---
OA_type: closed access
_id: '20972'
abstract:
- lang: eng
text: Small amounts of stress are thought to have beneficial effects. A new study
reports a mechanism by which the psychedelic drug, psilocybin, causes acute release
of stress hormones, despite its known long-term anti-anxiety effects.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Hakan
full_name: Kücükdereli, Hakan
id: 5d5f6ea4-ef9e-11f0-a10a-85e12a3552af
last_name: Kücükdereli
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
citation:
ama: 'Kücükdereli H, Douglass AM. Neuroscience: What doesn’t kill you makes you
stronger. Current Biology. 2026;36(1):R27-R29. doi:10.1016/j.cub.2025.11.056'
apa: 'Kücükdereli, H., & Douglass, A. M. (2026). Neuroscience: What doesn’t
kill you makes you stronger. Current Biology. Elsevier. https://doi.org/10.1016/j.cub.2025.11.056'
chicago: 'Kücükdereli, Hakan, and Amelia M. Douglass. “Neuroscience: What Doesn’t
Kill You Makes You Stronger.” Current Biology. Elsevier, 2026. https://doi.org/10.1016/j.cub.2025.11.056.'
ieee: 'H. Kücükdereli and A. M. Douglass, “Neuroscience: What doesn’t kill you makes
you stronger,” Current Biology, vol. 36, no. 1. Elsevier, pp. R27–R29,
2026.'
ista: 'Kücükdereli H, Douglass AM. 2026. Neuroscience: What doesn’t kill you makes
you stronger. Current Biology. 36(1), R27–R29.'
mla: 'Kücükdereli, Hakan, and Amelia M. Douglass. “Neuroscience: What Doesn’t Kill
You Makes You Stronger.” Current Biology, vol. 36, no. 1, Elsevier, 2026,
pp. R27–29, doi:10.1016/j.cub.2025.11.056.'
short: H. Kücükdereli, A.M. Douglass, Current Biology 36 (2026) R27–R29.
corr_author: '1'
date_created: 2026-01-11T23:01:33Z
date_published: 2026-01-05T00:00:00Z
date_updated: 2026-01-12T10:09:13Z
day: '05'
department:
- _id: AmDo
- _id: SiHi
doi: 10.1016/j.cub.2025.11.056
external_id:
pmid:
- '41494523'
intvolume: ' 36'
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: R27-R29
pmid: 1
publication: Current Biology
publication_identifier:
eissn:
- 1879-0445
issn:
- 0960-9822
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Neuroscience: What doesn’t kill you makes you stronger'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2026'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '21744'
abstract:
- lang: eng
text: The paraventricular hypothalamus (PVH) controls behavioral and physiologic
processes, including appetite, social behavior, autonomic outflow, and pituitary
hormone secretion. However, molecular markers for centrally projecting PVH neuron
populations remain largely undefined, and a complete census of PVH cell types
has not been established. Therefore, we performed extensive single-cell/nucleus
RNA sequencing to catalog PVH neuron subtypes and multiplexed error-robust fluorescence
in situ hybridization (MERFISH) to map them spatially. Our spatial transcriptomic
atlas resolves 26 Sim1+ and 29 GABAergic neuron populations from the PVH and surrounding
areas. Additionally, projection-based profiling identified neurons that project
to the parabrachial region (PB) and spinal cord, helping to determine PVH populations
that regulate satiety and sympathetic nervous system activity, respectively. Notably,
activation of PB-projecting PVH neurons expressing Brs3 reduces food intake, and
silencing them causes obesity. Together, this atlas contributes high-resolution
PVH spatial and circuit-based gene expression profiles, representing a valuable
resource for the field of homeostasis.
acknowledgement: "We would like to thank Drs. Mark Andermann, Joel Geerling, and Clifford\r\nSaper,
as well as the Lowell, Tsai, and Resch laboratories for helpful discussions;\r\nAlysia
Berns, Jia Yu, and Yanfang Li for technical support; the BNORC\r\nFunctional Genomics
and Bioinformatics Core (P30DK046200) and the Iowa\r\nInstitute for Human Genetics
Genomics Division (IIHG, RRID: SCR_023422)\r\nfor helpful discussions and technical
assistance with sc/snRNA-seq; Zachary\r\nNiziolek and the Bauer Core Facility at
Harvard University, the BIDMC Flow Cytometry\r\nCore, and Heath Vignes, Michael
Shey, and Thomas Kaufman of the\r\nFlow Cytometry Facility at the University of
Iowa Carver College of Medicine\r\nfor helpful discussions and technical support;
the ICCB-Longwood Screening\r\nFacility of Harvard Medical School for assistance
with the snRNA-seq\r\nexperiments; Dr. Sayak Mitter and Vizgen support for technical
assistance\r\nwith the MERSCOPE platform; and Mara Jendro and Li-Chun (Queena) Lin\r\nfor
their assistance with MERSCOPE experiments within the Iowa\r\nNeuroBank Core in
the Iowa Neuroscience Institute at the University of Iowa\r\nCarver College of Medicine.
