Abstract

Imipramine, amitriptyline and desmethylimipramine given alone depressed or did not affect the spinal monosynaptic reflex (MSR). 5-Hydroxytryptophan (5-HTP) alone produced a slowly developing moderate facilitation of the MSR. The 5-HTP-induced increase in the MSR was more rapid in onset and much greater in cats pretreated with imipramine. Imipramine, amitriptyline and desmethylimipramine administered after 5-HTP, when spinal cord serotonin content was elevated, produced, respectively, 4-, 3- and 2-fold increases in the monosynaptic spike height. Cinanserin or methysergide injected subsequent to 5-HTP plus a tricyclic compound caused the MSR to return abruptly toward the predrug height. Similar findings were observed in cats treated with α-methyl-5-HTP. Increased deafferentation of the cord did not reduce facilitation of the MSR by imipramine in 5-HTP-treated animals, but the effect was abolished by chronic spinal transection and greatly reduced by pretreatment (before 5-HTP) with a decarboxylase inhibitor. Our findings indicate that antidepressants given before or after 5-HTP potentiate the 5-HTP-induced facilitation of the MSR via central interaction with serotonin formed from 5-HTP. Decreased neuronal uptake of serotonin may be the mechanism involved in this interaction.