---
_id: '2647'
abstract:
- lang: eng
  text: 'Our understanding of the role played by neurotransmitter receptors in the
    developing brain has advanced in recent years. The major excitatory and inhibitory
    neurotransmitters in the brain, glutamate and GABA, activate both ionotropic (ligand-gated
    ion channels) and metabotropic (G protein-coupled) receptors, and are generally
    associated with neuronal communication in the mature brain. However, before the
    emergence of their role in neurotransmission in adulthood, they also act to influence
    earlier developmental events, some of which occur prior to synapse formation:
    such as proliferation, migration, differentiation or survival processes during
    neural development. To fulfill these actions in the constructing of the nervous
    system, different types of glutamate and GABA receptors need to be expressed both
    at the right time and at the right place. The identification by molecular cloning
    of 16 ionotropic glutamate receptor subunits, eight metabotropic glutamate receptor
    subtypes, 21 ionotropic and two metabotropic GABA receptor subunits, some of which
    exist in alternatively splice variants, has enriched our appreciation of how molecular
    diversity leads to functional diversity in the brain. It now appears that many
    different types of glutamate and GABA receptor subunits have prominent expression
    in the embryonic and/or postnatal brain, whereas others are mainly present in
    the adult brain. Although the significance of this differential expression of
    subunits is not fully understood, it appears that the change in subunit composition
    is essential for normal development in particular brain regions. This review focuses
    on emerging information relating to the expression and role of glutamatergic and
    GABAergic neurotransmitter receptors during prenatal and postnatal development.'
author:
- first_name: Rafael
  full_name: Luján, Rafael
  last_name: Luján
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Guillermina
  full_name: López-Bendito, Guillermina
  last_name: López Bendito
citation:
  ama: Luján R, Shigemoto R, López Bendito G. Glutamate and GABA receptor signalling
    in the developing brain. <i>Neuroscience</i>. 2005;130(3):567-580. doi:<a href="https://doi.org/10.1016/j.neuroscience.2004.09.042">10.1016/j.neuroscience.2004.09.042</a>
  apa: Luján, R., Shigemoto, R., &#38; López Bendito, G. (2005). Glutamate and GABA
    receptor signalling in the developing brain. <i>Neuroscience</i>. Elsevier. <a
    href="https://doi.org/10.1016/j.neuroscience.2004.09.042">https://doi.org/10.1016/j.neuroscience.2004.09.042</a>
  chicago: Luján, Rafael, Ryuichi Shigemoto, and Guillermina López Bendito. “Glutamate
    and GABA Receptor Signalling in the Developing Brain.” <i>Neuroscience</i>. Elsevier,
    2005. <a href="https://doi.org/10.1016/j.neuroscience.2004.09.042">https://doi.org/10.1016/j.neuroscience.2004.09.042</a>.
  ieee: R. Luján, R. Shigemoto, and G. López Bendito, “Glutamate and GABA receptor
    signalling in the developing brain,” <i>Neuroscience</i>, vol. 130, no. 3. Elsevier,
    pp. 567–580, 2005.
  ista: Luján R, Shigemoto R, López Bendito G. 2005. Glutamate and GABA receptor signalling
    in the developing brain. Neuroscience. 130(3), 567–580.
  mla: Luján, Rafael, et al. “Glutamate and GABA Receptor Signalling in the Developing
    Brain.” <i>Neuroscience</i>, vol. 130, no. 3, Elsevier, 2005, pp. 567–80, doi:<a
    href="https://doi.org/10.1016/j.neuroscience.2004.09.042">10.1016/j.neuroscience.2004.09.042</a>.
  short: R. Luján, R. Shigemoto, G. López Bendito, Neuroscience 130 (2005) 567–580.
date_created: 2018-12-11T11:58:51Z
date_published: 2005-01-01T00:00:00Z
date_updated: 2020-07-14T12:45:44Z
day: '01'
doi: 10.1016/j.neuroscience.2004.09.042
extern: 1
intvolume: '       130'
issue: '3'
month: '01'
page: 567 - 580
publication: Neuroscience
publication_status: published
publisher: Elsevier
publist_id: '4250'
quality_controlled: 0
status: public
title: Glutamate and GABA receptor signalling in the developing brain
type: review
volume: 130
year: '2005'
...
---
_id: '2648'
abstract:
- lang: eng
  text: Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels are
    involved in the control of neuronal excitability and plasticity. In this study,
    we used immunoblotting and immunohistochemical techniques to reveal the developmental
    expression and subcellular distribution of the HCN1 subunit in the cerebellar
    cortex. During postnatal development, the spatio-temporal expression of HCN1 correlated
    well with the morphological events occurring during the ontogenesis of cerebellar
    interneurons. Using immunoblotting techniques, HCN1 was weakly detected during
    the first postnatal week and continued to increase throughout postnatal development,
    peaking at postnatal day (P)15. At the light-microscopic level, HCN1 immunoreactivity
    was very weak until P7 whereas from P10-12 to adulthood it was strongly detected
    in the lower third of the molecular layer and in the Purkinje cell layer. HCN1
    was present in axons running through the molecular layer and in the pericellular
    basket around Purkinje cells at P12, but in the periaxonal plexus (the pinceau)
    surrounding their initial segment only after P15. Using immunofluorescence, HCN1
    colocalized with GAD65 and synaptophysin, demonstrating that the subunit was present
    in inhibitory axons and axon terminals. At the electron-microscopic level, in
    adulthood, HCN1 immunoparticles were detected at postsynaptic sites in basket
    and Purkinje cells but most immunoparticles were found at presynaptic sites in
    basket cell axons and in terminals. In the axon terminals, the distribution of
    HCN1 was relatively uniform along the extrasynaptic plasma membrane; this was
    confirmed using quantitative techniques. The present findings suggest that HCN1
    channels may provide a significant route for modulating co-ordinated cerebellar
    synaptic transmission through basket cells.
author:
- first_name: Rafael
  full_name: Luján, Rafael
  last_name: Luján
- first_name: José
  full_name: Albasanz, José L
  last_name: Albasanz
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: José
  full_name: Juíz, José M
  last_name: Juíz
citation:
  ama: Luján R, Albasanz J, Shigemoto R, Juíz J. Preferential localization of the
    hyperpolarization-activated cyclic nucleotide-gated cation channel subunit HCN1
    in basket cell terminals of the rat cerebellum. <i>European Journal of Neuroscience</i>.
    2005;21(8):2073-2082. doi:<a href="https://doi.org/10.1111/j.1460-9568.2005.04043.x">10.1111/j.1460-9568.2005.04043.x</a>
  apa: Luján, R., Albasanz, J., Shigemoto, R., &#38; Juíz, J. (2005). Preferential
    localization of the hyperpolarization-activated cyclic nucleotide-gated cation
    channel subunit HCN1 in basket cell terminals of the rat cerebellum. <i>European
    Journal of Neuroscience</i>. Wiley-Blackwell. <a href="https://doi.org/10.1111/j.1460-9568.2005.04043.x">https://doi.org/10.1111/j.1460-9568.2005.04043.x</a>
  chicago: Luján, Rafael, José Albasanz, Ryuichi Shigemoto, and José Juíz. “Preferential
    Localization of the Hyperpolarization-Activated Cyclic Nucleotide-Gated Cation
    Channel Subunit HCN1 in Basket Cell Terminals of the Rat Cerebellum.” <i>European
    Journal of Neuroscience</i>. Wiley-Blackwell, 2005. <a href="https://doi.org/10.1111/j.1460-9568.2005.04043.x">https://doi.org/10.1111/j.1460-9568.2005.04043.x</a>.
  ieee: R. Luján, J. Albasanz, R. Shigemoto, and J. Juíz, “Preferential localization
    of the hyperpolarization-activated cyclic nucleotide-gated cation channel subunit
    HCN1 in basket cell terminals of the rat cerebellum,” <i>European Journal of Neuroscience</i>,
    vol. 21, no. 8. Wiley-Blackwell, pp. 2073–2082, 2005.
  ista: Luján R, Albasanz J, Shigemoto R, Juíz J. 2005. Preferential localization
    of the hyperpolarization-activated cyclic nucleotide-gated cation channel subunit
    HCN1 in basket cell terminals of the rat cerebellum. European Journal of Neuroscience.
    21(8), 2073–2082.
  mla: Luján, Rafael, et al. “Preferential Localization of the Hyperpolarization-Activated
    Cyclic Nucleotide-Gated Cation Channel Subunit HCN1 in Basket Cell Terminals of
    the Rat Cerebellum.” <i>European Journal of Neuroscience</i>, vol. 21, no. 8,
    Wiley-Blackwell, 2005, pp. 2073–82, doi:<a href="https://doi.org/10.1111/j.1460-9568.2005.04043.x">10.1111/j.1460-9568.2005.04043.x</a>.
  short: R. Luján, J. Albasanz, R. Shigemoto, J. Juíz, European Journal of Neuroscience
    21 (2005) 2073–2082.
date_created: 2018-12-11T11:58:52Z
date_published: 2005-04-01T00:00:00Z
date_updated: 2021-01-12T06:58:48Z
day: '01'
doi: 10.1111/j.1460-9568.2005.04043.x
extern: 1
intvolume: '        21'
issue: '8'
month: '04'
page: 2073 - 2082
publication: European Journal of Neuroscience
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4248'
quality_controlled: 0
status: public
title: Preferential localization of the hyperpolarization-activated cyclic nucleotide-gated
  cation channel subunit HCN1 in basket cell terminals of the rat cerebellum
type: journal_article
volume: 21
year: '2005'
...
---
_id: '2649'
abstract:
- lang: eng
  text: The number of ionotropic receptors in synapses is an essential factor for
    determining the efficacy of fast transmission. We estimated the number of functional
    AMPA receptors at single postsynaptic sites by a combination of two-photon uncaging
    of glutamate and the nonstationary fluctuation analysis in immature rat Purkinje
    cells (PCs), which receive a single type of excitatory input from climbing fibers.
    Areas of postsynaptic membrane specialization at the recorded synapses were measured
    by reconstruction of serial ultrathin sections. The number of functional AMPA
    receptors was proportional to the synaptic area with a density of ∼ 1280 receptors/μm
    2. Moreover, highly sensitive freeze-fracture replica labeling revealed a homogeneous
    density of immunogold particles for AMPA receptors in synaptic sites (910 ± 36
    particles/μm 2) and much lower density in extrasynaptic sites (19 ± 2 particles/μm
    2) in the immature PCs. Our results indicate that in this developing synapse,
    the efficacy of transmission is determined by the synaptic area.
author:
- first_name: Junichi
  full_name: Tanaka, Junichi
  last_name: Tanaka
- first_name: Masanori
  full_name: Matsuzaki, Masanori
  last_name: Matsuzaki
- first_name: Etsuko
  full_name: Tarusawa, Etsuko
  last_name: Tarusawa
- first_name: Akiko
  full_name: Momiyama, Akiko
  last_name: Momiyama
- first_name: Elek
  full_name: Molnár, Elek
  last_name: Molnár
- first_name: Haruo
  full_name: Kasai, Haruo
  last_name: Kasai
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
citation:
  ama: Tanaka J, Matsuzaki M, Tarusawa E, et al. Number and density of AMPA receptors
    in single synapses in immature cerebellum. <i>Journal of Neuroscience</i>. 2005;25(4):799-807.
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.4256-04.2005">10.1523/JNEUROSCI.4256-04.2005</a>
  apa: Tanaka, J., Matsuzaki, M., Tarusawa, E., Momiyama, A., Molnár, E., Kasai, H.,
    &#38; Shigemoto, R. (2005). Number and density of AMPA receptors in single synapses
    in immature cerebellum. <i>Journal of Neuroscience</i>. Society for Neuroscience.
