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Serotonin 5‐HT 1A Receptor Activation Increases Cyclic AMP Formation in the Rat Hippocampus In Vivo
Author(s) -
Cadogan A. K.,
Kendall D. A.,
Marsden C. A.
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62051816.x
Subject(s) - forskolin , microdialysis , endocrinology , medicine , agonist , 5 ht1a receptor , 8 oh dpat , serotonin , efflux , chemistry , in vivo , extracellular , 5 ht receptor , receptor antagonist , receptor , biology , antagonist , stimulation , biochemistry , central nervous system , microbiology and biotechnology
In vivo microdialysis was used to examine the efflux of cyclic AMP (cAMP) into the extracellular fluid of the ventral hippocampus in the freely moving rat. The changes in extracellular cAMP concentration were monitored in response to forskolin and the serotonin 5‐HT 1A receptor agonist 8‐hydroxy‐2‐(di‐ n ‐propylamino)tetralin (8‐OH‐DPAT). The basal level of hippocampal extracellular cAMP was 2.3 ± 0.2 pmol/ml (n = 6), after a 3‐h postsur‐ gery stabilisation period. Perfusion of forskolin (100 μ M ) through the probe for 30 min significantly increased the efflux of cAMP, which returned to baseline levels within 90 min. 8‐OH‐DPAT (0.3 mg/kg s.c.) also significantly increased cAMP efflux, whereas a similar volume of saline had no effect. Desensitisation of the 8‐OH‐DPAT‐induced increase in cAMP efflux was observed following a second administration of 8‐OH‐DPAT after a 4‐h interval. Administration of 8‐OH‐DPAT did not alter the efflux of cAMP when forskolin was perfused through the probe. Pretreatment with WAY 100135 [ N‐tert ‐butyl 3–4‐(2‐methoxyphenyl)piperazine‐1 ‐yl‐2‐phenylpropanamide dihydrochloride] (5 mg/kg s.c.), a specific 5‐HT 1A receptor antagonist, prevented the 8‐OH‐DPAT‐induced increase in cAMP efflux. The data indicate that the 8‐OH‐DPAT‐induced increase in cAMP efflux in vivo is mediated by a 5‐HT 1A receptor.