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Neuropharmacology. 2016 Aug;107:239-250. doi: 10.1016/j.neuropharm.2016.03.029. Epub 2016 Mar 22.

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

Author information

1
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.
2
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.
3
Department of Pharmacology & Physiology, Georgetown University School of Medicine, Washington, DC 20007, USA.
4
Department of Biology, Georgetown University School of Medicine, Washington, DC 20007, USA.
5
Interdisciplinary Program in Neuroscience, Georgetown University School of Medicine, Washington, DC 20007, USA; Department of Obstetrics & Gynecology, University of Washington, Seattle, WA 98195, USA.
6
Abramson Pediatric Research Center, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.

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.

KEYWORDS:

ChR2; Chronic unpredictable stress; Corticotropin releasing factor; GABA

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