    <a href="https://doi.org/10.1523/JNEUROSCI.4256-04.2005">https://doi.org/10.1523/JNEUROSCI.4256-04.2005</a>
  chicago: Tanaka, Junichi, Masanori Matsuzaki, Etsuko Tarusawa, Akiko Momiyama, Elek
    Molnár, Haruo Kasai, and Ryuichi Shigemoto. “Number and Density of AMPA Receptors
    in Single Synapses in Immature Cerebellum.” <i>Journal of Neuroscience</i>. Society
    for Neuroscience, 2005. <a href="https://doi.org/10.1523/JNEUROSCI.4256-04.2005">https://doi.org/10.1523/JNEUROSCI.4256-04.2005</a>.
  ieee: J. Tanaka <i>et al.</i>, “Number and density of AMPA receptors in single synapses
    in immature cerebellum,” <i>Journal of Neuroscience</i>, vol. 25, no. 4. Society
    for Neuroscience, pp. 799–807, 2005.
  ista: Tanaka J, Matsuzaki M, Tarusawa E, Momiyama A, Molnár E, Kasai H, Shigemoto
    R. 2005. Number and density of AMPA receptors in single synapses in immature cerebellum.
    Journal of Neuroscience. 25(4), 799–807.
  mla: Tanaka, Junichi, et al. “Number and Density of AMPA Receptors in Single Synapses
    in Immature Cerebellum.” <i>Journal of Neuroscience</i>, vol. 25, no. 4, Society
    for Neuroscience, 2005, pp. 799–807, doi:<a href="https://doi.org/10.1523/JNEUROSCI.4256-04.2005">10.1523/JNEUROSCI.4256-04.2005</a>.
  short: J. Tanaka, M. Matsuzaki, E. Tarusawa, A. Momiyama, E. Molnár, H. Kasai, R.
    Shigemoto, Journal of Neuroscience 25 (2005) 799–807.
date_created: 2018-12-11T11:58:52Z
date_published: 2005-01-26T00:00:00Z
date_updated: 2021-01-12T06:58:48Z
day: '26'
doi: 10.1523/JNEUROSCI.4256-04.2005
extern: 1
intvolume: '        25'
issue: '4'
month: '01'
page: 799 - 807
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '4249'
quality_controlled: 0
status: public
title: Number and density of AMPA receptors in single synapses in immature cerebellum
type: journal_article
volume: 25
year: '2005'
...
---
_id: '2650'
abstract:
- lang: eng
  text: 'Septohippocampal cholinergic neurons play key roles in learning and memory
    processes, and in the generation of hippocampal theta rhythm. The range of receptors
    for endogenous modulators expressed on these neurons is unclear. Here we describe
    GABAB 1a/b receptor (GABABR) and type 1 cannabinoid receptor (CB1R) expression
    in rat septal cholinergic [i.e. choline acetyltransferase (ChAT)-positive] cells.
    Using double immunofluorescent staining, we found that almost two-thirds of the
    cholinergic cells in the rat medial septum were GABABR positive, and that these
    cells had significantly larger somata than did GABABR-negative cholinergic neurons.
    We detected CB1R labelling in somata after axonal protein transport was blocked
    by colchicine. In these animals about one-third of the cholinergic cells were
    CB1R positive. These cells again had larger somata than CB1R-negative cholinergic
    neurons. The analyses confirmed that the size of GABABR-positive and CB 1R-positive
    cholinergic cells were alike, and all CB 1R-positive cholinergic cells were GABABR
    positive as well. CB1R-positive cells were invariably ChAT positive. All retrogradely
    labelled septohippocampal cholinergic cells were positive for GABABR and at least
    half of them also for CB1R. These data shed light on the existence of at least
    two cholinergic cell types in the medial septum: one expresses GABABR and CB1R,
    has large somata and projects to the hippocampus, whereas the other is negative
    for GABABR and CB1R and has smaller somata. The results also suggest that cholinergic
    transmission in the hippocampus is fine-tuned by endocannabinoid signalling.'
author:
- first_name: Gábor
  full_name: Nyíri, Gábor
  last_name: Nyíri
- first_name: Eszter
  full_name: Szabadits, Eszter
  last_name: Szabadits
- first_name: Csaba
  full_name: Cserép, Csaba
  last_name: Cserép
- first_name: Ken
  full_name: Mackie, Ken P
  last_name: Mackie
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Tamás
  full_name: Freund, Tamás F
  last_name: Freund
citation:
  ama: Nyíri G, Szabadits E, Cserép C, Mackie K, Shigemoto R, Freund T. GABAB and
    CB1 cannabinoid receptor expression identifies two types of septal cholinergic
    neurons. <i>European Journal of Neuroscience</i>. 2005;21(11):3034-3042. doi:<a
    href="https://doi.org/10.1111/j.1460-9568.2005.04146.x">10.1111/j.1460-9568.2005.04146.x</a>
  apa: Nyíri, G., Szabadits, E., Cserép, C., Mackie, K., Shigemoto, R., &#38; Freund,
    T. (2005). GABAB and CB1 cannabinoid receptor expression identifies two types
    of septal cholinergic neurons. <i>European Journal of Neuroscience</i>. Wiley-Blackwell.
    <a href="https://doi.org/10.1111/j.1460-9568.2005.04146.x">https://doi.org/10.1111/j.1460-9568.2005.04146.x</a>
  chicago: Nyíri, Gábor, Eszter Szabadits, Csaba Cserép, Ken Mackie, Ryuichi Shigemoto,
    and Tamás Freund. “GABAB and CB1 Cannabinoid Receptor Expression Identifies Two
    Types of Septal Cholinergic Neurons.” <i>European Journal of Neuroscience</i>.
    Wiley-Blackwell, 2005. <a href="https://doi.org/10.1111/j.1460-9568.2005.04146.x">https://doi.org/10.1111/j.1460-9568.2005.04146.x</a>.
  ieee: G. Nyíri, E. Szabadits, C. Cserép, K. Mackie, R. Shigemoto, and T. Freund,
    “GABAB and CB1 cannabinoid receptor expression identifies two types of septal
    cholinergic neurons,” <i>European Journal of Neuroscience</i>, vol. 21, no. 11.
    Wiley-Blackwell, pp. 3034–3042, 2005.
  ista: Nyíri G, Szabadits E, Cserép C, Mackie K, Shigemoto R, Freund T. 2005. GABAB
    and CB1 cannabinoid receptor expression identifies two types of septal cholinergic
    neurons. European Journal of Neuroscience. 21(11), 3034–3042.
  mla: Nyíri, Gábor, et al. “GABAB and CB1 Cannabinoid Receptor Expression Identifies
    Two Types of Septal Cholinergic Neurons.” <i>European Journal of Neuroscience</i>,
    vol. 21, no. 11, Wiley-Blackwell, 2005, pp. 3034–42, doi:<a href="https://doi.org/10.1111/j.1460-9568.2005.04146.x">10.1111/j.1460-9568.2005.04146.x</a>.
  short: G. Nyíri, E. Szabadits, C. Cserép, K. Mackie, R. Shigemoto, T. Freund, European
    Journal of Neuroscience 21 (2005) 3034–3042.
date_created: 2018-12-11T11:58:52Z
date_published: 2005-06-01T00:00:00Z
date_updated: 2021-01-12T06:58:49Z
day: '01'
doi: 10.1111/j.1460-9568.2005.04146.x
extern: 1
intvolume: '        21'
issue: '11'
month: '06'
page: 3034 - 3042
publication: European Journal of Neuroscience
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4247'
quality_controlled: 0
status: public
title: GABAB and CB1 cannabinoid receptor expression identifies two types of septal
  cholinergic neurons
type: journal_article
volume: 21
year: '2005'
...
---
_id: '2651'
abstract:
- lang: eng
  text: The GABAergic system, a major inhibitory regulator in the central nervous
    system, may also play important roles in peripheral nonneuronal tissues and cells.
    Recent studies showed that GABAB receptor is expressed in testis and sperm. To
    understand the role of the GABAergic system in spermiogenesis, we examined cellular
    localization of GABA and GABAB receptor subunits in rat spermatids by immunocytochemistry.
    Immunoreactivity for GABA was detected around acrosomal granules of spermatids
    during the Golgi and cap phases. GABAB(1) immunoreactivity was observed in the
    acrosomal vesicle of spermatids in Golgi phase, and during cap phase, this reactivity
    expanded to the entire region of the acrosome covering the nuclear membrane. The
    level of reactivity decreased gradually with maturation of spermatids. In contrast,
    GABAB(2) immunoreactivity was not observed in spermatids during Golgi phase but
    was detected in the equatorial region during cap phase. Both GABA immunoreactivity
    and GABAB(2) immunoreactivity were transferred to the residual cytoplasm during
    the release of spermatozoa. Electron microscopic immunocytochemistry revealed
    that, during cap phase, GABA and GABAB(1) were distributed within the whole acrosomal
    vesicle but not in the acrosomal granule. GABAB(2) immunoreactivity was observed
    in the narrow space between the inner acrosomal and nuclear membrane and was limited
    to the equatorial region of the spermatid head. These results indicate that the
    GABAergic system might be involved in regulation of spermiogenesis.
author:
- first_name: Kiyoto
  full_name: Kanbara, Kiyoto
  last_name: Kanbara
- first_name: Keiko
  full_name: Okamoto, Keiko
  last_name: Okamoto
- first_name: Sakashi
  full_name: Nomura, Sakashi
  last_name: Nomura
- first_name: Takeshi
  full_name: Kaneko, Takeshi
  last_name: Kaneko
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Haruhito
  full_name: Azuma, Haruhito
  last_name: Azuma
- first_name: Yoji
  full_name: Katsuoka, Yoji
  last_name: Katsuoka
- first_name: Masahiko
  full_name: Watanabe, Masahiko
  last_name: Watanabe
citation:
  ama: Kanbara K, Okamoto K, Nomura S, et al. Cellular localization of GABA and GABAB
    receptor subunit proteins during spermiogenesis in rat testis. <i>Journal of Andrology</i>.
    2005;26(4):485-493. doi:<a href="https://doi.org/10.2164/jandrol.04185">10.2164/jandrol.04185</a>
  apa: Kanbara, K., Okamoto, K., Nomura, S., Kaneko, T., Shigemoto, R., Azuma, H.,
    … Watanabe, M. (2005). Cellular localization of GABA and GABAB receptor subunit
    proteins during spermiogenesis in rat testis. <i>Journal of Andrology</i>. American
    Society of Andrology. <a href="https://doi.org/10.2164/jandrol.04185">https://doi.org/10.2164/jandrol.04185</a>
  chicago: Kanbara, Kiyoto, Keiko Okamoto, Sakashi Nomura, Takeshi Kaneko, Ryuichi
    Shigemoto, Haruhito Azuma, Yoji Katsuoka, and Masahiko Watanabe. “Cellular Localization
    of GABA and GABAB Receptor Subunit Proteins during Spermiogenesis in Rat Testis.”
    <i>Journal of Andrology</i>. American Society of Andrology, 2005. <a href="https://doi.org/10.2164/jandrol.04185">https://doi.org/10.2164/jandrol.04185</a>.
  ieee: K. Kanbara <i>et al.</i>, “Cellular localization of GABA and GABAB receptor
    subunit proteins during spermiogenesis in rat testis,” <i>Journal of Andrology</i>,
    vol. 26, no. 4. American Society of Andrology, pp. 485–493, 2005.
  ista: Kanbara K, Okamoto K, Nomura S, Kaneko T, Shigemoto R, Azuma H, Katsuoka Y,
    Watanabe M. 2005. Cellular localization of GABA and GABAB receptor subunit proteins
    during spermiogenesis in rat testis. Journal of Andrology. 26(4), 485–493.
  mla: Kanbara, Kiyoto, et al. “Cellular Localization of GABA and GABAB Receptor Subunit
    Proteins during Spermiogenesis in Rat Testis.” <i>Journal of Andrology</i>, vol.
