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Neuropeptide Y and corticotropin-releasing factor bi-directionally modulate inhibitory synaptic transmission in the bed nucleus of the stria terminalis.
Neuropharmacology 2006; 51(5):1013-22N

Abstract

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 (CRFR1). 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.

Authors+Show Affiliations

Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232-0615, USA.No affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16904135

Citation

Kash, Thomas L., and Danny G. Winder. "Neuropeptide Y and Corticotropin-releasing Factor Bi-directionally Modulate Inhibitory Synaptic Transmission in the Bed Nucleus of the Stria Terminalis." Neuropharmacology, vol. 51, no. 5, 2006, pp. 1013-22.
Kash TL, Winder DG. Neuropeptide Y and corticotropin-releasing factor bi-directionally modulate inhibitory synaptic transmission in the bed nucleus of the stria terminalis. Neuropharmacology. 2006;51(5):1013-22.
Kash, T. L., & Winder, D. G. (2006). Neuropeptide Y and corticotropin-releasing factor bi-directionally modulate inhibitory synaptic transmission in the bed nucleus of the stria terminalis. Neuropharmacology, 51(5), pp. 1013-22.
Kash TL, Winder DG. Neuropeptide Y and Corticotropin-releasing Factor Bi-directionally Modulate Inhibitory Synaptic Transmission in the Bed Nucleus of the Stria Terminalis. Neuropharmacology. 2006;51(5):1013-22. PubMed PMID: 16904135.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuropeptide Y and corticotropin-releasing factor bi-directionally modulate inhibitory synaptic transmission in the bed nucleus of the stria terminalis. AU - Kash,Thomas L, AU - Winder,Danny G, Y1 - 2006/08/10/ PY - 2006/03/21/received PY - 2006/06/06/revised PY - 2006/06/20/accepted PY - 2006/8/15/pubmed PY - 2007/1/16/medline PY - 2006/8/15/entrez SP - 1013 EP - 22 JF - Neuropharmacology JO - Neuropharmacology VL - 51 IS - 5 N2 - 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 (CRFR1). 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. SN - 0028-3908 UR - https://www.unboundmedicine.com/medline/citation/16904135/Neuropeptide_Y_and_corticotropin_releasing_factor_bi_directionally_modulate_inhibitory_synaptic_transmission_in_the_bed_nucleus_of_the_stria_terminalis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(06)00196-1 DB - PRIME DP - Unbound Medicine ER -