Neuropeptide Y and corticotropin-releasing factor bi-directionally modulate inhibitory synaptic transmission in the bed nucleus of the stria terminalis

被引:138
作者
Kash, Thomas L.
Winder, Danny G.
机构
[1] Vanderbilt Univ, Sch Med, Dept Physiol & Mol Biophys, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Sch Med, Ctr Mol Neurosci, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Sch Med, JF Kennedy Ctr Res Human Dev, Nashville, TN 37232 USA
关键词
electrophysiology; whole cell; CRF; neuropeptide Y; anxiety; extended amygdala;
D O I
10.1016/j.neuropharm.2006.06.011
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neuropeptide Y (NPY) and corticotropin-releasing factor (CRF) have opposing effects on stress and anxiety. Both can modify synaptic activity through their binding to NPY receptors (YRs) and CRF receptors (CRFRs) respectively. The bed nucleus of the stria terminalis (BNST) is a brain region with enriched expression of both NPY and YRs and CRF and CRFRs. A component of the "extended amygdala", the BNST is anatomically well-situated to integrate stress and reward-related processing in the CNS, regulating activation of the hypothalamic-pituitary-adrenal (HPA) axis and reward circuits. Using whole-cell recordings in a BNST slice preparation, we found that NPY and CRF inhibit and enhance GABAergic transmission, respectively. Pharmacological experiments suggest that NPY depresses GABAergic transmission through activation of the Y2 receptor (Y2R), while both pharmacological and genetic experiments suggest that CRF and urocortin enhance GABAergic transmission through activation of the CRF receptor 1 (CRFR 1). Further, the data suggest that NPY acts to regulate GABA release, while CRF enhances postsynaptic responses to GABA. These results suggest potential anatomical and cellular substrates for the robust behavioral interactions between NPY and CRF. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1013 / 1022
页数:10
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