These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Activation of 5-HT1A receptors in the rat basolateral amygdala induces both anxiolytic and antipanic-like effects.
    Author: Strauss CV, Vicente MA, Zangrossi H.
    Journal: Behav Brain Res; 2013 Jun 01; 246():103-10. PubMed ID: 23499701.
    Abstract:
    The relevance of 5-HT1A and 5-HT2C receptors of the basolateral nucleus of the amygdala (BLA) in the mediation of anxiety-related defensive responses has long been acknowledged. Whereas strong evidence supports that activation of the latter receptors provokes anxiety, conflicting findings have been reported on the role played by the former binding site. In this study we further investigated the involvement of 5-HT1A receptors (5-HT1A-Rs) in the regulation of anxiety- and panic-related defensive behaviors. The results showed that intra-BLA injection of the 5-HT1A-R agonist 8-OH-DPAT (0.4-16nmol) in male Wistar rats impaired the acquisition of inhibitory avoidance in the elevated T-maze, increased the percentage of time spent in the lit compartment of the light-dark transition model and enhanced the number of punished drinking events in the Vogel conflict test, all changes compatible with an anxiolytic effect. This agonist also impaired escape expression in the elevated T-maze, suggestive of a panicolytic-like effect. 8-OH-DPAT-induced changes in the elevated T-maze and light-dark tests were blocked by previous local administration of the 5-HT1A-R antagonist WAY-100635 (0.37nmol) and were also observed after intra-BLA microinjection of the benzodiazepine receptor agonist midazolam (10-40nmol). Thus, stimulation of 5-HT1A-Rs in the BLA causes both anxiolytic- and panicolytic-like effects, what may have implications for the pathophysiology and treatment of generalized anxiety and panic disorders.
    [Abstract] [Full Text] [Related] [New Search]