This research was funded by the following NIH\r\ngrants to L.T.T.: R01DK128406;
to B.B.L.: R01DK075632, R01DK134427,\r\nand R01DK096010; to J.M.R.: R00HL144923
and R01NS141072; and to M.C.M.: F31HL170784; T.C.B. and M.C.M. were supported by
a pharmacological\r\nsciences predoctoral training grant T32GM144636. Additional
funding\r\nto J.M.R. came from the American Heart Association (AHA 935362), a University\r\nof
Iowa Fraternal Order of Eagles Diabetes Research Center Pilot and\r\nFeasibility
Catalyst Grant, and an Iowa Neuroscience Institute Early Stage\r\nInvestigator award
from the Carver Trust. Y.L. was supported by a predoctoral\r\nfellowship from the
American Heart Association (AHA 25PRE1372983). A.M.D.\r\nwas supported by a postdoctoral
fellowship from the Charles A. King Trust."
article_number: '116904'
article_processing_charge: Yes
article_type: original
author:
- first_name: Yuxi
full_name: Li, Yuxi
last_name: Li
- first_name: Trevor C.
full_name: Butler, Trevor C.
last_name: Butler
- first_name: Stefano
full_name: Nardone, Stefano
last_name: Nardone
- first_name: Christopher L.
full_name: Jacobs, Christopher L.
last_name: Jacobs
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
- first_name: Joseph C.
full_name: Madara, Joseph C.
last_name: Madara
- first_name: Miriam C.
full_name: McDonough, Miriam C.
last_name: McDonough
- first_name: Jenkang
full_name: Tao, Jenkang
last_name: Tao
- first_name: Elijah D.
full_name: Lowenstein, Elijah D.
last_name: Lowenstein
- first_name: Luhong
full_name: Wang, Luhong
last_name: Wang
- first_name: Deepti
full_name: Pant, Deepti
last_name: Pant
- first_name: Samuel J.
full_name: Walker, Samuel J.
last_name: Walker
- first_name: Annette
full_name: Wang, Annette
last_name: Wang
- first_name: Harini
full_name: Srinivasan, Harini
last_name: Srinivasan
- first_name: Zongfang
full_name: Yang, Zongfang
last_name: Yang
- first_name: John N.
full_name: Campbell, John N.
last_name: Campbell
- first_name: Linus T.
full_name: Tsai, Linus T.
last_name: Tsai
- first_name: Bradford B.
full_name: Lowell, Bradford B.
last_name: Lowell
- first_name: Jon M.
full_name: Resch, Jon M.
last_name: Resch
citation:
ama: Li Y, Butler TC, Nardone S, et al. A spatial and projection-based transcriptomic
atlas of paraventricular hypothalamic cell types. Cell Reports. 2026;45(2).
doi:10.1016/j.celrep.2025.116904
apa: Li, Y., Butler, T. C., Nardone, S., Jacobs, C. L., Douglass, A. M., Madara,
J. C., … Resch, J. M. (2026). A spatial and projection-based transcriptomic atlas
of paraventricular hypothalamic cell types. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2025.116904
chicago: Li, Yuxi, Trevor C. Butler, Stefano Nardone, Christopher L. Jacobs, Amelia
M. Douglass, Joseph C. Madara, Miriam C. McDonough, et al. “A Spatial and Projection-Based
Transcriptomic Atlas of Paraventricular Hypothalamic Cell Types.” Cell Reports.
Elsevier, 2026. https://doi.org/10.1016/j.celrep.2025.116904.
ieee: Y. Li et al., “A spatial and projection-based transcriptomic atlas
of paraventricular hypothalamic cell types,” Cell Reports, vol. 45, no.
2. Elsevier, 2026.
ista: Li Y, Butler TC, Nardone S, Jacobs CL, Douglass AM, Madara JC, McDonough MC,
Tao J, Lowenstein ED, Wang L, Pant D, Walker SJ, Wang A, Srinivasan H, Yang Z,
Campbell JN, Tsai LT, Lowell BB, Resch JM. 2026. A spatial and projection-based
transcriptomic atlas of paraventricular hypothalamic cell types. Cell Reports.
45(2), 116904.
mla: Li, Yuxi, et al. “A Spatial and Projection-Based Transcriptomic Atlas of Paraventricular
Hypothalamic Cell Types.” Cell Reports, vol. 45, no. 2, 116904, Elsevier,
2026, doi:10.1016/j.celrep.2025.116904.
short: Y. Li, T.C. Butler, S. Nardone, C.L. Jacobs, A.M. Douglass, J.C. Madara,
M.C. McDonough, J. Tao, E.D. Lowenstein, L. Wang, D. Pant, S.J. Walker, A. Wang,
H. Srinivasan, Z. Yang, J.N. Campbell, L.T. Tsai, B.B. Lowell, J.M. Resch, Cell
Reports 45 (2026).
date_created: 2026-04-16T13:51:29Z
date_published: 2026-02-24T00:00:00Z
date_updated: 2026-05-04T12:00:31Z
day: '24'
ddc:
- '570'
department:
- _id: AmDo
doi: 10.1016/j.celrep.2025.116904
external_id:
pmid:
- '41581146'
file:
- access_level: open_access
checksum: 82098dd9d0ca609119f9f2c6beb4fc1e
content_type: application/pdf
creator: dernst
date_created: 2026-05-04T11:58:51Z
date_updated: 2026-05-04T11:58:51Z
file_id: '21793'
file_name: 2026_CellReports_Li.pdf
file_size: 38532865
relation: main_file
success: 1
file_date_updated: 2026-05-04T11:58:51Z
has_accepted_license: '1'
intvolume: ' 45'
issue: '2'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: Cell Reports
publication_identifier:
eissn:
- 2211-1247
issn:
- 2639-1856
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A spatial and projection-based transcriptomic atlas of paraventricular hypothalamic
cell types
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 45
year: '2026'
...
---
OA_place: repository
OA_type: green
_id: '21955'
abstract:
- lang: eng
text: 'AgRP neurons cause hunger, the drive to seek and consume food. Their activation
by fasting is key for survival and is thought to be triggered by feedback when
energy stores are low. However, we know that environmental cues can also regulate
AgRP neurons since cues that predict future food intake rapidly inhibit AgRP neurons,
but is the converse true: can the prediction of future fasting rapidly activate
AgRP neurons? Here, we show in mice that such rapid fasting activation of AgRP
neurons does occur. This rapid activation is driven by excitatory input from paraventricular
hypothalamic (PVH) neurons expressing Sim2, which are bidirectionally sensitive
to predictions of future energy state. Thus, cognitively processed contextual
information conveyed by PVHSim2 neurons strongly activates AgRP neurons. Lastly,
chronic silencing of PVHSim2 neurons causes persistent hypophagia. This PVHSim2-to-AgRP-neuron
circuit, by anticipating and preventing negative energy balance, provides an important
new dimension of hunger regulation.'
acknowledgement: "We thank all members of the B.B.L. laboratory for helpful discussions.