    26, no. 4, American Society of Andrology, 2005, pp. 485–93, doi:<a href="https://doi.org/10.2164/jandrol.04185">10.2164/jandrol.04185</a>.
  short: K. Kanbara, K. Okamoto, S. Nomura, T. Kaneko, R. Shigemoto, H. Azuma, Y.
    Katsuoka, M. Watanabe, Journal of Andrology 26 (2005) 485–493.
date_created: 2018-12-11T11:58:52Z
date_published: 2005-07-01T00:00:00Z
date_updated: 2021-01-12T06:58:50Z
day: '01'
doi: 10.2164/jandrol.04185
extern: 1
intvolume: '        26'
issue: '4'
month: '07'
page: 485 - 493
publication: Journal of Andrology
publication_status: published
publisher: American Society of Andrology
publist_id: '4246'
quality_controlled: 0
status: public
title: Cellular localization of GABA and GABAB receptor subunit proteins during spermiogenesis
  in rat testis
type: journal_article
volume: 26
year: '2005'
...
---
_id: '2652'
abstract:
- lang: eng
  text: We studied neurogliaform neurons in the stratum lacunosum moleculare of the
    CA1 hippocampal area. These interneurons have short stellate dendrites and an
    extensive axonal arbor mainly located in the stratum lacunosum moleculare. Single-cell
    reverse transcription-PCR showed that these neurons were GABAergic and that the
    majority expressed mRNA for neuropeptide Y. Most neurogliaform neurons tested
    were immunoreactive for α-actinin-2, and many stratum lacunosum moleculare interneurons
    coexpressed α-actinin-2 and neuropeptide Y. Neurogliaform neurons received monosynaptic,
    DNQX-sensitive excitatory input from the perforant path, and 40 Hz stimulation
    of this input evoked EPSCs displaying either depression or initial facilitation,
    followed by depression. Paired recordings performed between neurogliaform neurons
    showed that 85% of pairs were electrically connected and 70% were also connected
    via GABAergic synapses. Injection of sine waveforms into neurons during paired
    recordings resulted in transmission of the waveforms through the electrical synapse.
    Unitary IPSCs recorded from neurogliaform pairs readily fatigued, had a slow decay,
    and had a strong depression of the synaptic response at a 5 Hz stimulation frequency
    that was antagonized by the GABA B antagonist (2S)-3-[[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl](phenylmethyl)
    phosphinic acid (CGP55845). The amplitude of the first IPSC during the 5 Hz stimulation
    was also increased by CGP55845, suggesting a tonic inhibition of synaptic transmission.
    A small unitary GABA B-mediated IPSC could also be detected, providing the first
    evidence for such a component between GABAergic interneurons. Electron microscopic
    localization of the GABA B1 subunit at neurogliaform synapses revealed the protein
    in both presynaptic and postsynaptic membranes. Our data disclose a novel interneuronal
    network well suited for modulating the flow of information between the entorhinal
    cortex and CA1 hippocampus.
author:
- first_name: Christopher
  full_name: Price, Christopher J
  last_name: Price
- first_name: Bruno
  full_name: Cauli, Bruno
  last_name: Cauli
- first_name: Endre
  full_name: Kovács, Endre R
  last_name: Kovács
- first_name: Ákos
  full_name: Kulik, Ákos
  last_name: Kulik
- first_name: Bertrand
  full_name: Lambolez, Bertrand
  last_name: Lambolez
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Marco
  full_name: Capogna,Marco
  last_name: Capogna
citation:
  ama: Price C, Cauli B, Kovács E, et al. Neurogliaform neurons form a novel inhibitory
    network in the hippocampal CA1 area. <i>Journal of Neuroscience</i>. 2005;25(29):6775-6786.
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.1135-05.2005">10.1523/JNEUROSCI.1135-05.2005</a>
  apa: Price, C., Cauli, B., Kovács, E., Kulik, Á., Lambolez, B., Shigemoto, R., &#38;
    Capogna, M. (2005). Neurogliaform neurons form a novel inhibitory network in the
    hippocampal CA1 area. <i>Journal of Neuroscience</i>. Society for Neuroscience.
    <a href="https://doi.org/10.1523/JNEUROSCI.1135-05.2005">https://doi.org/10.1523/JNEUROSCI.1135-05.2005</a>
  chicago: Price, Christopher, Bruno Cauli, Endre Kovács, Ákos Kulik, Bertrand Lambolez,
    Ryuichi Shigemoto, and Marco Capogna. “Neurogliaform Neurons Form a Novel Inhibitory
    Network in the Hippocampal CA1 Area.” <i>Journal of Neuroscience</i>. Society
    for Neuroscience, 2005. <a href="https://doi.org/10.1523/JNEUROSCI.1135-05.2005">https://doi.org/10.1523/JNEUROSCI.1135-05.2005</a>.
  ieee: C. Price <i>et al.</i>, “Neurogliaform neurons form a novel inhibitory network
    in the hippocampal CA1 area,” <i>Journal of Neuroscience</i>, vol. 25, no. 29.
    Society for Neuroscience, pp. 6775–6786, 2005.
  ista: Price C, Cauli B, Kovács E, Kulik Á, Lambolez B, Shigemoto R, Capogna M. 2005.
    Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area.
    Journal of Neuroscience. 25(29), 6775–6786.
  mla: Price, Christopher, et al. “Neurogliaform Neurons Form a Novel Inhibitory Network
    in the Hippocampal CA1 Area.” <i>Journal of Neuroscience</i>, vol. 25, no. 29,
    Society for Neuroscience, 2005, pp. 6775–86, doi:<a href="https://doi.org/10.1523/JNEUROSCI.1135-05.2005">10.1523/JNEUROSCI.1135-05.2005</a>.
  short: C. Price, B. Cauli, E. Kovács, Á. Kulik, B. Lambolez, R. Shigemoto, M. Capogna,
    Journal of Neuroscience 25 (2005) 6775–6786.
date_created: 2018-12-11T11:58:53Z
date_published: 2005-07-20T00:00:00Z
date_updated: 2021-01-12T06:58:50Z
day: '20'
doi: 10.1523/JNEUROSCI.1135-05.2005
extern: 1
intvolume: '        25'
issue: '29'
month: '07'
page: 6775 - 6786
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '4245'
quality_controlled: 0
status: public
title: Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1
  area
type: journal_article
volume: 25
year: '2005'
...
---
_id: '2653'
abstract:
- lang: eng
  text: Synaptic vesicle release occurs at a specialized membrane domain known as
    the presynaptic active zone (AZ). Several membrane proteins are involved in the
    vesicle release processes such as docking, priming, and exocytotic fusion. Cytomatrix
    at the active zone (CAZ) proteins are structural components of the AZ and are
    highly concentrated in it. Localization of other release-related proteins including
    target soluble N-ethylmaleimide-sensitive-factor attachment protein receptor (t-SNARE)
    proteins, however, has not been well demonstrated in the AZ. Here, we used sodium
    dodecyl sulfate-digested freeze-fracture replica labeling (SDS-FRL) to analyze
    quantitatively the distribution of CAZ and t-SNARE proteins in the hippocampal
    CA3 area. The AZ in replicated membrane was identified by immunolabeling for CAZ
    proteins (CAZ-associated structural protein [CAST] and Bassoon). Clusters of immunogold
    particles for these proteins were found on the P-face of presynaptic terminals
    of the mossy fiber and associational/commissural (AJC) fiber. Co-labeling with
    CAST revealed distribution of the t-SNARE proteins syntaxin and synaptosomal-associated
    protein of 25 kDa (SNAP-25) in the AZ as well as in the extrasynaptic membrane
    surrounding the AZ (SZ). Quantitative analysis demonstrated that the density of
    immunoparticles for CAST in the AZ was more than 100 times higher than in the
    SZ, whereas that for syntaxin and SNAP-25 was not significantly different between
    the AZ and SZ in both the A/C and mossy fiber terminals. These results support
    the involvement of the t-SNARE proteins in exocytotic fusion in the AZ and the
    role of CAST in specialization of the membrane domain for the AZ.
author:
- first_name: Akari
  full_name: Hagiwara, Akari
  last_name: Hagiwara
- first_name: Yugo
  full_name: Fukazawa, Yugo
  last_name: Fukazawa
- first_name: Maki
  full_name: Deguchi-Tawarada, Maki
  last_name: Deguchi Tawarada
- first_name: Toshihisa
  full_name: Ohtsuka, Toshihisa
  last_name: Ohtsuka
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
citation:
  ama: Hagiwara A, Fukazawa Y, Deguchi Tawarada M, Ohtsuka T, Shigemoto R. Differential
    distribution of release-related proteins in the hippocampal CA3 area as revealed
    by freeze-fracture replica labeling. <i>Journal of Comparative Neurology</i>.
    2005;489(2):195-216. doi:<a href="https://doi.org/10.1002/cne.20633">10.1002/cne.20633</a>
  apa: Hagiwara, A., Fukazawa, Y., Deguchi Tawarada, M., Ohtsuka, T., &#38; Shigemoto,
    R. (2005). Differential distribution of release-related proteins in the hippocampal
    CA3 area as revealed by freeze-fracture replica labeling. <i>Journal of Comparative
    Neurology</i>. Wiley-Blackwell. <a href="https://doi.org/10.1002/cne.20633">https://doi.org/10.1002/cne.20633</a>
  chicago: Hagiwara, Akari, Yugo Fukazawa, Maki Deguchi Tawarada, Toshihisa Ohtsuka,
    and Ryuichi Shigemoto. “Differential Distribution of Release-Related Proteins
    in the Hippocampal CA3 Area as Revealed by Freeze-Fracture Replica Labeling.”
    <i>Journal of Comparative Neurology</i>. Wiley-Blackwell, 2005. <a href="https://doi.org/10.1002/cne.20633">https://doi.org/10.1002/cne.20633</a>.
  ieee: A. Hagiwara, Y. Fukazawa, M. Deguchi Tawarada, T. Ohtsuka, and R. Shigemoto,
    “Differential distribution of release-related proteins in the hippocampal CA3
    area as revealed by freeze-fracture replica labeling,” <i>Journal of Comparative
    Neurology</i>, vol. 489, no. 2. Wiley-Blackwell, pp. 195–216, 2005.
  ista: Hagiwara A, Fukazawa Y, Deguchi Tawarada M, Ohtsuka T, Shigemoto R. 2005.
    Differential distribution of release-related proteins in the hippocampal CA3 area
    as revealed by freeze-fracture replica labeling. Journal of Comparative Neurology.
    489(2), 195–216.
  mla: Hagiwara, Akari, et al. “Differential Distribution of Release-Related Proteins
    in the Hippocampal CA3 Area as Revealed by Freeze-Fracture Replica Labeling.”
    <i>Journal of Comparative Neurology</i>, vol. 489, no. 2, Wiley-Blackwell, 2005,
    pp. 195–216, doi:<a href="https://doi.org/10.1002/cne.20633">10.1002/cne.20633</a>.
  short: A. Hagiwara, Y. Fukazawa, M. Deguchi Tawarada, T. Ohtsuka, R. Shigemoto,
    Journal of Comparative Neurology 489 (2005) 195–216.
date_created: 2018-12-11T11:58:53Z
date_published: 2005-08-22T00:00:00Z
date_updated: 2021-01-12T06:58:50Z
day: '22'
doi: 10.1002/cne.20633
extern: 1
intvolume: '       489'
issue: '2'
month: '08'
page: 195 - 216
publication: Journal of Comparative Neurology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4244'
quality_controlled: 0
status: public
title: Differential distribution of release-related proteins in the hippocampal CA3
  area as revealed by freeze-fracture replica labeling
type: journal_article
volume: 489
year: '2005'
...
