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Vol. 288, Issue 2, 843-848, February 1999
Departments of
Neuropsychiatry (K.T., K.K., N.U., T.S., T.K.) and
Pharmacology (K.I.), Nihon University, School of Medicine, Tokyo, Japan
Recent behavioral studies indicate that conditioned fear response
to contextual stimuli is reduced effectively by anxiolytic 5-hydroxytryptame (5-HT)1A agonists. Since the hippocampus
seems to play an essential role in associative fear memories evoked by
context, it is important to assess the effect of 5-HT1A
agonists on pyramidal cell activity in the hippocampus. We examined the effects of 5-HT1A agonists on the spontaneous firing rate
of hippocampal CA1 pyramidal neurons in unanesthetized, unrestrained
rats. Systemic administration of selective 5-HT1A agonists,
8-hydroxy-2-(di-n-propylamino)tetralin, buspirone,
ipsapirone, and flesinoxan produced a dose-dependent inhibition of
neuronal activity. Putative 5-HT1A antagonists NAN-190 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]piperazine and
(
)-pindolol did not change neuronal activity of CA1 pyramidal
neurons. The suppression of neuronal activity by buspirone was
antagonized by NAN-190 but not by ()-pindolol. Lack of antagonistic
activity of ()-pindolol for the suppression of pyramidal neurons via
a postsynaptic mechanism is consistent with the results of recent electrophysiological experiments in anesthetized rats. Pretreatment with parachlorphenylalanine did not change the spontaneous firing rates
of hippocampal CA1 pyramidal neurons or abolish the suppressant effects
of buspirone on these neurons. Taken together, the present results
strongly suggest that suppression of the hippocampal CA1 pyramidal
neuronal activity by anxiolytic 5-HT1A agonists in awake rats is mediated by postsynaptic 5-HT1A receptors located
on pyramidal neurons.
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