We\r\nthank the BADERC and BNORC transgenic cores (NIH P30DK057521 and\r\nP30DK046200)
for performing embryo injections to generate knockin mouse\r\nlines. We also thank
the BIDMC Energy Balance Core (supported by NIH\r\nS10OD028635 and the Boston Area
Diabetes Endocrinology Research Centers, P30DK135043), where Marissa Cortopassi
performed indirect calorimetry experiments and Alexander Banks assisted with data
analysis and interpretation. Confocal imaging was performed at BIDMC’s Confocal
Imaging\r\nCore. We thank Chen Wu for assistance in designing knockin mouse lines.\r\nThis
work was supported by the NIH (R01DK134427, R01DK096010, and\r\nR01DK075632 to B.B.L.).
Authors were supported by an EMBO Long-Term\r\nFellowship (770-2018, S.J.W.), a
T32 Postdoctoral Training Fellowship\r\n(5T32DK007516, E.D.L.), the Charles A. King
Trust Postdoctoral Research\r\nFellowship program (A.M.D.), and a K99 Career Development
Award\r\n(K99HL144923, J.M.R.)."
article_processing_charge: No
article_type: original
author:
- first_name: Samuel J.
full_name: Walker, Samuel J.
last_name: Walker
- first_name: Elijah D.
full_name: Lowenstein, Elijah D.
last_name: Lowenstein
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
- first_name: Callum M.P.
full_name: Thomas, Callum M.P.
last_name: Thomas
- first_name: Joseph C.
full_name: Madara, Joseph C.
last_name: Madara
- first_name: Hakan
full_name: Kucukdereli, Hakan
last_name: Kucukdereli
- first_name: Eunice A.
full_name: Barbosa-Meillon, Eunice A.
last_name: Barbosa-Meillon
- first_name: Jenkang
full_name: Tao, Jenkang
last_name: Tao
- first_name: Jon M.
full_name: Resch, Jon M.
last_name: Resch
- first_name: Bradford B.
full_name: Lowell, Bradford B.
last_name: Lowell
citation:
ama: Walker SJ, Lowenstein ED, Douglass AM, et al. A hypothalamic circuit for anticipating
future changes in energy balance. Neuron. doi:10.1016/j.neuron.2026.05.010
apa: Walker, S. J., Lowenstein, E. D., Douglass, A. M., Thomas, C. M. P., Madara,
J. C., Kucukdereli, H., … Lowell, B. B. (n.d.). A hypothalamic circuit for anticipating
future changes in energy balance. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2026.05.010
chicago: Walker, Samuel J., Elijah D. Lowenstein, Amelia M. Douglass, Callum M.P.
Thomas, Joseph C. Madara, Hakan Kucukdereli, Eunice A. Barbosa-Meillon, Jenkang
Tao, Jon M. Resch, and Bradford B. Lowell. “A Hypothalamic Circuit for Anticipating
Future Changes in Energy Balance.” Neuron. Elsevier, n.d. https://doi.org/10.1016/j.neuron.2026.05.010.
ieee: S. J. Walker et al., “A hypothalamic circuit for anticipating future
changes in energy balance,” Neuron. Elsevier.
ista: Walker SJ, Lowenstein ED, Douglass AM, Thomas CMP, Madara JC, Kucukdereli
H, Barbosa-Meillon EA, Tao J, Resch JM, Lowell BB. A hypothalamic circuit for
anticipating future changes in energy balance. Neuron.
mla: Walker, Samuel J., et al. “A Hypothalamic Circuit for Anticipating Future Changes
in Energy Balance.” Neuron, Elsevier, doi:10.1016/j.neuron.2026.05.010.
short: S.J. Walker, E.D. Lowenstein, A.M. Douglass, C.M.P. Thomas, J.C. Madara,
H. Kucukdereli, E.A. Barbosa-Meillon, J. Tao, J.M. Resch, B.B. Lowell, Neuron
(n.d.).
date_created: 2026-06-08T09:24:25Z
date_published: 2026-06-03T00:00:00Z
date_updated: 2026-06-16T08:35:11Z
day: '03'
department:
- _id: AmDo
doi: 10.1016/j.neuron.2026.05.010
external_id:
pmid:
- '42235510'
keyword:
- hunger
- hypothalamus
- AGRP neurons
- neuroscience
- metabolism
- homeostasis
- feeding
- food intake
- energy balance
- appetite
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2025.09.27.678865
month: '06'
oa: 1
oa_version: Preprint
pmid: 1
publication: Neuron
publication_identifier:
eissn:
- ' 1097-4199'
issn:
- 0896-6273
publication_status: inpress
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A hypothalamic circuit for anticipating future changes in energy balance
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2026'
...
---
OA_type: closed access
_id: '19470'
abstract:
- lang: eng
text: When food is freely available, eating occurs without energy deficit. While
agouti-related peptide (AgRP) neurons are likely involved, their activation is
thought to require negative energy balance. To investigate this, we implemented
long-term, continuous in vivo fiber-photometry recordings in mice. We discovered
new forms of AgRP neuron regulation, including fast pre-ingestive decreases in
activity and unexpectedly rapid activation by fasting. Furthermore, AgRP neuron
activity has a circadian rhythm that peaks concurrent with the daily feeding onset.
