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Corticotropin releasing factor and catecholamines enhance glutamatergic neurotransmission in the lateral subdivision of the central amygdala.
Neuropharmacology 2013; 70:316-23N

Abstract

Glutamatergic neurotransmission in the central nucleus of the amygdala (CeA) plays an important role in many behaviors including anxiety, memory consolidation and cardiovascular responses. While these behaviors can be modulated by corticotropin releasing factor (CRF) and catecholamine signaling, the mechanism(s) by which these signals modify CeA glutamatergic neurotransmission remains unclear. Utilizing whole-cell patch-clamp electrophysiology recordings from neurons in the lateral subdivision of the CeA (CeAL), we show that CRF, dopamine (DA) and the β-adrenergic receptor agonist isoproterenol (ISO) all enhance the frequency of spontaneous excitatory postsynaptic currents (sEPSC) without altering sEPSC kinetics, suggesting they increase presynaptic glutamate release. The effect of CRF on sEPSCs was mediated by a combination of CRFR1 and CRFR2 receptors. While previous work from our lab suggests that CRFRs mediate the effect of catecholamines on excitatory transmission in other subregions of the extended amygdala, blockade of CRFRs in the CeAL failed to significantly alter effects of DA and ISO on glutamatergic transmission. These findings suggest that catecholamine and CRF enhancement of glutamatergic transmission onto CeAL neurons occurs via distinct mechanisms. While CRF increased spontaneous glutamate release in the CeAL, CRF caused no significant changes to optogenetically evoked glutamate release in this region. The dissociable effects of CRF on different types of glutamatergic neurotransmission suggest that CRF may specifically regulate spontaneous excitatory transmission.

Authors+Show Affiliations

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

Pub Type(s)

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

Language

eng

PubMed ID

23470280

Citation

Silberman, Yuval, and Danny G. Winder. "Corticotropin Releasing Factor and Catecholamines Enhance Glutamatergic Neurotransmission in the Lateral Subdivision of the Central Amygdala." Neuropharmacology, vol. 70, 2013, pp. 316-23.
Silberman Y, Winder DG. Corticotropin releasing factor and catecholamines enhance glutamatergic neurotransmission in the lateral subdivision of the central amygdala. Neuropharmacology. 2013;70:316-23.
Silberman, Y., & Winder, D. G. (2013). Corticotropin releasing factor and catecholamines enhance glutamatergic neurotransmission in the lateral subdivision of the central amygdala. Neuropharmacology, 70, pp. 316-23. doi:10.1016/j.neuropharm.2013.02.014.
Silberman Y, Winder DG. Corticotropin Releasing Factor and Catecholamines Enhance Glutamatergic Neurotransmission in the Lateral Subdivision of the Central Amygdala. Neuropharmacology. 2013;70:316-23. PubMed PMID: 23470280.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Corticotropin releasing factor and catecholamines enhance glutamatergic neurotransmission in the lateral subdivision of the central amygdala. AU - Silberman,Yuval, AU - Winder,Danny G, Y1 - 2013/03/05/ PY - 2012/11/29/received PY - 2013/02/15/revised PY - 2013/02/19/accepted PY - 2013/3/9/entrez PY - 2013/3/9/pubmed PY - 2013/12/16/medline SP - 316 EP - 23 JF - Neuropharmacology JO - Neuropharmacology VL - 70 N2 - Glutamatergic neurotransmission in the central nucleus of the amygdala (CeA) plays an important role in many behaviors including anxiety, memory consolidation and cardiovascular responses. While these behaviors can be modulated by corticotropin releasing factor (CRF) and catecholamine signaling, the mechanism(s) by which these signals modify CeA glutamatergic neurotransmission remains unclear. Utilizing whole-cell patch-clamp electrophysiology recordings from neurons in the lateral subdivision of the CeA (CeAL), we show that CRF, dopamine (DA) and the β-adrenergic receptor agonist isoproterenol (ISO) all enhance the frequency of spontaneous excitatory postsynaptic currents (sEPSC) without altering sEPSC kinetics, suggesting they increase presynaptic glutamate release. The effect of CRF on sEPSCs was mediated by a combination of CRFR1 and CRFR2 receptors. While previous work from our lab suggests that CRFRs mediate the effect of catecholamines on excitatory transmission in other subregions of the extended amygdala, blockade of CRFRs in the CeAL failed to significantly alter effects of DA and ISO on glutamatergic transmission. These findings suggest that catecholamine and CRF enhancement of glutamatergic transmission onto CeAL neurons occurs via distinct mechanisms. While CRF increased spontaneous glutamate release in the CeAL, CRF caused no significant changes to optogenetically evoked glutamate release in this region. The dissociable effects of CRF on different types of glutamatergic neurotransmission suggest that CRF may specifically regulate spontaneous excitatory transmission. SN - 1873-7064 UR - https://www.unboundmedicine.com/medline/citation/23470280/Corticotropin_releasing_factor_and_catecholamines_enhance_glutamatergic_neurotransmission_in_the_lateral_subdivision_of_the_central_amygdala_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(13)00071-3 DB - PRIME DP - Unbound Medicine ER -