---
_id: '490'
abstract:
- lang: eng
  text: 'BioSig is an open source software library for biomedical signal processing.
    The aim of the BioSig project is to foster research in biomedical signal processing
    by providing free and open source software tools for many different application
    areas. Some of the areas where BioSig can be employed are neuroinformatics, brain-computer
    interfaces, neurophysiology, psychology, cardiovascular systems, and sleep research.
    Moreover, the analysis of biosignals such as the electroencephalogram (EEG), electrocorticogram
    (ECoG), electrocardiogram (ECG), electrooculogram (EOG), electromyogram (EMG),
    or respiration signals is a very relevant element of the BioSig project. Specifically,
    BioSig provides solutions for data acquisition, artifact processing, quality control,
    feature extraction, classification, modeling, and data visualization, to name
    a few. In this paper, we highlight several methods to help students and researchers
    to work more efficiently with biomedical signals. '
article_number: '935364'
article_processing_charge: No
author:
- first_name: Alois
  full_name: Schlögl, Alois
  id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
  last_name: Schlögl
  orcid: 0000-0002-5621-8100
- first_name: Carmen
  full_name: Vidaurre, Carmen
  last_name: Vidaurre
- first_name: Tilmann
  full_name: Sander, Tilmann
  last_name: Sander
citation:
  ama: 'Schlögl A, Vidaurre C, Sander T. BioSig: The free and open source software
    library for biomedical signal processing. <i>Computational Intelligence and Neuroscience</i>.
    2011;2011. doi:<a href="https://doi.org/10.1155/2011/935364">10.1155/2011/935364</a>'
  apa: 'Schlögl, A., Vidaurre, C., &#38; Sander, T. (2011). BioSig: The free and open
    source software library for biomedical signal processing. <i>Computational Intelligence
    and Neuroscience</i>. Hindawi Publishing Corporation. <a href="https://doi.org/10.1155/2011/935364">https://doi.org/10.1155/2011/935364</a>'
  chicago: 'Schlögl, Alois, Carmen Vidaurre, and Tilmann Sander. “BioSig: The Free
    and Open Source Software Library for Biomedical Signal Processing.” <i>Computational
    Intelligence and Neuroscience</i>. Hindawi Publishing Corporation, 2011. <a href="https://doi.org/10.1155/2011/935364">https://doi.org/10.1155/2011/935364</a>.'
  ieee: 'A. Schlögl, C. Vidaurre, and T. Sander, “BioSig: The free and open source
    software library for biomedical signal processing,” <i>Computational Intelligence
    and Neuroscience</i>, vol. 2011. Hindawi Publishing Corporation, 2011.'
  ista: 'Schlögl A, Vidaurre C, Sander T. 2011. BioSig: The free and open source software
    library for biomedical signal processing. Computational Intelligence and Neuroscience.
    2011, 935364.'
  mla: 'Schlögl, Alois, et al. “BioSig: The Free and Open Source Software Library
    for Biomedical Signal Processing.” <i>Computational Intelligence and Neuroscience</i>,
    vol. 2011, 935364, Hindawi Publishing Corporation, 2011, doi:<a href="https://doi.org/10.1155/2011/935364">10.1155/2011/935364</a>.'
  short: A. Schlögl, C. Vidaurre, T. Sander, Computational Intelligence and Neuroscience
    2011 (2011).
corr_author: '1'
date_created: 2018-12-11T11:46:45Z
date_published: 2011-01-01T00:00:00Z
date_updated: 2025-09-30T09:24:43Z
day: '01'
ddc:
- '005'
department:
- _id: ScienComp
- _id: PeJo
doi: 10.1155/2011/935364
external_id:
  isi:
  - '000208906100033'
file:
- access_level: open_access
  checksum: 8263bbf255171f2054f43f3db5f53b6e
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:07:44Z
  date_updated: 2020-07-14T12:46:35Z
  file_id: '4642'
  file_name: IST-2018-947-v1+1_2011_Schloegl_BioSig.pdf
  file_size: 2863551
  relation: main_file
file_date_updated: 2020-07-14T12:46:35Z
has_accepted_license: '1'
intvolume: '      2011'
isi: 1
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '01'
oa: 1
oa_version: Published Version
publication: Computational Intelligence and Neuroscience
publication_status: published
publisher: Hindawi Publishing Corporation
publist_id: '7330'
pubrep_id: '947'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'BioSig: The free and open source software library for biomedical signal processing'
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 2011
year: '2011'
...