Importantly, this rhythm persists when nutrition is provided via constant-rate
gastric infusions. Hence, it is not secondary to a circadian feeding rhythm. The
AgRP neuron rhythm is driven by the circadian clock, the suprachiasmatic nucleus
(SCN), as SCN ablation abolishes the circadian rhythm in AgRP neuron activity
and feeding. The SCN activates AgRP neurons via excitatory afferents from thyrotrophin-releasing
hormone-expressing neurons in the dorsomedial hypothalamus (DMHTrh neurons) to
drive daily feeding rhythms.
article_processing_charge: No
article_type: original
author:
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
- first_name: Hakan
full_name: Kucukdereli, Hakan
last_name: Kucukdereli
- first_name: Joseph C.
full_name: Madara, Joseph C.
last_name: Madara
- first_name: Daqing
full_name: Wang, Daqing
last_name: Wang
- first_name: Chen
full_name: Wu, Chen
last_name: Wu
- first_name: Elijah D.
full_name: Lowenstein, Elijah D.
last_name: Lowenstein
- first_name: Jenkang
full_name: Tao, Jenkang
last_name: Tao
- first_name: Bradford B.
full_name: Lowell, Bradford B.
last_name: Lowell
citation:
ama: Douglass AM, Kucukdereli H, Madara JC, et al. Acute and circadian feedforward
regulation of agouti-related peptide hunger neurons. Cell Metabolism. 2024;37(3):708-722.e5.
doi:10.1016/j.cmet.2024.11.009
apa: Douglass, A. M., Kucukdereli, H., Madara, J. C., Wang, D., Wu, C., Lowenstein,
E. D., … Lowell, B. B. (2024). Acute and circadian feedforward regulation of agouti-related
peptide hunger neurons. Cell Metabolism. Elsevier. https://doi.org/10.1016/j.cmet.2024.11.009
chicago: Douglass, Amelia M., Hakan Kucukdereli, Joseph C. Madara, Daqing Wang,
Chen Wu, Elijah D. Lowenstein, Jenkang Tao, and Bradford B. Lowell. “Acute and
Circadian Feedforward Regulation of Agouti-Related Peptide Hunger Neurons.” Cell
Metabolism. Elsevier, 2024. https://doi.org/10.1016/j.cmet.2024.11.009.
ieee: A. M. Douglass et al., “Acute and circadian feedforward regulation
of agouti-related peptide hunger neurons,” Cell Metabolism, vol. 37, no.
3. Elsevier, p. 708–722.e5, 2024.
ista: Douglass AM, Kucukdereli H, Madara JC, Wang D, Wu C, Lowenstein ED, Tao J,
Lowell BB. 2024. Acute and circadian feedforward regulation of agouti-related
peptide hunger neurons. Cell Metabolism. 37(3), 708–722.e5.
mla: Douglass, Amelia M., et al. “Acute and Circadian Feedforward Regulation of
Agouti-Related Peptide Hunger Neurons.” Cell Metabolism, vol. 37, no. 3,
Elsevier, 2024, p. 708–722.e5, doi:10.1016/j.cmet.2024.11.009.
short: A.M. Douglass, H. Kucukdereli, J.C. Madara, D. Wang, C. Wu, E.D. Lowenstein,
J. Tao, B.B. Lowell, Cell Metabolism 37 (2024) 708–722.e5.
date_created: 2025-04-03T12:27:39Z
date_published: 2024-03-04T00:00:00Z
date_updated: 2025-07-10T11:51:40Z
day: '04'
doi: 10.1016/j.cmet.2024.11.009
extern: '1'
external_id:
pmid:
- '39719709'
intvolume: ' 37'
issue: '3'
language:
- iso: eng
month: '03'
oa_version: None
page: 708-722.e5
pmid: 1
publication: Cell Metabolism
publication_identifier:
issn:
- 1550-4131
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Acute and circadian feedforward regulation of agouti-related peptide hunger
neurons
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 37
year: '2024'
...
---
OA_place: repository
OA_type: green
_id: '19471'
abstract:
- lang: eng
text: 'Fasting initiates a multitude of adaptations to allow survival. Activation
of the hypothalamic–pituitary–adrenal (HPA) axis and subsequent release of glucocorticoid
hormones is a key response that mobilizes fuel stores to meet energy demands1,2,3,4,5.
Despite the importance of the HPA axis response, the neural mechanisms that drive
its activation during energy deficit are unknown. Here, we show that fasting-activated
hypothalamic agouti-related peptide (AgRP)-expressing neurons trigger and are
essential for fasting-induced HPA axis activation. AgRP neurons do so through
projections to the paraventricular hypothalamus (PVH), where, in a mechanism not
previously described for AgRP neurons, they presynaptically inhibit the terminals
of tonically active GABAergic afferents from the bed nucleus of the stria terminalis
(BNST) that otherwise restrain activity of corticotrophin-releasing hormone (CRH)-expressing
neurons. This disinhibition of PVHCrh neurons requires γ-aminobutyric acid (GABA)/GABA-B
receptor signalling and potently activates the HPA axis. Notably, stimulation
of the HPA axis by AgRP neurons is independent of their induction of hunger, showing
that these canonical ‘hunger neurons’ drive many distinctly different adaptations
to the fasted state. Together, our findings identify the neural basis for fasting-induced
HPA axis activation and uncover a unique means by which AgRP neurons activate
downstream neurons: through presynaptic inhibition of GABAergic afferents. Given
the potency of this disinhibition of tonically active BNST afferents, other activators
of the HPA axis, such as psychological stress, may also work by reducing BNST
inhibitory tone onto PVHCrh neurons.'
article_processing_charge: No
article_type: original
author:
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
- first_name: Jon M.
full_name: Resch, Jon M.
last_name: Resch
- first_name: Joseph C.
full_name: Madara, Joseph C.
last_name: Madara
- first_name: Hakan
full_name: Kucukdereli, Hakan
last_name: Kucukdereli
- first_name: Ofer
full_name: Yizhar, Ofer
last_name: Yizhar
- first_name: Abhinav
full_name: Grama, Abhinav
last_name: Grama
- first_name: Masahito
full_name: Yamagata, Masahito
last_name: Yamagata
- first_name: Zongfang
full_name: Yang, Zongfang
last_name: Yang
- first_name: Bradford B.