---
_id: '2654'
abstract:
- lang: eng
  text: Presynaptic metabotropic glutamate receptors (mGluRs) show a highly selective
    expression and subcellular location in nerve terminals modulating neurotransmitter
    release. We have demonstrated that alternatively spliced variants of mGluR8, mGluR8a
    and mGluR8b, have an overlapping distribution in the hippocampus, and besides
    perforant path terminals, they are expressed in the presynaptic active zone of
    boutons making synapses selectively with several types of GABAergic interneurons,
    primarily in the stratum oriens. Boutons labeled for mGluR8 formed either type
    I or type II synapses, and the latter were GABAergic. Some mGluR8-positive boutons
    also expressed mGluR7 or vasoactive intestinal polypeptide. Interneurons strongly
    immunopositive for the muscarinic M2 or the mGlu1 receptors were the primary targets
    of mGluR8-containing terminals in the stratum oriens, but only neurochemically
    distinct subsets were innervated by mGluR8-enriched terminals. The majority of
    M2-positive neurons were mGluR8 innervated, but a minority, which expresses somatostatin,
    was not. Rare neurons coexpressing calretinin and M2 were consistently targeted
    by mGluR8-positive boutons. In vivo recording and labeling of an mGluR8-decorated
    and strongly M2-positive interneuron revealed a trilaminar cell with complex spike
    bursts during theta oscillations and strong discharge during sharp wave/ripple
    events. The trilaminar cell had a large projection from the CA1 area to the subiculum
    and a preferential innervation of interneurons in the CA1 area in addition to
    pyramidal cell somata and dendrites. The postsynaptic interneuron type-specific
    expression of the high-efficacy presynaptic mGluR8 in both putative glutamatergic
    and in identified GABAergic terminals predicts a role in adjusting the activity
    of interneurons depending on the level of network activity.
author:
- first_name: Francesco
  full_name: Ferraguti, Francesco
  last_name: Ferraguti
- first_name: Thomas
  full_name: Klausberger,Thomas
  last_name: Klausberger
- first_name: Philip
  full_name: Cobden, Philip M
  last_name: Cobden
- first_name: Agnès
  full_name: Baude, Agnès
  last_name: Baude
- first_name: John
  full_name: Roberts, John D
  last_name: Roberts
- first_name: Péter
  full_name: Szűcs, Péter
  last_name: Szűcs
- first_name: Ayae
  full_name: Kinoshita, Ayae
  last_name: Kinoshita
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Péter
  full_name: Somogyi, Péter
  last_name: Somogyi
- first_name: Yannis
  full_name: Dalezios, Yannis
  last_name: Dalezios
citation:
  ama: Ferraguti F, Klausberger T, Cobden P, et al.  Metabotropic glutamate receptor
    8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus.
    <i>Journal of Neuroscience</i>. 2005;25(45):10520-10536. doi:<a href="https://doi.org/10.1523/JNEUROSCI.2547-05.2005">10.1523/JNEUROSCI.2547-05.2005</a>
  apa: Ferraguti, F., Klausberger, T., Cobden, P., Baude, A., Roberts, J., Szűcs,
    P., … Dalezios, Y. (2005).  Metabotropic glutamate receptor 8-expressing nerve
    terminals target subsets of GABAergic neurons in the hippocampus. <i>Journal of
    Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.2547-05.2005">https://doi.org/10.1523/JNEUROSCI.2547-05.2005</a>
  chicago: Ferraguti, Francesco, Thomas Klausberger, Philip Cobden, Agnès Baude, John
    Roberts, Péter Szűcs, Ayae Kinoshita, Ryuichi Shigemoto, Péter Somogyi, and Yannis
    Dalezios. “ Metabotropic Glutamate Receptor 8-Expressing Nerve Terminals Target
    Subsets of GABAergic Neurons in the Hippocampus.” <i>Journal of Neuroscience</i>.
    Society for Neuroscience, 2005. <a href="https://doi.org/10.1523/JNEUROSCI.2547-05.2005">https://doi.org/10.1523/JNEUROSCI.2547-05.2005</a>.
  ieee: F. Ferraguti <i>et al.</i>, “ Metabotropic glutamate receptor 8-expressing
    nerve terminals target subsets of GABAergic neurons in the hippocampus,” <i>Journal
    of Neuroscience</i>, vol. 25, no. 45. Society for Neuroscience, pp. 10520–10536,
    2005.
  ista: Ferraguti F, Klausberger T, Cobden P, Baude A, Roberts J, Szűcs P, Kinoshita
    A, Shigemoto R, Somogyi P, Dalezios Y. 2005.  Metabotropic glutamate receptor
    8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus.
    Journal of Neuroscience. 25(45), 10520–10536.
  mla: Ferraguti, Francesco, et al. “ Metabotropic Glutamate Receptor 8-Expressing
    Nerve Terminals Target Subsets of GABAergic Neurons in the Hippocampus.” <i>Journal
    of Neuroscience</i>, vol. 25, no. 45, Society for Neuroscience, 2005, pp. 10520–36,
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.2547-05.2005">10.1523/JNEUROSCI.2547-05.2005</a>.
  short: F. Ferraguti, T. Klausberger, P. Cobden, A. Baude, J. Roberts, P. Szűcs,
    A. Kinoshita, R. Shigemoto, P. Somogyi, Y. Dalezios, Journal of Neuroscience 25
    (2005) 10520–10536.
date_created: 2018-12-11T11:58:53Z
date_published: 2005-11-09T00:00:00Z
date_updated: 2021-01-12T06:58:51Z
day: '09'
doi: 10.1523/JNEUROSCI.2547-05.2005
extern: 1
intvolume: '        25'
issue: '45'
month: '11'
page: 10520 - 10536
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '4242'
quality_controlled: 0
status: public
title: ' Metabotropic glutamate receptor 8-expressing nerve terminals target subsets
  of GABAergic neurons in the hippocampus'
type: journal_article
volume: 25
year: '2005'
...
---
_id: '2655'
abstract:
- lang: eng
  text: Input-dependent left-right asymmetry of NMDA receptor ε2 (NR2B) subunit allocation
    was discovered in hippocampal Schaffer collateral (Sch) and commissural fiber
    pyramidal cell synapses (Kawakami et al., 2003). To investigate whether this asymmetrical
    ε2 allocation is also related to the types of the postsynaptic cells, we compared
    postembedding immunogold labeling for ε2 in left and right Sch synapses on pyramidal
    cells and interneurons. To facilitate the detection of ε2 density difference,
    we used ε1 (NR2A) knock-out (KO) mice, which have a simplified NMDA receptor subunit
    composition. The labeling density for ε2 but not ζ1 (NR1) and subtype 2/3 glutamate
    receptor (GluR2/3) in Sch-CA1 pyramidal cell synapses was significantly different
    between the left and right hippocampus with opposite directions in strata oriens
    and radiatum; the left to right ratio of ε2 labeling density was 1:1.50 in stratum
    oriens and 1.44:1 in stratum radiatum. No significant difference, however, was
    detected in CA1 stratum radiatum between the left and right Sch-GluR4-positive
    (mostly parvalbumin-positive) and Sch-GluR4-negative interneuron synapses. Consistent
    with the anatomical asymmetry, the amplitude ratio of NMDA EPSCs to non-NMDA EPSCs
    in pyramidal cells was approximately two times larger in right than left stratum
    radiatum and vice versa in stratum oriens of ε1 KO mice. Moreover, the amplitude
    of long-term potentiation in the Sch-CA1 synapses of left stratum radiatum was
    significantly larger than that in the right corresponding synapses. These results
    indicate that the asymmetry of ε2 distribution is target cell specific, resulting
    in the left-right difference in NMDA receptor content and plasticity in Sch-CA1
    pyramidal cell synapses in ε1 KO mice.
author:
- first_name: Yue
  full_name: Wu, Yue
  last_name: Wu
- first_name: Ryosuke
  full_name: Kawakami, Ryosuke
  last_name: Kawakami
- first_name: Yoshiaki
  full_name: Shinohara, Yoshiaki
  last_name: Shinohara
- first_name: Masahiro
  full_name: Fukaya, Masahiro
  last_name: Fukaya
- first_name: Kenji
  full_name: Sakimura, Kenji
  last_name: Sakimura
- first_name: Masayoshi
  full_name: Mishina, Masayoshi
  last_name: Mishina
- first_name: Masahiko
  full_name: Watanabe, Masahiko
  last_name: Watanabe
- first_name: Isao
  full_name: Ito, Isao
  last_name: Ito
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
citation:
  ama: Wu Y, Kawakami R, Shinohara Y, et al. Target-cell-specific left-right asymmetry
    of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out
    mice. <i>Journal of Neuroscience</i>. 2005;25(40):9213-9226. doi:<a href="https://doi.org/10.1523/JNEUROSCI.2134-05.2005">10.1523/JNEUROSCI.2134-05.2005</a>
  apa: Wu, Y., Kawakami, R., Shinohara, Y., Fukaya, M., Sakimura, K., Mishina, M.,
    … Shigemoto, R. (2005). Target-cell-specific left-right asymmetry of NMDA receptor
    content in Schaffer collateral synapses in ε1/NR2A knock-out mice. <i>Journal
    of Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.2134-05.2005">https://doi.org/10.1523/JNEUROSCI.2134-05.2005</a>
  chicago: Wu, Yue, Ryosuke Kawakami, Yoshiaki Shinohara, Masahiro Fukaya, Kenji Sakimura,
    Masayoshi Mishina, Masahiko Watanabe, Isao Ito, and Ryuichi Shigemoto. “Target-Cell-Specific
    Left-Right Asymmetry of NMDA Receptor Content in Schaffer Collateral Synapses
    in Ε1/NR2A Knock-out Mice.” <i>Journal of Neuroscience</i>. Society for Neuroscience,
    2005. <a href="https://doi.org/10.1523/JNEUROSCI.2134-05.2005">https://doi.org/10.1523/JNEUROSCI.2134-05.2005</a>.
  ieee: Y. Wu <i>et al.</i>, “Target-cell-specific left-right asymmetry of NMDA receptor
    content in Schaffer collateral synapses in ε1/NR2A knock-out mice,” <i>Journal
    of Neuroscience</i>, vol. 25, no. 40. Society for Neuroscience, pp. 9213–9226,
    2005.
  ista: Wu Y, Kawakami R, Shinohara Y, Fukaya M, Sakimura K, Mishina M, Watanabe M,
    Ito I, Shigemoto R. 2005. Target-cell-specific left-right asymmetry of NMDA receptor
    content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal of
    Neuroscience. 25(40), 9213–9226.
  mla: Wu, Yue, et al. “Target-Cell-Specific Left-Right Asymmetry of NMDA Receptor
    Content in Schaffer Collateral Synapses in Ε1/NR2A Knock-out Mice.” <i>Journal
    of Neuroscience</i>, vol. 25, no. 40, Society for Neuroscience, 2005, pp. 9213–26,
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.2134-05.2005">10.1523/JNEUROSCI.2134-05.2005</a>.
  short: Y. Wu, R. Kawakami, Y. Shinohara, M. Fukaya, K. Sakimura, M. Mishina, M.
