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

NEUROPHARMACOLOGY

卷:107

Article

Partridge, John G.^1,2  Forcelli, Patrick A.^1,2  Luo, Ruixi¹  Cashdan, Jonah M.³  Schulkin, Jay^2,4  Valentino, Rita J.⁵  Vicini, Stefano^1,2 

[1] Georgetown Univ, Sch Med, Dept Pharmacol & Physiol, Basic Sci Bldg,Rm 235,3900 Reservoir Rd, Washington, DC 20007 USA

[2] Georgetown Univ, Sch Med, Interdisciplinary Program Neurosci, Washington, DC 20007 USA

[3] Georgetown Univ, Sch Med, Dept Biol, Washington, DC 20007 USA

[4] Univ Washington, Dept Obstet & Gynecol, Seattle, WA 98195 USA

[5] Childrens Hosp Philadelphia, Abramson Pediat Res Ctr, Philadelphia, PA 19104 USA

关键词: ChR2;    GABA;    Chronic unpredictable stress;    Corticotropin releasing factor;   

DOI  :  10.1016/j.neuropharm.2016.03.029

来源: Elsevier

【 摘 要 】

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. (C) 2016 Elsevier Ltd. All rights reserved.

【 授权许可】

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