full_name: Lowell, Bradford B.
last_name: Lowell
citation:
ama: Douglass AM, Resch JM, Madara JC, et al. Neural basis for fasting activation
of the hypothalamic–pituitary–adrenal axis. Nature. 2023;620(7972):154-162.
doi:10.1038/s41586-023-06358-0
apa: Douglass, A. M., Resch, J. M., Madara, J. C., Kucukdereli, H., Yizhar, O.,
Grama, A., … Lowell, B. B. (2023). Neural basis for fasting activation of the
hypothalamic–pituitary–adrenal axis. Nature. Springer Nature. https://doi.org/10.1038/s41586-023-06358-0
chicago: Douglass, Amelia M., Jon M. Resch, Joseph C. Madara, Hakan Kucukdereli,
Ofer Yizhar, Abhinav Grama, Masahito Yamagata, Zongfang Yang, and Bradford B.
Lowell. “Neural Basis for Fasting Activation of the Hypothalamic–Pituitary–Adrenal
Axis.” Nature. Springer Nature, 2023. https://doi.org/10.1038/s41586-023-06358-0.
ieee: A. M. Douglass et al., “Neural basis for fasting activation of the
hypothalamic–pituitary–adrenal axis,” Nature, vol. 620, no. 7972. Springer
Nature, pp. 154–162, 2023.
ista: Douglass AM, Resch JM, Madara JC, Kucukdereli H, Yizhar O, Grama A, Yamagata
M, Yang Z, Lowell BB. 2023. Neural basis for fasting activation of the hypothalamic–pituitary–adrenal
axis. Nature. 620(7972), 154–162.
mla: Douglass, Amelia M., et al. “Neural Basis for Fasting Activation of the Hypothalamic–Pituitary–Adrenal
Axis.” Nature, vol. 620, no. 7972, Springer Nature, 2023, pp. 154–62, doi:10.1038/s41586-023-06358-0.
short: A.M. Douglass, J.M. Resch, J.C. Madara, H. Kucukdereli, O. Yizhar, A. Grama,
M. Yamagata, Z. Yang, B.B. Lowell, Nature 620 (2023) 154–162.
date_created: 2025-04-03T12:28:51Z
date_published: 2023-08-03T00:00:00Z
date_updated: 2025-07-10T11:51:40Z
day: '03'
doi: 10.1038/s41586-023-06358-0
extern: '1'
external_id:
pmid:
- '37495689 '
intvolume: ' 620'
issue: '7972'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://pmc.ncbi.nlm.nih.gov/articles/PMC11168300/
month: '08'
oa: 1
oa_version: Submitted Version
page: 154-162
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neural basis for fasting activation of the hypothalamic–pituitary–adrenal axis
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 620
year: '2023'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '19472'
abstract:
- lang: eng
text: The forebrain hemispheres are predominantly separated during embryogenesis
by the interhemispheric fissure (IHF). Radial astroglia remodel the IHF to form
a continuous substrate between the hemispheres for midline crossing of the corpus
callosum (CC) and hippocampal commissure (HC). Deleted in colorectal carcinoma
(DCC) and netrin 1 (NTN1) are molecules that have an evolutionarily conserved
function in commissural axon guidance. The CC and HC are absent in Dcc
and Ntn1 knockout mice, while other commissures are
only partially affected, suggesting an additional aetiology in forebrain commissure
formation. Here, we find that these molecules play a critical role in regulating
astroglial development and IHF remodelling during CC and HC formation. Human subjects
with DCC mutations display disrupted IHF remodelling
associated with CC and HC malformations. Thus, axon guidance molecules such as
DCC and NTN1 first regulate the formation of a midline substrate for dorsal commissures
prior to their role in regulating axonal growth and guidance across it.
article_number: '61769'
article_processing_charge: Yes
article_type: original
author:
- first_name: Laura
full_name: Morcom, Laura
last_name: Morcom
- first_name: Ilan
full_name: Gobius, Ilan
last_name: Gobius
- first_name: Ashley PL
full_name: Marsh, Ashley PL
last_name: Marsh
- first_name: Rodrigo
full_name: Suárez, Rodrigo
last_name: Suárez
- first_name: Jonathan WC
full_name: Lim, Jonathan WC
last_name: Lim
- first_name: Caitlin
full_name: Bridges, Caitlin
last_name: Bridges
- first_name: Yunan
full_name: Ye, Yunan
last_name: Ye
- first_name: Laura R
full_name: Fenlon, Laura R
last_name: Fenlon
- first_name: Yvrick
full_name: Zagar, Yvrick
last_name: Zagar
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
- first_name: Amber-Lee S
full_name: Donahoo, Amber-Lee S
last_name: Donahoo
- first_name: Thomas
full_name: Fothergill, Thomas
last_name: Fothergill
- first_name: Samreen
full_name: Shaikh, Samreen
last_name: Shaikh
- first_name: Peter
full_name: Kozulin, Peter
last_name: Kozulin
- first_name: Timothy J
full_name: Edwards, Timothy J
last_name: Edwards
- first_name: Helen M
full_name: Cooper, Helen M
last_name: Cooper
- first_name: Elliott H
full_name: Sherr, Elliott H
last_name: Sherr
- first_name: Alain
full_name: Chédotal, Alain
last_name: Chédotal
- first_name: Richard J
full_name: Leventer, Richard J
last_name: Leventer
- first_name: Paul J
full_name: Lockhart, Paul J
last_name: Lockhart
- first_name: Linda J
full_name: Richards, Linda J
last_name: Richards
citation:
ama: Morcom L, Gobius I, Marsh AP, et al. DCC regulates astroglial development essential
for telencephalic morphogenesis and corpus callosum formation. eLife. 2021;10.
doi:10.7554/elife.61769
apa: Morcom, L., Gobius, I., Marsh, A. P., Suárez, R., Lim, J. W., Bridges, C.,
… Richards, L. J. (2021). DCC regulates astroglial development essential for telencephalic
morphogenesis and corpus callosum formation. ELife. eLife Sciences Publications.
https://doi.org/10.7554/elife.61769
chicago: Morcom, Laura, Ilan Gobius, Ashley PL Marsh, Rodrigo Suárez, Jonathan WC
Lim, Caitlin Bridges, Yunan Ye, et al. “DCC Regulates Astroglial Development Essential
for Telencephalic Morphogenesis and Corpus Callosum Formation.” ELife.
eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.61769.
ieee: L. Morcom et al., “DCC regulates astroglial development essential for
telencephalic morphogenesis and corpus callosum formation,” eLife, vol.