    Watanabe, I. Ito, R. Shigemoto, Journal of Neuroscience 25 (2005) 9213–9226.
date_created: 2018-12-11T11:58:54Z
date_published: 2005-10-05T00:00:00Z
date_updated: 2021-01-12T06:58:51Z
day: '05'
doi: 10.1523/JNEUROSCI.2134-05.2005
extern: 1
intvolume: '        25'
issue: '40'
month: '10'
page: 9213 - 9226
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '4243'
quality_controlled: 0
status: public
title: Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer
  collateral synapses in ε1/NR2A knock-out mice
type: journal_article
volume: 25
year: '2005'
...
---
_id: '2656'
abstract:
- lang: eng
  text: Previous studies have shown that neurons in the sacral dorsal commissural
    nucleus (SDCN) express neurokinin-1 receptor (NK1R) and can be modulated by the
    co-release of GABA and glycine (Gly) from single presynaptic terminal. These results
    raise the possibility that GABA/Gly-cocontaining terminals might make synaptic
    contacts with NK1R-expressing neurons in the SDCN. In order to provide morphological
    evidence for this hypothesis, the triple-immunohistochemical studies were performed
    in the SDCN. Triple-immunofluorescence histochemical study showed that some axon
    terminals in close association with NK1R-immunopositive (NK1R-ip) neurons in the
    SDCN were immunopositive for both glutamic acid decarboxylase (GAD) and glycine
    transporter 2 (GlyT2). In electron microscopic dual- and triple-immunohistochemistry
    for GAD/GlyT2, GAD/NK1R, GlyT2/NK1R, or GAD/GlyT2/NK1R also revealed dually labeled
    (GAD/GlyT2-ip) synaptic terminals upon SDCN neurons, as well as GAD- and/or GlyT2-ip
    axon terminals in synaptic contact with NK1R-ip SDCN neurons. These results suggested
    that some synaptic terminals upon NK1R-expressing SDCN neurons co-released both
    GABA and Gly.
author:
- first_name: Yu
  full_name: Feng, Yu-Peng
  last_name: Feng
- first_name: Yun
  full_name: Li, Yun-Qing
  last_name: Li
- first_name: Wen
  full_name: Wang, Wen
  last_name: Wang
- first_name: Sheng
  full_name: Wu, Sheng-Xi
  last_name: Wu
- first_name: Tao
  full_name: Chen, Tao
  last_name: Chen
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Noboru
  full_name: Mizuno, Noboru
  last_name: Mizuno
citation:
  ama: Feng Y, Li Y, Wang W, et al. Morphological evidence for GABA/glycine-cocontaining
    terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in
    the sacral dorsal commissural nucleus of the rat. <i>Neuroscience Letters</i>.
    2005;388(3):144-148. doi:<a href="https://doi.org/10.1016/j.neulet.2005.06.068">10.1016/j.neulet.2005.06.068</a>
  apa: Feng, Y., Li, Y., Wang, W., Wu, S., Chen, T., Shigemoto, R., &#38; Mizuno,
    N. (2005). Morphological evidence for GABA/glycine-cocontaining terminals in synaptic
    contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural
    nucleus of the rat. <i>Neuroscience Letters</i>. Elsevier. <a href="https://doi.org/10.1016/j.neulet.2005.06.068">https://doi.org/10.1016/j.neulet.2005.06.068</a>
  chicago: Feng, Yu, Yun Li, Wen Wang, Sheng Wu, Tao Chen, Ryuichi Shigemoto, and
    Noboru Mizuno. “Morphological Evidence for GABA/Glycine-Cocontaining Terminals
    in Synaptic Contact with Neurokinin-1 Receptor-Expressing Neurons in the Sacral
    Dorsal Commissural Nucleus of the Rat.” <i>Neuroscience Letters</i>. Elsevier,
    2005. <a href="https://doi.org/10.1016/j.neulet.2005.06.068">https://doi.org/10.1016/j.neulet.2005.06.068</a>.
  ieee: Y. Feng <i>et al.</i>, “Morphological evidence for GABA/glycine-cocontaining
    terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in
    the sacral dorsal commissural nucleus of the rat,” <i>Neuroscience Letters</i>,
    vol. 388, no. 3. Elsevier, pp. 144–148, 2005.
  ista: Feng Y, Li Y, Wang W, Wu S, Chen T, Shigemoto R, Mizuno N. 2005. Morphological
    evidence for GABA/glycine-cocontaining terminals in synaptic contact with neurokinin-1
    receptor-expressing neurons in the sacral dorsal commissural nucleus of the rat.
    Neuroscience Letters. 388(3), 144–148.
  mla: Feng, Yu, et al. “Morphological Evidence for GABA/Glycine-Cocontaining Terminals
    in Synaptic Contact with Neurokinin-1 Receptor-Expressing Neurons in the Sacral
    Dorsal Commissural Nucleus of the Rat.” <i>Neuroscience Letters</i>, vol. 388,
    no. 3, Elsevier, 2005, pp. 144–48, doi:<a href="https://doi.org/10.1016/j.neulet.2005.06.068">10.1016/j.neulet.2005.06.068</a>.
  short: Y. Feng, Y. Li, W. Wang, S. Wu, T. Chen, R. Shigemoto, N. Mizuno, Neuroscience
    Letters 388 (2005) 144–148.
date_created: 2018-12-11T11:58:54Z
date_published: 2005-11-18T00:00:00Z
date_updated: 2021-01-12T06:58:51Z
day: '18'
doi: 10.1016/j.neulet.2005.06.068
extern: 1
intvolume: '       388'
issue: '3'
month: '11'
page: 144 - 148
publication: Neuroscience Letters
publication_status: published
publisher: Elsevier
publist_id: '4241'
quality_controlled: 0
status: public
title: Morphological evidence for GABA/glycine-cocontaining terminals in synaptic
  contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural
  nucleus of the rat
type: journal_article
volume: 388
year: '2005'
...
---
_id: '2658'
abstract:
- lang: eng
  text: Enhanced glutamatergic neurotransmission via the subthalamopallidal or subthalamonigral
    projection seems crucial for developing parkinsonian motor signs. In the present
    study, the possible changes in the expression of metabotropic glutamate receptors
    (mGluRs) were examined in the basal ganglia of a primate model for Parkinson's
    disease. When the patterns of immunohistochemical localization of mGluRs in monkeys
    administered systemically with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
    were analysed in comparison with normal controls, we found that expression of
    mGluR1α, but not of other subtypes, was significantly reduced in the internal
    and external segments of the globus pallidus and the substantia nigra pars reticulata.
    To elucidate the functional role of mGluR1 in the control of pallidal neuron activity,
    extracellular unit recordings combined with intrapallidal microinjections of mGluR1-related
    agents were then performed in normal and parkinsonian monkeys. In normal awake
    conditions, the spontaneous firing rates of neurons in the pallidal complex were
    increased by DHPG, a selective agonist of group I mGluRs, whereas they were decreased
    by AIDA, a selective antagonist of group I mGluRs, or LY367385, a selective antagonist
    of mGluR1. These electrophysiological data strongly indicate that the excitatory
    mechanism of pallidal neurons by glutamate is mediated at least partly through
    mGluR1. The effects of the mGluR1-related agents on neuronal firing in the internal
    pallidal segment became rather obscure after MPTP treatment. Our results suggest
    that the specific down-regulation of pallidal and nigral mGluR1 ot in the parkinsonian
    state may exert a compensatory action to reverse the overactivity of the subthalamic
    nucleus-derived glutamatergic input that is generated in the disease.
author:
- first_name: Katsuyuki
  full_name: Kaneda, Katsuyuki
  last_name: Kaneda
- first_name: Yoshihisa
  full_name: Tachibana, Yoshihisa
  last_name: Tachibana
- first_name: Michiko
  full_name: Imanishi, Michiko
  last_name: Imanishi
- first_name: Hitoshi
  full_name: Kita, Hitoshi
  last_name: Kita
- first_name: Ryuichi
  full_name: Ryuichi Shigemoto
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Atsushi
  full_name: Nambu, Atsushi
  last_name: Nambu
- first_name: Masahiko
  full_name: Takada, Masahiko
  last_name: Takada
citation:
  ama: Kaneda K, Tachibana Y, Imanishi M, et al. Down-regulation of metabotropic glutamate
    receptor 1α in globus pallidus and substantia nigra of parkinsonian monkeys. <i>European
    Journal of Neuroscience</i>. 2005;22(12):3241-3254. doi:<a href="https://doi.org/10.1111/j.1460-9568.2005.04488.x">10.1111/j.1460-9568.2005.04488.x</a>
  apa: Kaneda, K., Tachibana, Y., Imanishi, M., Kita, H., Shigemoto, R., Nambu, A.,
    &#38; Takada, M. (2005). Down-regulation of metabotropic glutamate receptor 1α
    in globus pallidus and substantia nigra of parkinsonian monkeys. <i>European Journal
    of Neuroscience</i>. Wiley-Blackwell. <a href="https://doi.org/10.1111/j.1460-9568.2005.04488.x">https://doi.org/10.1111/j.1460-9568.2005.04488.x</a>
  chicago: Kaneda, Katsuyuki, Yoshihisa Tachibana, Michiko Imanishi, Hitoshi Kita,
    Ryuichi Shigemoto, Atsushi Nambu, and Masahiko Takada. “Down-Regulation of Metabotropic
    Glutamate Receptor 1α in Globus Pallidus and Substantia Nigra of Parkinsonian
    Monkeys.” <i>European Journal of Neuroscience</i>. Wiley-Blackwell, 2005. <a href="https://doi.org/10.1111/j.1460-9568.2005.04488.x">https://doi.org/10.1111/j.1460-9568.2005.04488.x</a>.
  ieee: K. Kaneda <i>et al.</i>, “Down-regulation of metabotropic glutamate receptor
    1α in globus pallidus and substantia nigra of parkinsonian monkeys,” <i>European
    Journal of Neuroscience</i>, vol. 22, no. 12. Wiley-Blackwell, pp. 3241–3254,
    2005.
  ista: Kaneda K, Tachibana Y, Imanishi M, Kita H, Shigemoto R, Nambu A, Takada M.
    2005. Down-regulation of metabotropic glutamate receptor 1α in globus pallidus
    and substantia nigra of parkinsonian monkeys. European Journal of Neuroscience.
    22(12), 3241–3254.
  mla: Kaneda, Katsuyuki, et al. “Down-Regulation of Metabotropic Glutamate Receptor
    1α in Globus Pallidus and Substantia Nigra of Parkinsonian Monkeys.” <i>European
    Journal of Neuroscience</i>, vol. 22, no. 12, Wiley-Blackwell, 2005, pp. 3241–54,
    doi:<a href="https://doi.org/10.1111/j.1460-9568.2005.04488.x">10.1111/j.1460-9568.2005.04488.x</a>.
  short: K. Kaneda, Y. Tachibana, M. Imanishi, H. Kita, R. Shigemoto, A. Nambu, M.
    Takada, European Journal of Neuroscience 22 (2005) 3241–3254.
date_created: 2018-12-11T11:58:55Z
date_published: 2005-12-01T00:00:00Z
date_updated: 2021-01-12T06:58:52Z
day: '01'
doi: 10.1111/j.1460-9568.2005.04488.x
extern: 1
intvolume: '        22'
issue: '12'
month: '12'
page: 3241 - 3254
publication: European Journal of Neuroscience
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4240'
quality_controlled: 0
status: public
title: Down-regulation of metabotropic glutamate receptor 1α in globus pallidus and
  substantia nigra of parkinsonian monkeys
type: journal_article
volume: 22
year: '2005'
...