---
_id: '3318'
abstract:
- lang: eng
  text: Parvalbumin is thought to act in a manner similar to EGTA, but how a slow
    Ca2+ buffer affects nanodomain-coupling regimes at GABAergic synapses is unclear.
    Direct measurements of parvalbumin concentration and paired recordings in rodent
    hippocampus and cerebellum revealed that parvalbumin affects synaptic dynamics
    only when expressed at high levels. Modeling suggests that, in high concentrations,
    parvalbumin may exert BAPTA-like effects, modulating nanodomain coupling via competition
    with local saturation of endogenous fixed buffers.
article_processing_charge: No
author:
- first_name: Emmanuel
  full_name: Eggermann, Emmanuel
  last_name: Eggermann
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Eggermann E, Jonas PM. How the “slow” Ca(2+) buffer parvalbumin affects transmitter
    release in nanodomain coupling regimes at GABAergic synapses. <i>Nature Neuroscience</i>.
    2011;15:20-22. doi:<a href="https://doi.org/10.1038/nn.3002">10.1038/nn.3002</a>
  apa: Eggermann, E., &#38; Jonas, P. M. (2011). How the “slow” Ca(2+) buffer parvalbumin
    affects transmitter release in nanodomain coupling regimes at GABAergic synapses.
    <i>Nature Neuroscience</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/nn.3002">https://doi.org/10.1038/nn.3002</a>
  chicago: Eggermann, Emmanuel, and Peter M Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin
    Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.”
    <i>Nature Neuroscience</i>. Nature Publishing Group, 2011. <a href="https://doi.org/10.1038/nn.3002">https://doi.org/10.1038/nn.3002</a>.
  ieee: E. Eggermann and P. M. Jonas, “How the ‘slow’ Ca(2+) buffer parvalbumin affects
    transmitter release in nanodomain coupling regimes at GABAergic synapses,” <i>Nature
    Neuroscience</i>, vol. 15. Nature Publishing Group, pp. 20–22, 2011.
  ista: Eggermann E, Jonas PM. 2011. How the “slow” Ca(2+) buffer parvalbumin affects
    transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature
    Neuroscience. 15, 20–22.
  mla: Eggermann, Emmanuel, and Peter M. Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin
    Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.”
    <i>Nature Neuroscience</i>, vol. 15, Nature Publishing Group, 2011, pp. 20–22,
    doi:<a href="https://doi.org/10.1038/nn.3002">10.1038/nn.3002</a>.
  short: E. Eggermann, P.M. Jonas, Nature Neuroscience 15 (2011) 20–22.
corr_author: '1'
date_created: 2018-12-11T12:02:38Z
date_published: 2011-12-04T00:00:00Z
date_updated: 2025-09-30T09:20:05Z
day: '04'
department:
- _id: PeJo
doi: 10.1038/nn.3002
external_id:
  isi:
  - '000298414400008'
intvolume: '        15'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631701/
month: '12'
oa: 1
oa_version: Submitted Version
page: 20 - 22
publication: Nature Neuroscience
publication_status: published
publisher: Nature Publishing Group
publist_id: '3321'
quality_controlled: '1'
scopus_import: '1'
status: public
title: How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain
  coupling regimes at GABAergic synapses
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 15
year: '2011'
...
