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Behavioural evidence for a functional interaction between central 5‐HT 2 and 5‐HT 1A receptors
Author(s) -
Backus Lisa I.,
Sharp Trevor,
GrahameSmith David G.
Publication year - 1990
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1990.tb14094.x
Subject(s) - ritanserin , ketanserin , 5 ht2 receptor , agonist , medicine , quipazine , 5 ht receptor , endocrinology , prazosin , antagonist , chemistry , serotonin agonist , serotonin , receptor antagonist , pharmacology , receptor
1 The possibility of 5‐HT 2 receptor modulation of central 5‐HT 1A receptor function has been examined using the 5‐hydroxytryptamine (5‐HT) behavioural syndrome induced by 5‐HT 1A receptor active drugs in rats. 2 The 5‐HT 2 /5‐HT 1C antagonist ritanserin (0.1–2 mg kg −1 ) increased the 5‐HT behavioural syndrome induced by submaximally effective doses of 8‐hydroxy‐2‐(di‐n‐propylamino)tetralin (8‐OH‐DPAT), 5‐methoxy‐N,N‐dimethyltryptamine (5‐MeODMT) and gepirone. 3 Pretreatment with the 5‐HT 2 /5‐HT 1C antagonist ICI 170,809 (0.25–5 mg kg −1 ) also enhanced the behavioural syndrome induced by 8‐OH‐DPAT or 5‐MeODMT. 4 The 5‐HT 2 /α 1 ‐adrenoceptor antagonist ketanserin in a low dose (0.25 mg kg −1 ) significantly increased the 5‐HT behavioural syndrome induced by 8‐OH‐DPAT or 5‐MeODMT, while in a higher dose (2.5 mg kg −1 ) this drug decreased the response. Experiments with prazosin indicate that the higher dose of ketanserin might reduce the 5‐HT behavioural syndrome through blockade of α 1 ‐adrenoceptors. 5 Ritanserin and ICI 170,809 had no effect on apomorphine‐induced stereotypy or hyperactivity, indicating that these drugs do not produce non‐specific behavioural activation. 6 Ritanserin and ICI 170,809 inhibited quipazine‐induced wet dog shakes at doses similar to those enhancing the 5‐HT behavioural syndrome. 7 We suggest that ritanserin, ICI 170,809 and ketanserin enhance 5‐HT 1A agonist‐induced behaviour through blockade of an inhibitory 5‐HT 2 receptor regulating or coupled to 5‐HT 1A receptor‐mediated function.