Local 5,7-dihydroxytryptamine lesions of rat amygdala: Release of punisheddrinking, unaffected plus-maze behavior and ethanol consumption

Citation
W. Sommer et al., Local 5,7-dihydroxytryptamine lesions of rat amygdala: Release of punisheddrinking, unaffected plus-maze behavior and ethanol consumption, NEUROPSYCH, 24(4), 2001, pp. 430-440
Citations number
52
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROPSYCHOPHARMACOLOGY
ISSN journal
0893133X → ACNP
Volume
24
Issue
4
Year of publication
2001
Pages
430 - 440
Database
ISI
SICI code
0893-133X(200104)24:4<430:L5LORA>2.0.ZU;2-4
Abstract
several serotonergic drugs are effective for anxiety disorders but underlyi ng mechanisms are unclear, adn findings in experimental animals are difficu lt to reconcile with human data. It has been proposed that differential eff ects of serotonin within specific anatomical systems may account for these difficulties, and the amygdala has been suggested as one of the structures involved. To examine this hypothesis, the neurotoxin 5,7-dihydroxytryptamin e was administered locally in rat amygdala. Within the amygdala, serotonin was depleted by approximately 80%, with other transmitters unaffected and s erotonin transporter labelling was decreased by approximately 85%. Cortical areas near the lesion site were also affected, although to a lesser degree . Other forebrain areas were unaffected. Lesion resulted in a specific anti -conflict effect in a punished drinking test, but did not influence elevate d plus-maze behavior (under basline conditions and after restraint stress), locomotor activity or ethanol intake. These data suggest that the punished drinking test and the elevated plus-maze may activate different components of fear circuitry, and that the serotonergic input to the amygdala specifi cally participates in fear-related behavioral suppression mediated by this structure. (C) 2001 American College of Neuropsychopharmacology. Published by Elsevier Science Inc.