---
_id: '3369'
abstract:
- lang: eng
  text: Rab3 interacting molecules (RIMs) are highly enriched in the active zones
    of presynaptic terminals. It is generally thought that they operate as effectors
    of the small G protein Rab3. Three recent papers, by Han et al. (this issue of
    Neuron), Deng et al. (this issue of Neuron), and Kaeser et al. (a recent issue
    of Cell), shed new light on the functional role of RIM in presynaptic terminals.
    First, RIM tethers Ca2+ channels to active zones. Second, RIM contributes to priming
    of synaptic vesicles by interacting with another presynaptic protein, Munc13.
article_processing_charge: No
author:
- first_name: Alejandro
  full_name: Pernia-Andrade, Alejandro
  id: 36963E98-F248-11E8-B48F-1D18A9856A87
  last_name: Pernia-Andrade
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Pernia-Andrade A, Jonas PM. The multiple faces of RIM. <i>Neuron</i>. 2011;69(2):185-187.
    doi:<a href="https://doi.org/10.1016/j.neuron.2011.01.010">10.1016/j.neuron.2011.01.010</a>
  apa: Pernia-Andrade, A., &#38; Jonas, P. M. (2011). The multiple faces of RIM. <i>Neuron</i>.
    Elsevier. <a href="https://doi.org/10.1016/j.neuron.2011.01.010">https://doi.org/10.1016/j.neuron.2011.01.010</a>
  chicago: Pernia-Andrade, Alejandro, and Peter M Jonas. “The Multiple Faces of RIM.”
    <i>Neuron</i>. Elsevier, 2011. <a href="https://doi.org/10.1016/j.neuron.2011.01.010">https://doi.org/10.1016/j.neuron.2011.01.010</a>.
  ieee: A. Pernia-Andrade and P. M. Jonas, “The multiple faces of RIM,” <i>Neuron</i>,
    vol. 69, no. 2. Elsevier, pp. 185–187, 2011.
  ista: Pernia-Andrade A, Jonas PM. 2011. The multiple faces of RIM. Neuron. 69(2),
    185–187.
  mla: Pernia-Andrade, Alejandro, and Peter M. Jonas. “The Multiple Faces of RIM.”
    <i>Neuron</i>, vol. 69, no. 2, Elsevier, 2011, pp. 185–87, doi:<a href="https://doi.org/10.1016/j.neuron.2011.01.010">10.1016/j.neuron.2011.01.010</a>.
  short: A. Pernia-Andrade, P.M. Jonas, Neuron 69 (2011) 185–187.
corr_author: '1'
date_created: 2018-12-11T12:02:56Z
date_published: 2011-01-27T00:00:00Z
date_updated: 2025-09-30T09:01:26Z
day: '27'
department:
- _id: PeJo
doi: 10.1016/j.neuron.2011.01.010
external_id:
  isi:
  - '000286792900002'
intvolume: '        69'
isi: 1
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 185 - 187
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '3243'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The multiple faces of RIM
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 69
year: '2011'
...
---
_id: '3718'
abstract:
- lang: eng
  text: Long-term depression (LTD) is a form of synaptic plasticity that may contribute
    to information storage in the central nervous system. Here we report that LTD
    can be elicited in layer 5 pyramidal neurons of the rat prefrontal cortex by pairing
    low frequency stimulation with a modest postsynaptic depolarization. The induction
    of LTD required the activation of both metabotropic glutamate receptors of the
    mGlu1 subtype and voltage-sensitive Ca(2+) channels (VSCCs) of the T/R, P/Q and
    N types, leading to the stimulation of intracellular inositol trisphosphate (IP3)
    receptors by IP3 and Ca(2+). The subsequent release of Ca(2+) from intracellular
    stores activated the protein phosphatase cascade involving calcineurin and protein
    phosphatase 1. The activation of purinergic P2Y(1) receptors blocked LTD. This
    effect was prevented by P2Y(1) receptor antagonists and was absent in mice lacking
    P2Y(1) but not P2Y(2) receptors. We also found that activation of P2Y(1) receptors
    inhibits Ca(2+) transients via VSCCs in the apical dendrites and spines of pyramidal
    neurons. In addition, we show that the release of ATP under hypoxia is able to
    inhibit LTD by acting on postsynaptic P2Y(1) receptors. In conclusion, these data
    suggest that the reduction of Ca(2+) influx via VSCCs caused by the activation
    of P2Y(1) receptors by ATP is the possible mechanism for the inhibition of LTD
    in prefrontal cortex.