---
_id: '2743'
abstract:
- lang: eng
  text: We consider the supersymmetric quantum mechanical system which is obtained
    by dimensionally reducing d = 6, N = 1 supersymmetric gauge theory with gauge
    group U(1) and a single charged hypermultiplet. Using the deformation method and
    ideas introduced by Porrati and Rozenberg [1], we present a detailed proof of
    the existence of a normalizable ground state for this system.
author:
- first_name: László
  full_name: László Erdös
  id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
  last_name: Erdös
  orcid: 0000-0001-5366-9603
- first_name: David
  full_name: Hasler, David G
  last_name: Hasler
- first_name: Jan
  full_name: Solovej, Jan P
  last_name: Solovej
citation:
  ama: 'Erdös L, Hasler D, Solovej J. Existence of the D0-D4 bound state: A detailed
    proof. <i>Annales Henri Poincare</i>. 2005;6(2):247-267. doi:<a href="https://doi.org/10.1007/s00023-005-0205-0">10.1007/s00023-005-0205-0</a>'
  apa: 'Erdös, L., Hasler, D., &#38; Solovej, J. (2005). Existence of the D0-D4 bound
    state: A detailed proof. <i>Annales Henri Poincare</i>. Birkhäuser. <a href="https://doi.org/10.1007/s00023-005-0205-0">https://doi.org/10.1007/s00023-005-0205-0</a>'
  chicago: 'Erdös, László, David Hasler, and Jan Solovej. “Existence of the D0-D4
    Bound State: A Detailed Proof.” <i>Annales Henri Poincare</i>. Birkhäuser, 2005.
    <a href="https://doi.org/10.1007/s00023-005-0205-0">https://doi.org/10.1007/s00023-005-0205-0</a>.'
  ieee: 'L. Erdös, D. Hasler, and J. Solovej, “Existence of the D0-D4 bound state:
    A detailed proof,” <i>Annales Henri Poincare</i>, vol. 6, no. 2. Birkhäuser, pp.
    247–267, 2005.'
  ista: 'Erdös L, Hasler D, Solovej J. 2005. Existence of the D0-D4 bound state: A
    detailed proof. Annales Henri Poincare. 6(2), 247–267.'
  mla: 'Erdös, László, et al. “Existence of the D0-D4 Bound State: A Detailed Proof.”
    <i>Annales Henri Poincare</i>, vol. 6, no. 2, Birkhäuser, 2005, pp. 247–67, doi:<a
    href="https://doi.org/10.1007/s00023-005-0205-0">10.1007/s00023-005-0205-0</a>.'
  short: L. Erdös, D. Hasler, J. Solovej, Annales Henri Poincare 6 (2005) 247–267.
date_created: 2018-12-11T11:59:22Z
date_published: 2005-04-01T00:00:00Z
date_updated: 2021-01-12T06:59:24Z
day: '01'
doi: 10.1007/s00023-005-0205-0
extern: 1
intvolume: '         6'
issue: '2'
month: '04'
page: 247 - 267
publication: Annales Henri Poincare
publication_status: published
publisher: Birkhäuser
publist_id: '4149'
quality_controlled: 0
status: public
title: 'Existence of the D0-D4 bound state: A detailed proof'
type: journal_article
volume: 6
year: '2005'
...
---
_id: '2744'
abstract:
- lang: eng
  text: We study the long time evolution of a quantum particle interacting with a
    random potential in the Boltzmann-Grad low density limit. We prove that the phase
    space density of the quantum evolution defined through the Husimi function converges
    weakly to a linear Boltzmann equation. The Boltzmann collision kernel is given
    by the full quantum scattering cross-section of the obstacle potential.
author:
- first_name: David
  full_name: Eng, David
  last_name: Eng
- first_name: László
  full_name: László Erdös
  id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
  last_name: Erdös
  orcid: 0000-0001-5366-9603
citation:
  ama: Eng D, Erdös L. The linear Boltzmann equation as the low density limit of a
    random Schrödinger equation. <i>Reviews in Mathematical Physics</i>. 2005;17(6):669-743.
    doi:<a href="https://doi.org/10.1142/S0129055X0500242X">10.1142/S0129055X0500242X</a>
  apa: Eng, D., &#38; Erdös, L. (2005). The linear Boltzmann equation as the low density
    limit of a random Schrödinger equation. <i>Reviews in Mathematical Physics</i>.
    World Scientific Publishing. <a href="https://doi.org/10.1142/S0129055X0500242X">https://doi.org/10.1142/S0129055X0500242X</a>
  chicago: Eng, David, and László Erdös. “The Linear Boltzmann Equation as the Low
    Density Limit of a Random Schrödinger Equation.” <i>Reviews in Mathematical Physics</i>.
    World Scientific Publishing, 2005. <a href="https://doi.org/10.1142/S0129055X0500242X">https://doi.org/10.1142/S0129055X0500242X</a>.
  ieee: D. Eng and L. Erdös, “The linear Boltzmann equation as the low density limit
    of a random Schrödinger equation,” <i>Reviews in Mathematical Physics</i>, vol.
    17, no. 6. World Scientific Publishing, pp. 669–743, 2005.
  ista: Eng D, Erdös L. 2005. The linear Boltzmann equation as the low density limit
    of a random Schrödinger equation. Reviews in Mathematical Physics. 17(6), 669–743.
  mla: Eng, David, and László Erdös. “The Linear Boltzmann Equation as the Low Density
    Limit of a Random Schrödinger Equation.” <i>Reviews in Mathematical Physics</i>,
    vol. 17, no. 6, World Scientific Publishing, 2005, pp. 669–743, doi:<a href="https://doi.org/10.1142/S0129055X0500242X">10.1142/S0129055X0500242X</a>.
  short: D. Eng, L. Erdös, Reviews in Mathematical Physics 17 (2005) 669–743.
date_created: 2018-12-11T11:59:22Z
date_published: 2005-07-01T00:00:00Z
date_updated: 2021-01-12T06:59:25Z
day: '01'
doi: 10.1142/S0129055X0500242X
extern: 1
intvolume: '        17'
issue: '6'
month: '07'
page: 669 - 743
publication: Reviews in Mathematical Physics
publication_status: published
publisher: World Scientific Publishing
publist_id: '4148'
quality_controlled: 0
status: public
title: The linear Boltzmann equation as the low density limit of a random Schrödinger
  equation
type: journal_article
volume: 17
year: '2005'
...
---
_id: '2788'
abstract:
- lang: eng
  text: We present the results of an experimental investigation into the nature and
    structure of turbulent pipe flow at moderate Reynolds numbers. A turbulence regeneration
    mechanism is identified which sustains a symmetric traveling wave within the flow.
    The periodicity of the mechanism allows comparison to the wavelength of numerically
    observed exact traveling wave solutions and close agreement is found. The advection
    speed of the upstream turbulence laminar interface in the experimental flow is
    observed to form a lower bound on the phase velocities of the exact traveling
    wave solutions. Overall our observations suggest that the dynamics of the turbulent
    flow at moderate Reynolds numbers are governed by unstable nonlinear traveling
    waves.
author:
- first_name: Björn
  full_name: Björn Hof
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
- first_name: Casimir
  full_name: van Doorne, Casimir W
  last_name: Van Doorne
- first_name: Jerry
  full_name: Westerweel, Jerry
  last_name: Westerweel
- first_name: Frans
  full_name: Nieuwstadt, Frans T
  last_name: Nieuwstadt
citation:
  ama: Hof B, Van Doorne C, Westerweel J, Nieuwstadt F. Turbulence regeneration in
    pipe flow at moderate reynolds numbers. <i>Physical Review Letters</i>. 2005;95(21).
    doi:<a href="https://doi.org/10.1103/PhysRevLett.95.214502">10.1103/PhysRevLett.95.214502</a>
  apa: Hof, B., Van Doorne, C., Westerweel, J., &#38; Nieuwstadt, F. (2005). Turbulence
    regeneration in pipe flow at moderate reynolds numbers. <i>Physical Review Letters</i>.
    American Physical Society. <a href="https://doi.org/10.1103/PhysRevLett.95.214502">https://doi.org/10.1103/PhysRevLett.95.214502</a>
  chicago: Hof, Björn, Casimir Van Doorne, Jerry Westerweel, and Frans Nieuwstadt.
    “Turbulence Regeneration in Pipe Flow at Moderate Reynolds Numbers.” <i>Physical
    Review Letters</i>. American Physical Society, 2005. <a href="https://doi.org/10.1103/PhysRevLett.95.214502">https://doi.org/10.1103/PhysRevLett.95.214502</a>.
  ieee: B. Hof, C. Van Doorne, J. Westerweel, and F. Nieuwstadt, “Turbulence regeneration
    in pipe flow at moderate reynolds numbers,” <i>Physical Review Letters</i>, vol.
    95, no. 21. American Physical Society, 2005.
  ista: Hof B, Van Doorne C, Westerweel J, Nieuwstadt F. 2005. Turbulence regeneration
    in pipe flow at moderate reynolds numbers. Physical Review Letters. 95(21).
  mla: Hof, Björn, et al. “Turbulence Regeneration in Pipe Flow at Moderate Reynolds
    Numbers.” <i>Physical Review Letters</i>, vol. 95, no. 21, American Physical Society,
    2005, doi:<a href="https://doi.org/10.1103/PhysRevLett.95.214502">10.1103/PhysRevLett.95.214502</a>.
  short: B. Hof, C. Van Doorne, J. Westerweel, F. Nieuwstadt, Physical Review Letters
    95 (2005).
date_created: 2018-12-11T11:59:36Z
date_published: 2005-11-17T00:00:00Z
date_updated: 2021-01-12T06:59:43Z
day: '17'
doi: 10.1103/PhysRevLett.95.214502
extern: 1
intvolume: '        95'
issue: '21'
month: '11'
publication: Physical Review Letters
publication_status: published
publisher: American Physical Society
publist_id: '4101'
quality_controlled: 0
status: public
title: Turbulence regeneration in pipe flow at moderate reynolds numbers
type: journal_article
volume: 95
year: '2005'
...
---
_id: '2789'
abstract:
- lang: eng
  text: Transitional pipe flow is investigated in two different experimental set-ups.
    In the first the stability threshold and the initial growth of localized perturbations
    are studied. Good agreement is found with an earlier investigation of the transition
    threshold. The measurement technique applied in the last part of this study allows
    the reconstruction of the streamwise vorticity in a turbulent puff.
author:
- first_name: Björn
  full_name: Björn Hof
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
citation:
  ama: Hof B. Transition to turbulence in pipe flow. <i>Fluid Mechanics and its Applications</i>.
    2005;77:221-231. doi:<a href="https://doi.org/10.1007/1-4020-4049-0_12">10.1007/1-4020-4049-0_12</a>
  apa: Hof, B. (2005). Transition to turbulence in pipe flow. <i>Fluid Mechanics and
    Its Applications</i>. Springer. <a href="https://doi.org/10.1007/1-4020-4049-0_12">https://doi.org/10.1007/1-4020-4049-0_12</a>
  chicago: Hof, Björn. “Transition to Turbulence in Pipe Flow.” <i>Fluid Mechanics
    and Its Applications</i>. Springer, 2005. <a href="https://doi.org/10.1007/1-4020-4049-0_12">https://doi.org/10.1007/1-4020-4049-0_12</a>.
  ieee: B. Hof, “Transition to turbulence in pipe flow,” <i>Fluid Mechanics and its
    Applications</i>, vol. 77. Springer, pp. 221–231, 2005.
  ista: Hof B. 2005. Transition to turbulence in pipe flow. Fluid Mechanics and its
    Applications. 77, 221–231.
  mla: Hof, Björn. “Transition to Turbulence in Pipe Flow.” <i>Fluid Mechanics and
    Its Applications</i>, vol. 77, Springer, 2005, pp. 221–31, doi:<a href="https://doi.org/10.1007/1-4020-4049-0_12">10.1007/1-4020-4049-0_12</a>.
  short: B. Hof, Fluid Mechanics and Its Applications 77 (2005) 221–231.
date_created: 2018-12-11T11:59:36Z
date_published: 2005-09-19T00:00:00Z
date_updated: 2021-01-12T06:59:43Z
day: '19'
doi: 10.1007/1-4020-4049-0_12
extern: 1
intvolume: '        77'
month: '09'
page: 221 - 231
publication: Fluid Mechanics and its Applications
publication_status: published
publisher: Springer
publist_id: '4100'
quality_controlled: 0
status: public
title: Transition to turbulence in pipe flow
type: journal_article
volume: 77
year: '2005'
...