10. eLife Sciences Publications, 2021.
ista: Morcom L, Gobius I, Marsh AP, Suárez R, Lim JW, Bridges C, Ye Y, Fenlon LR,
Zagar Y, Douglass AM, Donahoo A-LS, Fothergill T, Shaikh S, Kozulin P, Edwards
TJ, Cooper HM, Sherr EH, Chédotal A, Leventer RJ, Lockhart PJ, Richards LJ. 2021.
DCC regulates astroglial development essential for telencephalic morphogenesis
and corpus callosum formation. eLife. 10, 61769.
mla: Morcom, Laura, et al. “DCC Regulates Astroglial Development Essential for Telencephalic
Morphogenesis and Corpus Callosum Formation.” ELife, vol. 10, 61769, eLife
Sciences Publications, 2021, doi:10.7554/elife.61769.
short: L. Morcom, I. Gobius, A.P. Marsh, R. Suárez, J.W. Lim, C. Bridges, Y. Ye,
L.R. Fenlon, Y. Zagar, A.M. Douglass, A.-L.S. Donahoo, T. Fothergill, S. Shaikh,
P. Kozulin, T.J. Edwards, H.M. Cooper, E.H. Sherr, A. Chédotal, R.J. Leventer,
P.J. Lockhart, L.J. Richards, ELife 10 (2021).
date_created: 2025-04-03T12:29:29Z
date_published: 2021-04-19T00:00:00Z
date_updated: 2025-07-10T11:51:41Z
day: '19'
doi: 10.7554/elife.61769
extern: '1'
external_id:
pmid:
- '33871356'
has_accepted_license: '1'
intvolume: ' 10'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
main_file_link:
- open_access: '1'
url: https://doi.org/10.7554/eLife.61769
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: DCC regulates astroglial development essential for telencephalic morphogenesis
and corpus callosum formation
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2021'
...
---
OA_place: publisher
OA_type: hybrid
_id: '19473'
abstract:
- lang: eng
text: Leptin informs the brain about sufficiency of fuel stores. When insufficient,
leptin levels fall, triggering compensatory increases in appetite. Falling leptin
is first sensed by hypothalamic neurons, which then initiate adaptive responses.
With regard to hunger, it is thought that leptin-sensing neurons work entirely
via circuits within the central nervous system (CNS). Very unexpectedly, however,
we now show this is not the case. Instead, stimulation of hunger requires an intervening
endocrine step, namely activation of the hypothalamic–pituitary–adrenocortical
(HPA) axis. Increased corticosterone then activates AgRP neurons to fully increase
hunger. Importantly, this is true for 2 forms of low leptin-induced hunger, fasting
and poorly controlled type 1 diabetes. Hypoglycemia, which also stimulates hunger
by activating CNS neurons, albeit independently of leptin, similarly recruits
and requires this pathway by which HPA axis activity stimulates AgRP neurons.
Thus, HPA axis regulation of AgRP neurons is a previously underappreciated step
in homeostatic regulation of hunger.
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Rachel J.
full_name: Perry, Rachel J.
last_name: Perry
- first_name: Jon M.
full_name: Resch, Jon M.
last_name: Resch
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
- first_name: Joseph C.
full_name: Madara, Joseph C.
last_name: Madara
- first_name: Aviva
full_name: Rabin-Court, Aviva
last_name: Rabin-Court
- first_name: Hakan
full_name: Kucukdereli, Hakan
last_name: Kucukdereli
- first_name: Chen
full_name: Wu, Chen
last_name: Wu
- first_name: Joongyu D.
full_name: Song, Joongyu D.
last_name: Song
- first_name: Bradford B.
full_name: Lowell, Bradford B.
last_name: Lowell
- first_name: Gerald I.
full_name: Shulman, Gerald I.
last_name: Shulman
citation:
ama: Perry RJ, Resch JM, Douglass AM, et al. Leptin’s hunger-suppressing effects
are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents. Proceedings
of the National Academy of Sciences. 2019;116(27):13670-13679. doi:10.1073/pnas.1901795116
apa: Perry, R. J., Resch, J. M., Douglass, A. M., Madara, J. C., Rabin-Court, A.,
Kucukdereli, H., … Shulman, G. I. (2019). Leptin’s hunger-suppressing effects
are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents. Proceedings
of the National Academy of Sciences. National Academy of Sciences. https://doi.org/10.1073/pnas.1901795116
chicago: Perry, Rachel J., Jon M. Resch, Amelia M. Douglass, Joseph C. Madara, Aviva
Rabin-Court, Hakan Kucukdereli, Chen Wu, Joongyu D. Song, Bradford B. Lowell,
and Gerald I. Shulman. “Leptin’s Hunger-Suppressing Effects Are Mediated by the
Hypothalamic–Pituitary–Adrenocortical Axis in Rodents.” Proceedings of the
National Academy of Sciences. National Academy of Sciences, 2019. https://doi.org/10.1073/pnas.1901795116.