acknowledgement: " The financial support of the Deutsche Forschungsgemeinschaft (IL
  20/12-1, KI 677/2-4) is gratefully acknowledged.\r\nWe thank B. H. Koller (Department
  of Genetics and Molecular Biology, University of North Carolina at Chapel Hill,
  NC, USA) for the generous supply of P2Y1−/− and P2Y2−/− mice. We are grateful to
  Dr. A. Schulz for reanalysing the genotype of the P2Y1−/− mice. The authors thank
  P. Jonas and U. Heinemann for many helpful comments and A-K. Krause, L Feige and
  M. Eberts for their excellent technical support."
article_processing_charge: No
author:
- first_name: José
  full_name: Guzmán, José
  id: 30CC5506-F248-11E8-B48F-1D18A9856A87
  last_name: Guzmán
  orcid: 0000-0003-2209-5242
- first_name: Hartmut
  full_name: Schmidt, Hartmut
  last_name: Schmidt
- first_name: Heike
  full_name: Franke, Heike
  last_name: Franke
- first_name: Ute
  full_name: Krügel, Ute
  last_name: Krügel
- first_name: Jens
  full_name: Eilers, Jens
  last_name: Eilers
- first_name: Peter
  full_name: Illes, Peter
  last_name: Illes
- first_name: Zoltan
  full_name: Gerevich, Zoltan
  last_name: Gerevich
citation:
  ama: Guzmán J, Schmidt H, Franke H, et al. P2Y1 receptors inhibit long-term depression
    in the prefrontal cortex. <i>Neuropharmacology</i>. 2010;59(6):406-415. doi:<a
    href="https://doi.org/10.1016/j.neuropharm.2010.05.013">10.1016/j.neuropharm.2010.05.013</a>
  apa: Guzmán, J., Schmidt, H., Franke, H., Krügel, U., Eilers, J., Illes, P., &#38;
    Gerevich, Z. (2010). P2Y1 receptors inhibit long-term depression in the prefrontal
    cortex. <i>Neuropharmacology</i>. Elsevier. <a href="https://doi.org/10.1016/j.neuropharm.2010.05.013">https://doi.org/10.1016/j.neuropharm.2010.05.013</a>
  chicago: Guzmán, José, Hartmut Schmidt, Heike Franke, Ute Krügel, Jens Eilers, Peter
    Illes, and Zoltan Gerevich. “P2Y1 Receptors Inhibit Long-Term Depression in the
    Prefrontal Cortex.” <i>Neuropharmacology</i>. Elsevier, 2010. <a href="https://doi.org/10.1016/j.neuropharm.2010.05.013">https://doi.org/10.1016/j.neuropharm.2010.05.013</a>.
  ieee: J. Guzmán <i>et al.</i>, “P2Y1 receptors inhibit long-term depression in the
    prefrontal cortex.,” <i>Neuropharmacology</i>, vol. 59, no. 6. Elsevier, pp. 406–415,
    2010.
  ista: Guzmán J, Schmidt H, Franke H, Krügel U, Eilers J, Illes P, Gerevich Z. 2010.
    P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology.
