ARE 5-HT1A AUTORECEPTORS INVOLVED IN THE INHIBITORY EFFECT OF IPSAPIRONE ON COLD-ELICITED THYROTROPIN SECRETION
Neuroendocrinology. 1993-01-01; 57(4): 640-647
DOI: 10.1159/000126419
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1. Neuroendocrinology. 1993 Apr;57(4):640-7.
Are 5-HT1A autoreceptors involved in the inhibitory effect of ipsapirone on
cold-elicited thyrotropin secretion?
Broqua P(1), Laude D, Bluet-Pajot MT, Schmidt B, Baudrie V, Chaouloff F.
Author information:
(1)Laboratoire de Pharmacologie, CNRS, CHU Necker-EM, Paris, France.
Administration of the serotonin (5-HT)1A receptor agonist ipsapirone has been
shown to decrease cold-elicited thyrotropin (TSH) secretion. We have analyzed (1)
the influence of 5-HT1A receptors and ipsapirone metabolism into
1-(2-pyrimidinyl)-piperazine (1-PP, an alpha 2-adrenoceptor antagonist) on the
effect of ipsapirone on TSH release, and (2) the interaction between the
corticosterone-releasing effect of ipsapirone and its inhibitory influence on TSH
release. Pretreatment with proadifen (50 mg/kg, 5 h before ipsapirone), i.e. an
inhibitor of ipsapirone metabolism into 1-PP, did not affect ipsapirone-induced
inhibition of cold-elicited TSH secretion. Pretreatment (15 min before
ipsapirone) with the 5-HT1/5-HT2 receptor antagonist metergoline 2 mg/kg) or with
the 5-HT1A receptor blocker (-)-pindolol (5 mg/kg) increased baseline and
cold-elicited TSH release but the inhibitory influence of ipsapirone on
cold-elicited TSH release was alleviated by (-)-pindolol pretreatment only. Cold
exposure increased corticosterone release, an effect which was insensitive to
(-)-pindolol pretreatment. Lastly, pretreatment with the 5-HT synthesis inhibitor
p-chlorophenylalanine prevented the immediate inhibitory effect of the selective
5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) upon
cold-induced TSH release, but it amplified the late release of TSH in
cold-exposed 8-OH-DPAT-injected rats. These results suggest that presynaptic
5-HT1A receptors mediate ipsapirone-induced inhibition of cold-elicited TSH
release, an effect which may be partially opposed by postsynaptic 5-HT1A receptor
stimulation.
DOI: 10.1159/000126419
PMID: 7690117 [Indexed for MEDLINE]