---
_id: '2790'
abstract:
- lang: eng
  text: We present the results of an experimental investigation of the effect of a
    magnetic field on the stability of convection in a liquid metal. A rectangular
    container of gallium is subjected to a horizontal temperature gradient and a uniform
    magnetic field is applied separately in three directions. The magnetic field suppresses
    the oscillation most effectively when it is applied in the vertical direction
    and is least efficient when applied in the direction of the temperature gradient.
    The critical temperature difference required for the onset of oscillations is
    found to scale exponentially with the magnitude of the magnetic field for all
    three orientations. Comparisons are made with available theory and qualitative
    differences are discussed.
author:
- first_name: Björn
  full_name: Björn Hof
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
- first_name: Anne
  full_name: Juel, Anne
  last_name: Juel
- first_name: Tom
  full_name: Mullin, Tom P
  last_name: Mullin
citation:
  ama: Hof B, Juel A, Mullin T. Magnetohydrodynamic damping of oscillations in low-Prandtl-number
    convection. <i>Journal of Fluid Mechanics</i>. 2005;545:193-201. doi:<a href="https://doi.org/10.1017/S0022112005006762">10.1017/S0022112005006762</a>
  apa: Hof, B., Juel, A., &#38; Mullin, T. (2005). Magnetohydrodynamic damping of
    oscillations in low-Prandtl-number convection. <i>Journal of Fluid Mechanics</i>.
    Cambridge University Press. <a href="https://doi.org/10.1017/S0022112005006762">https://doi.org/10.1017/S0022112005006762</a>
  chicago: Hof, Björn, Anne Juel, and Tom Mullin. “Magnetohydrodynamic Damping of
    Oscillations in Low-Prandtl-Number Convection.” <i>Journal of Fluid Mechanics</i>.
    Cambridge University Press, 2005. <a href="https://doi.org/10.1017/S0022112005006762">https://doi.org/10.1017/S0022112005006762</a>.
  ieee: B. Hof, A. Juel, and T. Mullin, “Magnetohydrodynamic damping of oscillations
    in low-Prandtl-number convection,” <i>Journal of Fluid Mechanics</i>, vol. 545.
    Cambridge University Press, pp. 193–201, 2005.
  ista: Hof B, Juel A, Mullin T. 2005. Magnetohydrodynamic damping of oscillations
    in low-Prandtl-number convection. Journal of Fluid Mechanics. 545, 193–201.
  mla: Hof, Björn, et al. “Magnetohydrodynamic Damping of Oscillations in Low-Prandtl-Number
    Convection.” <i>Journal of Fluid Mechanics</i>, vol. 545, Cambridge University
    Press, 2005, pp. 193–201, doi:<a href="https://doi.org/10.1017/S0022112005006762">10.1017/S0022112005006762</a>.
  short: B. Hof, A. Juel, T. Mullin, Journal of Fluid Mechanics 545 (2005) 193–201.
date_created: 2018-12-11T11:59:37Z
date_published: 2005-12-25T00:00:00Z
date_updated: 2021-01-12T06:59:44Z
day: '25'
doi: 10.1017/S0022112005006762
extern: 1
intvolume: '       545'
month: '12'
page: 193 - 201
publication: Journal of Fluid Mechanics
publication_status: published
publisher: Cambridge University Press
publist_id: '4099'
quality_controlled: 0
status: public
title: Magnetohydrodynamic damping of oscillations in low-Prandtl-number convection
type: journal_article
volume: 545
year: '2005'
...
---
_id: '2867'
abstract:
- lang: eng
  text: The plant hormone auxin elicits many specific context-dependent developmental
    responses. Auxin promotes degradation of Aux/IAA proteins that prevent transcription
    factors of the auxin response factor (ARF) family from regulating auxin-responsive
    target genes. Aux/IAAs and ARFs are represented by large gene families in Arabidopsis.
    Here we show that stabilization of BDL/IAA12 or its sister protein IAA13 prevents
    MP/ARF5-dependent embryonic root formation whereas stabilized SHY2/IAA3 interferes
    with seedling growth. Although both bdl and shy2-2 proteins inhibited MP/ARF5-dependent
    reporter gene activation, shy2-2 was much less efficient than bdl to interfere
    with embryonic root initiation when expressed from the BDL promoter. Similarly,
    MP was much more efficient than ARF16 in this process. When expressed from the
    SHY2 promoter, both shy2-2 and bdl inhibited cell elongation and auxin-induced
    gene expression in the seedling hypocotyl. By contrast, gravitropism and auxin-induced
    gene expression in the root, which were promoted by functionally redundant NPH4/ARF7
    and ARF19 proteins, were inhibited by shy2-2, but not by bdl protein. Our results
    suggest that auxin signals are converted into specific responses by matching pairs
    of coexpressed ARF and Aux/IAA proteins.
author:
- first_name: Dolf
  full_name: Weijers, Dolf
  last_name: Weijers
- first_name: Eva
  full_name: Eva Benková
  id: 38F4F166-F248-11E8-B48F-1D18A9856A87
  last_name: Benková
  orcid: 0000-0002-8510-9739
- first_name: Katja
  full_name: Jäger, Katja E
  last_name: Jäger
- first_name: Alexandra
  full_name: Schlereth, Alexandra
  last_name: Schlereth
- first_name: Thorsten
  full_name: Hamann, Thorsten
  last_name: Hamann
- first_name: Marika
  full_name: Kientz, Marika
  last_name: Kientz
- first_name: Jill
  full_name: Wilmoth, Jill C
  last_name: Wilmoth
- first_name: Jason
  full_name: Reed, Jason W
  last_name: Reed
- first_name: Gerd
  full_name: Jürgens, Gerd
  last_name: Jürgens
citation:
  ama: Weijers D, Benková E, Jäger K, et al. Developmental specificity of auxin response
    by pairs of ARF and Aux/IAA transcriptional regulators. <i>EMBO Journal</i>. 2005;24(10):1874-1885.
    doi:<a href="https://doi.org/10.1038/sj.emboj.7600659">10.1038/sj.emboj.7600659</a>
  apa: Weijers, D., Benková, E., Jäger, K., Schlereth, A., Hamann, T., Kientz, M.,
    … Jürgens, G. (2005). Developmental specificity of auxin response by pairs of
    ARF and Aux/IAA transcriptional regulators. <i>EMBO Journal</i>. Wiley-Blackwell.
    <a href="https://doi.org/10.1038/sj.emboj.7600659">https://doi.org/10.1038/sj.emboj.7600659</a>
  chicago: Weijers, Dolf, Eva Benková, Katja Jäger, Alexandra Schlereth, Thorsten
    Hamann, Marika Kientz, Jill Wilmoth, Jason Reed, and Gerd Jürgens. “Developmental
    Specificity of Auxin Response by Pairs of ARF and Aux/IAA Transcriptional Regulators.”
    <i>EMBO Journal</i>. Wiley-Blackwell, 2005. <a href="https://doi.org/10.1038/sj.emboj.7600659">https://doi.org/10.1038/sj.emboj.7600659</a>.
  ieee: D. Weijers <i>et al.</i>, “Developmental specificity of auxin response by
    pairs of ARF and Aux/IAA transcriptional regulators,” <i>EMBO Journal</i>, vol.
    24, no. 10. Wiley-Blackwell, pp. 1874–1885, 2005.
  ista: Weijers D, Benková E, Jäger K, Schlereth A, Hamann T, Kientz M, Wilmoth J,
    Reed J, Jürgens G. 2005. Developmental specificity of auxin response by pairs
    of ARF and Aux/IAA transcriptional regulators. EMBO Journal. 24(10), 1874–1885.
  mla: Weijers, Dolf, et al. “Developmental Specificity of Auxin Response by Pairs
    of ARF and Aux/IAA Transcriptional Regulators.” <i>EMBO Journal</i>, vol. 24,
    no. 10, Wiley-Blackwell, 2005, pp. 1874–85, doi:<a href="https://doi.org/10.1038/sj.emboj.7600659">10.1038/sj.emboj.7600659</a>.
  short: D. Weijers, E. Benková, K. Jäger, A. Schlereth, T. Hamann, M. Kientz, J.
    Wilmoth, J. Reed, G. Jürgens, EMBO Journal 24 (2005) 1874–1885.
date_created: 2018-12-11T12:00:01Z
date_published: 2005-05-18T00:00:00Z
date_updated: 2021-01-12T07:00:22Z
day: '18'
doi: 10.1038/sj.emboj.7600659
extern: 1
intvolume: '        24'
issue: '10'
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142592/
month: '05'
oa: 1
page: 1874 - 1885
publication: EMBO Journal
publication_status: published
publisher: Wiley-Blackwell
publist_id: '3918'
quality_controlled: 0
status: public
title: Developmental specificity of auxin response by pairs of ARF and Aux/IAA transcriptional
  regulators
type: journal_article
volume: 24
year: '2005'
...
---
_id: '2895'
abstract:
- lang: eng
  text: One of the fundamental properties of the immune system is its capacity to
    avoid autoimmune diseases. The mechanism underlying this process, known as self-tolerance,
    is hitherto unresolved but seems to involve the control of clonal expansion of
    autoreactive lymphocytes. This article reviews mathematical modeling of self-tolerance,
    addressing two specific hypotheses. The first hypothesis posits that self-tolerance
    is mediated by tuning of activation thresholds, which makes autoreactive T lymphocytes
    reversibly &quot;anergic&quot; and unable to proliferate. The second hypothesis
    posits that the proliferation of autoreactive T lymphocytes is instead controlled
    by specific regulatory T lymphocytes. Models representing the population dynamics
    of autoreactive T lymphocytes according to these two hypotheses were derived.
    For each model we identified how cell density affects tolerance, and predicted
    the corresponding phase spaces and bifurcations. We show that the simple induction
    of proliferative anergy, as modeled here, has a density dependence that is only
    partially compatible with adoptive transfers of tolerance, and that the models
    of tolerance mediated by specific regulatory T cells are closer to the observations.
acknowledgement: 'The work was financially supported by Fundação para a Ciência e
  Tecnologia: grants  P/BIA/10094/1998,  POCTI/36413/99,  and  POCTI/MGI/46477/2002;
  and fellowships to JF (Praxis/BCC/18972/98), JS (BD/13546/97), KL (SFRH/BPD+/1157/2002),
  DM (SFRH/BD/2960/2000) and TP (SFRH/BD/10550/2002).'
author:
- first_name: Jorge
  full_name: Carneiro, Jorge
  last_name: Carneiro
- first_name: Tiago
  full_name: Tiago Paixao
  id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
  last_name: Paixao
  orcid: 0000-0003-2361-3953
- first_name: Dejan
  full_name: Milutinovic, Dejan
  last_name: Milutinovic
- first_name: João
  full_name: Sousa, João
  last_name: Sousa
- first_name: Kalet
  full_name: Leon, Kalet
  last_name: Leon
- first_name: Rui
  full_name: Gardner, Rui
  last_name: Gardner
- first_name: Jose
  full_name: Faro, Jose
  last_name: Faro
citation:
  ama: 'Carneiro J, Paixao T, Milutinovic D, et al. Immunological self tolerance:
    Lessons from mathematical modeling. <i>Journal of Computational and Applied Mathematics</i>.