    59(6), 406–415.
  mla: Guzmán, José, et al. “P2Y1 Receptors Inhibit Long-Term Depression in the Prefrontal
    Cortex.” <i>Neuropharmacology</i>, vol. 59, no. 6, Elsevier, 2010, pp. 406–15,
    doi:<a href="https://doi.org/10.1016/j.neuropharm.2010.05.013">10.1016/j.neuropharm.2010.05.013</a>.
  short: J. Guzmán, H. Schmidt, H. Franke, U. Krügel, J. Eilers, P. Illes, Z. Gerevich,
    Neuropharmacology 59 (2010) 406–415.
corr_author: '1'
date_created: 2018-12-11T12:04:47Z
date_published: 2010-11-01T00:00:00Z
date_updated: 2025-09-30T09:46:27Z
day: '01'
department:
- _id: PeJo
doi: 10.1016/j.neuropharm.2010.05.013
external_id:
  isi:
  - '000283453300006'
intvolume: '        59'
isi: 1
issue: '6'
language:
- iso: eng
month: '11'
oa_version: None
page: 406 - 415
publication: Neuropharmacology
publication_status: published
publisher: Elsevier
publist_id: '2512'
quality_controlled: '1'
scopus_import: '1'
status: public
title: P2Y1 receptors inhibit long-term depression in the prefrontal cortex.
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 59
year: '2010'
...
---
_id: '3832'
abstract:
- lang: eng
  text: A recent paper by von Engelhardt et al. identifies a novel auxiliary subunit
    of native AMPARs, termedCKAMP44. Unlike other auxiliary subunits, CKAMP44 accelerates
    desensitization and prolongs recovery from desensitization. CKAMP44 is highly
    expressed in hippocampal dentate gyrus granule cells and decreases the paired-pulse
    ratio at perforant path input synapses. Thus, both principal and auxiliary AMPAR
    subunits control the time course of signaling at glutamatergic synapses.
article_processing_charge: No
author:
- first_name: José
  full_name: Guzmán, José
  id: 30CC5506-F248-11E8-B48F-1D18A9856A87
  last_name: Guzmán
  orcid: 0000-0003-2209-5242
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: 'Guzmán J, Jonas PM. Beyond TARPs: The growing list of auxiliary AMPAR subunits.
    <i>Neuron</i>. 2010;66(1):8-10. doi:<a href="https://doi.org/10.1016/j.neuron.2010.04.003">10.1016/j.neuron.2010.04.003</a>'
  apa: 'Guzmán, J., &#38; Jonas, P. M. (2010). Beyond TARPs: The growing list of auxiliary
    AMPAR subunits. <i>Neuron</i>. Elsevier. <a href="https://doi.org/10.1016/j.neuron.2010.04.003">https://doi.org/10.1016/j.neuron.2010.04.003</a>'
  chicago: 'Guzmán, José, and Peter M Jonas. “Beyond TARPs: The Growing List of Auxiliary
    AMPAR Subunits.” <i>Neuron</i>. Elsevier, 2010. <a href="https://doi.org/10.1016/j.neuron.2010.04.003">https://doi.org/10.1016/j.neuron.2010.04.003</a>.'
  ieee: 'J. Guzmán and P. M. Jonas, “Beyond TARPs: The growing list of auxiliary AMPAR
    subunits,” <i>Neuron</i>, vol. 66, no. 1. Elsevier, pp. 8–10, 2010.'
  ista: 'Guzmán J, Jonas PM. 2010. Beyond TARPs: The growing list of auxiliary AMPAR
    subunits. Neuron. 66(1), 8–10.'
  mla: 'Guzmán, José, and Peter M. Jonas. “Beyond TARPs: The Growing List of Auxiliary
    AMPAR Subunits.” <i>Neuron</i>, vol. 66, no. 1, Elsevier, 2010, pp. 8–10, doi:<a
    href="https://doi.org/10.1016/j.neuron.2010.04.003">10.1016/j.neuron.2010.04.003</a>.'
  short: J. Guzmán, P.M. Jonas, Neuron 66 (2010) 8–10.
corr_author: '1'
date_created: 2018-12-11T12:05:25Z
date_published: 2010-04-15T00:00:00Z
date_updated: 2026-06-18T18:47:22Z
day: '15'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1016/j.neuron.2010.04.003
external_id:
  isi:
  - '000277016200004'
  pmid:
  - '20399724'
intvolume: '        66'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pubmed/20399724
month: '04'
oa: 1
oa_version: Published Version
page: 8 - 10
pmid: 1
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '2377'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Beyond TARPs: The growing list of auxiliary AMPAR subunits'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 66
year: '2010'
...
