5-HT1A AND BENZODIAZEPINE RECEPTORS IN THE BASOLATERAL AMYGDALA MODULATE ANXIETY IN THE SOCIAL-INTERACTION TEST, BUT NOT IN THE ELEVATED PLUS-MAZE

In order to investigate the role of the 5-HT1A receptors of the amygda la in modulating anxiety, rats were implanted with bilateral cannulae aimed at the basolateral nucleus of the amygdala complex and infused w ith either artificial cerebrospinal fluid (aCSF) or the selective 5-HT 1A receptor agonist 8-OH-DPAT (50-200 ng) and tested in two animal mod els of anxiety. In the elevated plus-maze test, no significant effects were detected in this dose range. In contrast, 8-OH-DPAT caused an ov erall reduction in levels of social investigation, thus indicating anx iogenic actions in the social interaction test. At 50 ng, 8-OH-DPAT ha d a selective action on anxiety, while at 200 ng there was a concomita nt reduction in locomotor activity and, in some animals, signs of the 5-HT1A syndrome. Evidence that the anxiogenic effect of 8-OH-DPAT (50 ng) was due to activation of 5-HT1A receptors came from the finding th at (-)-tertatolol, a 5-HT1A receptor antagonist, reversed this effect at a dose (1.5 mu g) which was silent when given alone. The benzodiaze pine receptor agonist, midazolam (1 and 2 mu g) was bilaterally admini stered into the basolateral nucleus of the amygdala and evoked clear-c ut anxiolytic effects in the social interaction test. These data indic ate that the agonist activation of post-synaptic 5-HT1A receptors in t he basolateral nucleus of the amygdala may produce anxiogenic effects, while agonist activation of BDZ receptors in the same areas evokes an xiolytic effects. Our results from the social interaction test are sim ilar to those previously reported from tests of anxiety using punished paradigms, but contrast with those found in the elevated plus-maze. T hus. it is concluded that either the two tests have different sensitiv ities to midazolam and 8-OH-DPAT or more intriguingly, the tests are e voking fundamentally different states of anxiety, with that evoked by the plus-maze being mediated via brain areas or receptors different fr om those studied here.