Cited by 81Neuroscience and Neuropharmacology ResearchNeuropeptides and Animal PhysiologyStress Responses and Cortisol

Stress increases GABAergic neurotransmission in CRF neurons of the central amygdala and bed nucleus stria terminalis

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Partridge, John G., Forcelli, Patrick A., Luo, Ruixi, Cashdan, Jonah M., Schulkin, Jay, Valentino, Rita J., Vicini, Stefano·2016·Neuropharmacology

Abstract

Corticotrophin Releasing Factor (CRF) is a critical stress-related neuropeptide in major output pathways of the amygdala, including the central nucleus (CeA), and in a key projection target of the CeA, the bed nucleus of the stria terminalis (BnST). While progress has been made in understanding the contributions and characteristics of CRF as a neuropeptide in rodent behavior, little attention has been committed to determine the properties and synaptic physiology of specific populations of CRF-expressing (CRF(+)) and non-expressing (CRF(-)) neurons in the CeA and BnST. Here, we fill this gap by electrophysiologically characterizing distinct neuronal subtypes in CeA and BnST. Crossing tdTomato or channelrhodopsin-2 (ChR2-YFP) reporter mice to those expressing Cre-recombinase under the CRF promoter allowed us to identify and manipulate CRF(+) and CRF(-) neurons in CeA and BnST, the two largest areas with fluorescently labeled neurons in these mice. We optogenetically activated CRF(+) neurons to elicit action potentials or synaptic responses in CRF(+) and CRF(-) neurons. We found that GABA is the predominant co-transmitter in CRF(+) neurons within the CeA and BnST. CRF(+) neurons are highly interconnected with CRF(-) neurons and to a lesser extent with CRF(+) neurons. CRF(+) and CRF(-) neurons differentially express tonic GABA currents. Chronic, unpredictable stress increase the amplitude of evoked IPSCs and connectivity between CRF(+) neurons, but not between CRF(+) and CRF(-) neurons in both regions. We propose that reciprocal inhibition of interconnected neurons controls CRF(+) output in these nuclei.

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Crossref · 10.1016/j.neuropharm.2016.03.029

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Authors
Partridge, J. G., Forcelli, P. A., Luo, R., Cashdan, J. M., Schulkin, J., Valentino, R. J., & Vicini, S.
Affiliations
  • Georgetown University (US)
  • Children's Hospital of Philadelphia (US)
Corresponding author
Partridge, John G.
Venue
Neuropharmacology
Publisher
Elsevier BV
Published
2016-08
Volume
107
Pages
239-250
ISSN
0028-3908 (ISSN-L)
OpenAlex
W2304290531
Cited by
81
References
83
Citations by year
2026: 7 · 2025: 6 · 2024: 5 · 2023: 8 · 2022: 9 · 2021: 8 · 2020: 9 · 2019: 9 · 2018: 7 · 2017: 11 · 2016: 2
FWCI
5.42
Type
journal article
Language
en
Open access
Locations
  • Neuropharmacology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
Georgetown University
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
corticotropin-releasing factor, CRF neurons, central amygdala, bed nucleus of the stria terminalis, GABAergic neurotransmission, inhibitory postsynaptic currents, chronic unpredictable mild stress, neuronal connectivity, reciprocal inhibition, optogenetic stimulation, stress response
MeSH terms
Animals, Corticotropin-Releasing Hormone, Female, gamma-Aminobutyric Acid, Male, Mice, Inbred C57BL, Mice, Transgenic, Synaptic Transmission, Organ Culture Techniques, Septal Nuclei, Stress, Psychological, Mice, GABAergic Neurons, Central Amygdaloid Nucleus

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