---
_id: '3833'
article_processing_charge: No
author:
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
- first_name: Stefan
  full_name: Hefft, Stefan
  last_name: Hefft
citation:
  ama: 'Jonas PM, Hefft S. GABA release at terminals of CCK-interneurons: Synchrony,
    asynchrony and modulation by cannabinoid receptors (commentary on Ali &#38;amp;
    Todorova). <i>The European Journal of Neuroscience</i>. 2010;31(7):1194-1195.
    doi:<a href="https://doi.org/10.1111/j.1460-9568.2010.07189.x">10.1111/j.1460-9568.2010.07189.x</a>'
  apa: 'Jonas, P. M., &#38; Hefft, S. (2010). GABA release at terminals of CCK-interneurons:
    Synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali
    &#38;amp; Todorova). <i>The European Journal of Neuroscience</i>. Wiley-Blackwell.
    <a href="https://doi.org/10.1111/j.1460-9568.2010.07189.x">https://doi.org/10.1111/j.1460-9568.2010.07189.x</a>'
  chicago: 'Jonas, Peter M, and Stefan Hefft. “GABA Release at Terminals of CCK-Interneurons:
    Synchrony, Asynchrony and Modulation by Cannabinoid Receptors (Commentary on Ali
    &#38;amp; Todorova).” <i>The European Journal of Neuroscience</i>. Wiley-Blackwell,
    2010. <a href="https://doi.org/10.1111/j.1460-9568.2010.07189.x">https://doi.org/10.1111/j.1460-9568.2010.07189.x</a>.'
  ieee: 'P. M. Jonas and S. Hefft, “GABA release at terminals of CCK-interneurons:
    Synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali
    &#38;amp; Todorova),” <i>The European Journal of Neuroscience</i>, vol. 31, no.
    7. Wiley-Blackwell, pp. 1194–1195, 2010.'
  ista: 'Jonas PM, Hefft S. 2010. GABA release at terminals of CCK-interneurons: Synchrony,
    asynchrony and modulation by cannabinoid receptors (commentary on Ali &#38;amp;
    Todorova). The European Journal of Neuroscience. 31(7), 1194–1195.'
  mla: 'Jonas, Peter M., and Stefan Hefft. “GABA Release at Terminals of CCK-Interneurons:
    Synchrony, Asynchrony and Modulation by Cannabinoid Receptors (Commentary on Ali
    &#38;amp; Todorova).” <i>The European Journal of Neuroscience</i>, vol. 31, no.
    7, Wiley-Blackwell, 2010, pp. 1194–95, doi:<a href="https://doi.org/10.1111/j.1460-9568.2010.07189.x">10.1111/j.1460-9568.2010.07189.x</a>.'
  short: P.M. Jonas, S. Hefft, The European Journal of Neuroscience 31 (2010) 1194–1195.
corr_author: '1'
date_created: 2018-12-11T12:05:25Z
date_published: 2010-03-19T00:00:00Z
date_updated: 2025-09-30T09:38:44Z
day: '19'
department:
- _id: PeJo
doi: 10.1111/j.1460-9568.2010.07189.x
external_id:
  isi:
  - '000276245400005'
intvolume: '        31'
isi: 1
issue: '7'
language:
- iso: eng
month: '03'
oa_version: None
page: 1194 - 1195
publication: The European Journal of Neuroscience
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2378'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'GABA release at terminals of CCK-interneurons: Synchrony, asynchrony and modulation
  by cannabinoid receptors (commentary on Ali &amp; Todorova)'
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 31
year: '2010'
...