ieee: R. J. Perry et al., “Leptin’s hunger-suppressing effects are mediated
by the hypothalamic–pituitary–adrenocortical axis in rodents,” Proceedings
of the National Academy of Sciences, vol. 116, no. 27. National Academy of
Sciences, pp. 13670–13679, 2019.
ista: Perry RJ, Resch JM, Douglass AM, Madara JC, Rabin-Court A, Kucukdereli H,
Wu C, Song JD, Lowell BB, Shulman GI. 2019. Leptin’s hunger-suppressing effects
are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents. Proceedings
of the National Academy of Sciences. 116(27), 13670–13679.
mla: Perry, Rachel J., et al. “Leptin’s Hunger-Suppressing Effects Are Mediated
by the Hypothalamic–Pituitary–Adrenocortical Axis in Rodents.” Proceedings
of the National Academy of Sciences, vol. 116, no. 27, National Academy of
Sciences, 2019, pp. 13670–79, doi:10.1073/pnas.1901795116.
short: R.J. Perry, J.M. Resch, A.M. Douglass, J.C. Madara, A. Rabin-Court, H. Kucukdereli,
C. Wu, J.D. Song, B.B. Lowell, G.I. Shulman, Proceedings of the National Academy
of Sciences 116 (2019) 13670–13679.
date_created: 2025-04-03T12:30:19Z
date_published: 2019-07-02T00:00:00Z
date_updated: 2025-07-10T11:51:42Z
day: '02'
ddc:
- '570'
doi: 10.1073/pnas.1901795116
extern: '1'
external_id:
pmid:
- '31213533'
has_accepted_license: '1'
intvolume: ' 116'
issue: '27'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1073/pnas.1901795116
month: '07'
oa: 1
oa_version: Published Version
page: 13670-13679
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
eissn:
- 1091-6490
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
scopus_import: '1'
status: public
title: Leptin’s hunger-suppressing effects are mediated by the hypothalamic–pituitary–adrenocortical
axis in rodents
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 116
year: '2019'
...
---
OA_place: repository
OA_type: green
_id: '19474'
abstract:
- lang: eng
text: The complex behaviors underlying reward seeking and consumption are integral
to organism survival. The hypothalamus and mesolimbic dopamine system are key
mediators of these behaviors, yet regulation of appetitive and consummatory behaviors
outside of these regions is poorly understood. The central nucleus of the amygdala
(CeA) has been implicated in feeding and reward, but the neurons and circuit mechanisms
that positively regulate these behaviors remain unclear. Here, we defined the
neuronal mechanisms by which CeA neurons promote food consumption. Using in vivo
activity manipulations and Ca2+ imaging in mice, we found that GABAergic serotonin
receptor 2a (Htr2a)-expressing CeA neurons modulate food consumption, promote
positive reinforcement and are active in vivo during eating. We demonstrated electrophysiologically,
anatomically and behaviorally that intra-CeA and long-range circuit mechanisms
underlie these behaviors. Finally, we showed that CeAHtr2a neurons receive inputs
from feeding-relevant brain regions. Our results illustrate how defined CeA neural
circuits positively regulate food consumption.
article_processing_charge: No
article_type: original
author:
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
- first_name: Hakan
full_name: Kucukdereli, Hakan
last_name: Kucukdereli
- first_name: Marion
full_name: Ponserre, Marion
last_name: Ponserre
- first_name: Milica
full_name: Markovic, Milica
last_name: Markovic
- first_name: Jan
full_name: Gründemann, Jan
last_name: Gründemann
- first_name: Cornelia
full_name: Strobel, Cornelia
last_name: Strobel
- first_name: Pilar L
full_name: Alcala Morales, Pilar L
last_name: Alcala Morales
- first_name: Karl-Klaus
full_name: Conzelmann, Karl-Klaus
last_name: Conzelmann
- first_name: Andreas
full_name: Lüthi, Andreas
last_name: Lüthi
- first_name: Rüdiger
full_name: Klein, Rüdiger
last_name: Klein
citation:
ama: Douglass AM, Kucukdereli H, Ponserre M, et al. Central amygdala circuits modulate
food consumption through a positive-valence mechanism. Nature Neuroscience.
2017;20(10):1384-1394. doi:10.1038/nn.4623
apa: Douglass, A. M., Kucukdereli, H., Ponserre, M., Markovic, M., Gründemann, J.,
Strobel, C., … Klein, R. (2017). Central amygdala circuits modulate food consumption
through a positive-valence mechanism. Nature Neuroscience. Springer Nature.
https://doi.org/10.1038/nn.4623
chicago: Douglass, Amelia M., Hakan Kucukdereli, Marion Ponserre, Milica Markovic,
Jan Gründemann, Cornelia Strobel, Pilar L Alcala Morales, Karl-Klaus Conzelmann,
Andreas Lüthi, and Rüdiger Klein. “Central Amygdala Circuits Modulate Food Consumption
through a Positive-Valence Mechanism.” Nature Neuroscience. Springer Nature,
2017. https://doi.org/10.1038/nn.4623.
ieee: A. M. Douglass et al., “Central amygdala circuits modulate food consumption
through a positive-valence mechanism,” Nature Neuroscience, vol. 20, no.
10. Springer Nature, pp. 1384–1394, 2017.
ista: Douglass AM, Kucukdereli H, Ponserre M, Markovic M, Gründemann J, Strobel
C, Alcala Morales PL, Conzelmann K-K, Lüthi A, Klein R. 2017. Central amygdala
circuits modulate food consumption through a positive-valence mechanism. Nature
Neuroscience. 20(10), 1384–1394.
mla: Douglass, Amelia M., et al. “Central Amygdala Circuits Modulate Food Consumption
through a Positive-Valence Mechanism.” Nature Neuroscience, vol. 20, no.
10, Springer Nature, 2017, pp. 1384–94, doi:10.1038/nn.4623.
short: A.M. Douglass, H. Kucukdereli, M. Ponserre, M. Markovic, J. Gründemann, C.