    2005;184(1):77-100. doi:<a href="https://doi.org/10.1016/j.cam.2004.10.025">10.1016/j.cam.2004.10.025</a>'
  apa: 'Carneiro, J., Paixao, T., Milutinovic, D., Sousa, J., Leon, K., Gardner, R.,
    &#38; Faro, J. (2005). Immunological self tolerance: Lessons from mathematical
    modeling. <i>Journal of Computational and Applied Mathematics</i>. Elsevier. <a
    href="https://doi.org/10.1016/j.cam.2004.10.025">https://doi.org/10.1016/j.cam.2004.10.025</a>'
  chicago: 'Carneiro, Jorge, Tiago Paixao, Dejan Milutinovic, João Sousa, Kalet Leon,
    Rui Gardner, and Jose Faro. “Immunological Self Tolerance: Lessons from Mathematical
    Modeling.” <i>Journal of Computational and Applied Mathematics</i>. Elsevier,
    2005. <a href="https://doi.org/10.1016/j.cam.2004.10.025">https://doi.org/10.1016/j.cam.2004.10.025</a>.'
  ieee: 'J. Carneiro <i>et al.</i>, “Immunological self tolerance: Lessons from mathematical
    modeling,” <i>Journal of Computational and Applied Mathematics</i>, vol. 184,
    no. 1. Elsevier, pp. 77–100, 2005.'
  ista: 'Carneiro J, Paixao T, Milutinovic D, Sousa J, Leon K, Gardner R, Faro J.
    2005. Immunological self tolerance: Lessons from mathematical modeling. Journal
    of Computational and Applied Mathematics. 184(1), 77–100.'
  mla: 'Carneiro, Jorge, et al. “Immunological Self Tolerance: Lessons from Mathematical
    Modeling.” <i>Journal of Computational and Applied Mathematics</i>, vol. 184,
    no. 1, Elsevier, 2005, pp. 77–100, doi:<a href="https://doi.org/10.1016/j.cam.2004.10.025">10.1016/j.cam.2004.10.025</a>.'
  short: J. Carneiro, T. Paixao, D. Milutinovic, J. Sousa, K. Leon, R. Gardner, J.
    Faro, Journal of Computational and Applied Mathematics 184 (2005) 77–100.
date_created: 2018-12-11T12:00:12Z
date_published: 2005-12-01T00:00:00Z
date_updated: 2021-01-12T07:00:32Z
day: '01'
doi: 10.1016/j.cam.2004.10.025
extern: 1
intvolume: '       184'
issue: '1'
month: '12'
page: 77 - 100
publication: Journal of Computational and Applied Mathematics
publication_status: published
publisher: Elsevier
publist_id: '3863'
quality_controlled: 0
status: public
title: 'Immunological self tolerance: Lessons from mathematical modeling'
type: journal_article
volume: 184
year: '2005'
...
---
_id: '3000'
abstract:
- lang: eng
  text: In plants, cell polarity is an issue more recurring than in other systems,
    because plants, due to their adaptive and flexible development, often change cell
    polarity postembryonically according to intrinsic cues and demands of the environment.
    Recent findings on the directional movement of the plant signalling molecule auxin
    provide a unique connection between individual cell polarity and the establishment
    of polarity at the tissue, organ, and whole-plant levels. Decisions about the
    subcellular polar targeting of PIN auxin transport components determine the direction
    of auxin flow between cells and consequently mediate multiple developmental events.
    In addition, mutations or chemical interference with PIN-based auxin transport
    result in abnormal cell divisions. Thus, the complicated links between cell polarity
    establishment, auxin transport, cytoskeleton, and oriented cell divisions now
    begin to emerge. Here we review the available literature on the issues of cell
    polarity in both plants and animals to extend our understanding on the generation,
    maintenance, and transmission of cell polarity in plants.
author:
- first_name: Pankaj
  full_name: Dhonukshe, Pankaj
  last_name: Dhonukshe
- first_name: Jürgen
  full_name: Kleine Vehn, Jürgen
  last_name: Kleine Vehn
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: 'Dhonukshe P, Kleine Vehn J, Friml J. Cell polarity, auxin transport and cytoskeleton
    mediated division planes: Who comes first? <i>Protoplasma</i>. 2005;226(1-2):67-73.
    doi:<a href="https://doi.org/10.1007/s00709-005-0104-8">10.1007/s00709-005-0104-8</a>'
  apa: 'Dhonukshe, P., Kleine Vehn, J., &#38; Friml, J. (2005). Cell polarity, auxin
    transport and cytoskeleton mediated division planes: Who comes first? <i>Protoplasma</i>.
    Springer. <a href="https://doi.org/10.1007/s00709-005-0104-8">https://doi.org/10.1007/s00709-005-0104-8</a>'
  chicago: 'Dhonukshe, Pankaj, Jürgen Kleine Vehn, and Jiří Friml. “Cell Polarity,
    Auxin Transport and Cytoskeleton Mediated Division Planes: Who Comes First?” <i>Protoplasma</i>.
    Springer, 2005. <a href="https://doi.org/10.1007/s00709-005-0104-8">https://doi.org/10.1007/s00709-005-0104-8</a>.'
  ieee: 'P. Dhonukshe, J. Kleine Vehn, and J. Friml, “Cell polarity, auxin transport
    and cytoskeleton mediated division planes: Who comes first?,” <i>Protoplasma</i>,
    vol. 226, no. 1–2. Springer, pp. 67–73, 2005.'
  ista: 'Dhonukshe P, Kleine Vehn J, Friml J. 2005. Cell polarity, auxin transport
    and cytoskeleton mediated division planes: Who comes first? Protoplasma. 226(1–2),
    67–73.'
  mla: 'Dhonukshe, Pankaj, et al. “Cell Polarity, Auxin Transport and Cytoskeleton
    Mediated Division Planes: Who Comes First?” <i>Protoplasma</i>, vol. 226, no.
    1–2, Springer, 2005, pp. 67–73, doi:<a href="https://doi.org/10.1007/s00709-005-0104-8">10.1007/s00709-005-0104-8</a>.'
  short: P. Dhonukshe, J. Kleine Vehn, J. Friml, Protoplasma 226 (2005) 67–73.
date_created: 2018-12-11T12:00:47Z
date_published: 2005-10-01T00:00:00Z
date_updated: 2021-01-12T07:40:22Z
day: '01'
doi: 10.1007/s00709-005-0104-8
extern: '1'
intvolume: '       226'
issue: 1-2
language:
- iso: eng
month: '10'
oa_version: None
page: 67 - 73
publication: Protoplasma
publication_status: published
publisher: Springer
publist_id: '3701'
quality_controlled: '1'
status: public
title: 'Cell polarity, auxin transport and cytoskeleton mediated division planes:
  Who comes first?'
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 226
year: '2005'
...
---
_id: '3001'
abstract:
- lang: eng
  text: 'One of the mechanisms by which signalling molecules regulate cellular behaviour
    is modulating subcellular protein translocation. This mode of regulation is often
    based on specialized vesicle trafficking, termed constitutive cycling, which consists
    of repeated internalization and recycling of proteins to and from the plasma membrane.
    No such mechanism of hormone action has been shown in plants although several
    proteins, including the PIN auxin efflux facilitators, exhibit constitutive cycling.
    Here we show that a major regulator of plant development, auxin, inhibits endocytosis.
    This effect is specific to biologically active auxins and requires activity of
    the Calossin-like protein BIG. By inhibiting the internalization step of PIN constitutive
    cycling, auxin increases levels of PINs at the plasma membrane. Concomitantly,
    auxin promotes its own efflux from cells by a vesicle-trafficking-dependent mechanism.
    Furthermore, asymmetric auxin translocation during gravitropism is correlated
    with decreased PIN internalization. Our data imply a previously undescribed mode
    of plant hormone action: by modulating PIN protein trafficking, auxin regulates
    PIN abundance and activity at the cell surface, providing a mechanism for the
    feedback regulation of auxin transport.'
author:
- first_name: Tomasz
  full_name: Paciorek, Tomasz
  last_name: Paciorek
- first_name: Eva
  full_name: Zažímalová, Eva
  last_name: Zažímalová
- first_name: Nadia
  full_name: Ruthardt, Nadia
  last_name: Ruthardt
- first_name: Jan
  full_name: Petrášek, Jan
  last_name: Petrášek
- first_name: York
  full_name: Stierhof, York-Dieter
  last_name: Stierhof
- first_name: Jürgen
  full_name: Kleine-Vehn, Jürgen
  last_name: Kleine Vehn
- first_name: David
  full_name: Morris, David A
  last_name: Morris
- first_name: Neil
  full_name: Emans, Neil
  last_name: Emans
- first_name: Gerd
  full_name: Jürgens, Gerd
  last_name: Jürgens
- first_name: Niko
  full_name: Geldner, Niko
  last_name: Geldner
- first_name: Jirí
  full_name: Jirí Friml
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: Paciorek T, Zažímalová E, Ruthardt N, et al. Auxin inhibits endocytosis and
    promotes its own efflux from cells. <i>Nature</i>. 2005;435(7046):1251-1256. doi:<a
    href="https://doi.org/10.1038/nature03633">10.1038/nature03633</a>
  apa: Paciorek, T., Zažímalová, E., Ruthardt, N., Petrášek, J., Stierhof, Y., Kleine
    Vehn, J., … Friml, J. (2005). Auxin inhibits endocytosis and promotes its own
    efflux from cells. <i>Nature</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/nature03633">https://doi.org/10.1038/nature03633</a>
  chicago: Paciorek, Tomasz, Eva Zažímalová, Nadia Ruthardt, Jan Petrášek, York Stierhof,
    Jürgen Kleine Vehn, David Morris, et al. “Auxin Inhibits Endocytosis and Promotes
    Its Own Efflux from Cells.” <i>Nature</i>. Nature Publishing Group, 2005. <a href="https://doi.org/10.1038/nature03633">https://doi.org/10.1038/nature03633</a>.
  ieee: T. Paciorek <i>et al.</i>, “Auxin inhibits endocytosis and promotes its own
    efflux from cells,” <i>Nature</i>, vol. 435, no. 7046. Nature Publishing Group,
    pp. 1251–1256, 2005.
  ista: Paciorek T, Zažímalová E, Ruthardt N, Petrášek J, Stierhof Y, Kleine Vehn
    J, Morris D, Emans N, Jürgens G, Geldner N, Friml J. 2005. Auxin inhibits endocytosis
    and promotes its own efflux from cells. Nature. 435(7046), 1251–1256.
  mla: Paciorek, Tomasz, et al. “Auxin Inhibits Endocytosis and Promotes Its Own Efflux
    from Cells.” <i>Nature</i>, vol. 435, no. 7046, Nature Publishing Group, 2005,
    pp. 1251–56, doi:<a href="https://doi.org/10.1038/nature03633">10.1038/nature03633</a>.
  short: T. Paciorek, E. Zažímalová, N. Ruthardt, J. Petrášek, Y. Stierhof, J. Kleine
    Vehn, D. Morris, N. Emans, G. Jürgens, N. Geldner, J. Friml, Nature 435 (2005)
    1251–1256.
date_created: 2018-12-11T12:00:47Z
date_published: 2005-06-30T00:00:00Z
date_updated: 2021-01-12T07:40:23Z
day: '30'
doi: 10.1038/nature03633
extern: 1
intvolume: '       435'
issue: '7046'
month: '06'
page: 1251 - 1256
publication: Nature
publication_status: published
publisher: Nature Publishing Group
publist_id: '3702'
quality_controlled: 0
status: public
title: Auxin inhibits endocytosis and promotes its own efflux from cells
type: journal_article
volume: 435
year: '2005'
...
