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Stress increases GABAergic neurotransmission in CRF neurons of the central amygdala and bed nucleus stria terminalis.
Neuropharmacology 2016; 107:239-250N

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.

Authors+Show Affiliations

Department of Pharmacology & Physiology, Georgetown University School of Medicine, Washington, DC 20007, USA; Interdisciplinary Program in Neuroscience, Georgetown University School of Medicine, Washington, DC 20007, USA. Electronic address: jp374@georgetown.edu.Department of Pharmacology & Physiology, Georgetown University School of Medicine, Washington, DC 20007, USA; Interdisciplinary Program in Neuroscience, Georgetown University School of Medicine, Washington, DC 20007, USA.Department of Pharmacology & Physiology, Georgetown University School of Medicine, Washington, DC 20007, USA.Department of Biology, Georgetown University School of Medicine, Washington, DC 20007, USA.Interdisciplinary Program in Neuroscience, Georgetown University School of Medicine, Washington, DC 20007, USA; Department of Obstetrics & Gynecology, University of Washington, Seattle, WA 98195, USA.Abramson Pediatric Research Center, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.Department of Pharmacology & Physiology, Georgetown University School of Medicine, Washington, DC 20007, USA; Interdisciplinary Program in Neuroscience, Georgetown University School of Medicine, Washington, DC 20007, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27016019

Citation

Partridge, John G., et al. "Stress Increases GABAergic Neurotransmission in CRF Neurons of the Central Amygdala and Bed Nucleus Stria Terminalis." Neuropharmacology, vol. 107, 2016, pp. 239-250.
Partridge JG, Forcelli PA, Luo R, et al. Stress increases GABAergic neurotransmission in CRF neurons of the central amygdala and bed nucleus stria terminalis. Neuropharmacology. 2016;107:239-250.
Partridge, J. G., Forcelli, P. A., Luo, R., Cashdan, J. M., Schulkin, J., Valentino, R. J., & Vicini, S. (2016). Stress increases GABAergic neurotransmission in CRF neurons of the central amygdala and bed nucleus stria terminalis. Neuropharmacology, 107, pp. 239-250. doi:10.1016/j.neuropharm.2016.03.029.
Partridge JG, et al. Stress Increases GABAergic Neurotransmission in CRF Neurons of the Central Amygdala and Bed Nucleus Stria Terminalis. Neuropharmacology. 2016;107:239-250. PubMed PMID: 27016019.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Stress increases GABAergic neurotransmission in CRF neurons of the central amygdala and bed nucleus stria terminalis. AU - Partridge,John G, AU - Forcelli,Patrick A, AU - Luo,Ruixi, AU - Cashdan,Jonah M, AU - Schulkin,Jay, AU - Valentino,Rita J, AU - Vicini,Stefano, Y1 - 2016/03/22/ PY - 2015/10/21/received PY - 2016/03/17/revised PY - 2016/03/21/accepted PY - 2016/3/27/entrez PY - 2016/3/27/pubmed PY - 2017/6/20/medline KW - ChR2 KW - Chronic unpredictable stress KW - Corticotropin releasing factor KW - GABA SP - 239 EP - 250 JF - Neuropharmacology JO - Neuropharmacology VL - 107 N2 - 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. SN - 1873-7064 UR - https://www.unboundmedicine.com/medline/citation/27016019/Stress_increases_GABAergic_neurotransmission_in_CRF_neurons_of_the_central_amygdala_and_bed_nucleus_stria_terminalis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(16)30101-0 DB - PRIME DP - Unbound Medicine ER -