Document Detail


5-hydroxytryptamine1A-like receptor activation in the bed nucleus of the stria terminalis: electrophysiological and behavioral studies.
MedLine Citation:
PMID:  15381287     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The anteriorlateral bed nucleus of the stria terminalis (BNST AL) and the serotonergic system are believed to modulate behavioral responses to stressful and/or anxiogenic stimuli. However, although the BNST AL receives heavy serotonergic innervation, the functional significance of this input is not known. Data obtained from in vitro whole-cell patch clamp recording in the rat BNST slice show that exogenous application of 5-hydroxytryptamine (5-HT) evoked a heterogeneous response in BNST AL neurons. The principal action of 5-HT in this region was inhibitory, evoking a membrane hyperpolarization (5-HTHyp) and a concomitant reduction in input resistance in the majority of neurons tested. The broad-spectrum 5-HT1 agonist, 5-carboxamindotryptamine (5-CT), but not R(+/-)8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT), mimicked the 5-HTHyp response in the BNST. Moreover, the outward current mediating 5-HTHyp was inwardly rectifying and sensitive to the G protein activated inwardly rectifying K+ (G IRK) channel blocker, tertiapin-Q. In the CNS 5-HT1A receptors are thought to couple to GIRK channels, suggesting that 5-HTHyp in BNST AL neurons was mediated by activation of 5-HT1A-like receptors. This was confirmed by the blockade of both 5-HTHyp and 5-CTHyp by the specific 5-HT1A receptor antagonist N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide maleate salt (WAY100635 200nM). Furthermore, an in vivo examination of the functional consequences of 5-HT1A-like induced inhibition of BNST neurons revealed that infusion of 5-CT into the BNST significantly reduced the acoustic startle response, without affecting the general motor activity of the animals. These data point to the possibility that 5-HT1A mediated inhibition of the BNST AL could contribute to an anxiolytic action. Hence, we propose that in response to stressful stimuli, enhanced levels of 5-HT in the BNST AL plays a critical homeostatic role in feedback inhibition of the anxiogenic response to these stimuli.
Authors:
L Levita; S E Hammack; I Mania; X-Y Li; M Davis; D G Rainnie
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Neuroscience     Volume:  128     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2004  
Date Detail:
Created Date:  2004-09-21     Completed Date:  2005-03-04     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  583-96     Citation Subset:  IM    
Affiliation:
Department of Psychiatry and Behavioral Neuroscience, Emory University, Yerkes Neuroscience Building, 954 Gatewood Drive, Room 5220, Atlanta, GA 30322, USA.
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MeSH Terms
Descriptor/Qualifier:
Afferent Pathways / drug effects,  metabolism*
Animals
G Protein-Coupled Inwardly-Rectifying Potassium Channels
Male
Membrane Potentials / drug effects,  physiology
Neural Inhibition / drug effects,  physiology
Neurons / drug effects,  metabolism*
Organ Culture Techniques
Patch-Clamp Techniques
Potassium Channel Blockers / pharmacology
Potassium Channels, Inwardly Rectifying / drug effects,  metabolism
Rats
Rats, Sprague-Dawley
Receptor, Serotonin, 5-HT1A / agonists,  metabolism*
Septal Nuclei / drug effects,  metabolism*
Serotonin / metabolism*,  pharmacology
Serotonin Agonists / pharmacology
Serotonin Antagonists / pharmacology
Startle Reaction / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
MH 57250/MH/NIMH NIH HHS; MH47840/MH/NIMH NIH HHS; MH59906/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/G Protein-Coupled Inwardly-Rectifying Potassium Channels; 0/Potassium Channel Blockers; 0/Potassium Channels, Inwardly Rectifying; 0/Serotonin Agonists; 0/Serotonin Antagonists; 112692-38-3/Receptor, Serotonin, 5-HT1A; 50-67-9/Serotonin

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