Strobel, P.L. Alcala Morales, K.-K. Conzelmann, A. Lüthi, R. Klein, Nature Neuroscience
20 (2017) 1384–1394.
date_created: 2025-04-03T12:30:57Z
date_published: 2017-10-01T00:00:00Z
date_updated: 2025-07-10T11:51:42Z
day: '01'
doi: 10.1038/nn.4623
extern: '1'
external_id:
pmid:
- '28825719 '
intvolume: ' 20'
issue: '10'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/145375
month: '10'
oa: 1
oa_version: Preprint
page: 1384-1394
pmid: 1
publication: Nature Neuroscience
publication_identifier:
eissn:
- 1546-1726
issn:
- 1097-6256
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Central amygdala circuits modulate food consumption through a positive-valence
mechanism
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 20
year: '2017'
...
---
OA_type: closed access
_id: '19475'
abstract:
- lang: eng
text: The left and right sides of the nervous system communicate via commissural
axons that cross the midline during development using evolutionarily conserved
molecules. These guidance cues have been particularly well studied in the mammalian
spinal cord, but it remains unclear whether these guidance mechanisms for commissural
axons are similar in the developing forebrain, in particular for the corpus callosum,
the largest and most important commissure for cortical function. Here, we show
that Netrin1 initially attracts callosal pioneering axons derived from the cingulate
cortex, but surprisingly is not attractive for the neocortical callosal axons
that make up the bulk of the projection. Instead, we show that Netrin-deleted
in colorectal cancer signaling acts in a fundamentally different manner, to prevent
the Slit2-mediated repulsion of precrossing axons thereby allowing them to approach
and cross the midline. These results provide the first evidence for how callosal
axons integrate multiple guidance cues to navigate the midline.
article_processing_charge: No
article_type: original
author:
- first_name: Thomas
full_name: Fothergill, Thomas
last_name: Fothergill
- first_name: Amber-Lee S.
full_name: Donahoo, Amber-Lee S.
last_name: Donahoo
- first_name: Amelia May Barnett
full_name: Douglass, Amelia May Barnett
id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289
last_name: Douglass
orcid: 0000-0001-5398-6473
- first_name: Oressia
full_name: Zalucki, Oressia
last_name: Zalucki
- first_name: Jiajia
full_name: Yuan, Jiajia
last_name: Yuan
- first_name: Tianzhi
full_name: Shu, Tianzhi
last_name: Shu
- first_name: Geoffrey J.
full_name: Goodhill, Geoffrey J.
last_name: Goodhill
- first_name: Linda J.
full_name: Richards, Linda J.
last_name: Richards
citation:
ama: Fothergill T, Donahoo A-LS, Douglass AM, et al. Netrin-DCC signaling regulates
corpus callosum formation through attraction of pioneering axons and by modulating
Slit2-mediated repulsion. Cerebral Cortex. 2014;24(5):1138-1151. doi:10.1093/cercor/bhs395
apa: Fothergill, T., Donahoo, A.-L. S., Douglass, A. M., Zalucki, O., Yuan, J.,
Shu, T., … Richards, L. J. (2014). Netrin-DCC signaling regulates corpus callosum
formation through attraction of pioneering axons and by modulating Slit2-mediated
repulsion. Cerebral Cortex. Oxford University Press. https://doi.org/10.1093/cercor/bhs395
chicago: Fothergill, Thomas, Amber-Lee S. Donahoo, Amelia M. Douglass, Oressia Zalucki,
Jiajia Yuan, Tianzhi Shu, Geoffrey J. Goodhill, and Linda J. Richards. “Netrin-DCC
Signaling Regulates Corpus Callosum Formation through Attraction of Pioneering
Axons and by Modulating Slit2-Mediated Repulsion.” Cerebral Cortex. Oxford
University Press, 2014. https://doi.org/10.1093/cercor/bhs395.
ieee: T. Fothergill et al., “Netrin-DCC signaling regulates corpus callosum
formation through attraction of pioneering axons and by modulating Slit2-mediated
repulsion,” Cerebral Cortex, vol. 24, no. 5. Oxford University Press, pp.
1138–1151, 2014.
ista: Fothergill T, Donahoo A-LS, Douglass AM, Zalucki O, Yuan J, Shu T, Goodhill
GJ, Richards LJ. 2014. Netrin-DCC signaling regulates corpus callosum formation
through attraction of pioneering axons and by modulating Slit2-mediated repulsion.
Cerebral Cortex. 24(5), 1138–1151.
mla: Fothergill, Thomas, et al. “Netrin-DCC Signaling Regulates Corpus Callosum
Formation through Attraction of Pioneering Axons and by Modulating Slit2-Mediated
Repulsion.” Cerebral Cortex, vol. 24, no. 5, Oxford University Press, 2014,
pp. 1138–51, doi:10.1093/cercor/bhs395.
short: T. Fothergill, A.-L.S. Donahoo, A.M. Douglass, O. Zalucki, J. Yuan, T. Shu,
G.J. Goodhill, L.J. Richards, Cerebral Cortex 24 (2014) 1138–1151.
date_created: 2025-04-03T12:31:58Z
date_published: 2014-05-01T00:00:00Z
date_updated: 2025-07-10T11:51:43Z
day: '01'
doi: 10.1093/cercor/bhs395
extern: '1'
external_id:
pmid:
- '23302812 '
intvolume: ' 24'
issue: '5'
language:
- iso: eng
month: '05'
oa_version: None
page: 1138-1151
pmid: 1
publication: Cerebral Cortex
publication_identifier:
eissn:
- 1460-2199
issn:
- 1047-3211
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Netrin-DCC signaling regulates corpus callosum formation through attraction
of pioneering axons and by modulating Slit2-mediated repulsion
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 24
year: '2014'
...