Abstract: The effect of the serotonergic receptor agonist 1‐(m‐trifluoromethylphenyl)piperazine (TFMPP) was studied on the K+‐evoked (3H)acetylcholine ((3H)ACh) release from guinea pig hippocampal synaptosomes loaded with (3H)choline. TFMPP (5–1,000 μM) inhibited the evoked ACh release in a dose‐dependent manner (IC50= 81.8 μM). The inhibitory effect of TFMPP was mimicked by CGS‐12066B (10, 30, and 100 μM), a 5‐hydroxytryptamine1B (5‐HT1B)/5‐HT1D receptor agonist; 1‐(m‐chlorophenyl)piperazine (100 μM), a 5‐HT1C/5‐HT1B receptor agonist; and 5‐carboxamidotryptamine (10 μM), a nonselective 5‐HT1 receptor agonist. 8‐Hydroxy‐2‐(di‐n‐propylamino)tetralin (10 and 100 μM), a 5‐HT1A receptor agonist, and quipazine (10 and 100 μM), a 5‐HT2 receptor agonist, did not have any significant effect. Serotonergic antagonists, such as dihydroergotamine (0.1 and 1 μM), metergoline (0.1 μM), methysergide (0.5 and 1 μM), or yohimbine (1 and 10 μM), blocked the TFMPP effect dose‐dependently. In contrast, methiotepine (0.3 and 1 μM), propranolol (1 μM), ketanserin (0.1 μM), mesulergine (0.1 μM), ICS 205930 (0.1 and 1 μM), and spiroperidol (1 and 7 μM) did not affect the TFMPP‐induced inhibition of the evoked ACh release. These data suggest that, in guinea pig hippocampus, the K+‐evoked ACh release is modulated by a 5‐HT1 receptor distinct from the 5‐HT1A, 5‐HT1B, and 5‐HT1C subtypes.
Journal of Neurochemistry – Wiley
Published: Jan 1, 1991
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