De- and regeneration of brain serotonin neurons following 5,7-dihydroxytryptamine treatment: Effects on serum LH, FSH and prolactin levels in male rats

Abstract

5,7-Dihydroxytryptamine (5,7-DHT), injected intraventricularly at a dose of 100 μg into adult male rats pretreated with desipramine (DMI), caused a substantial injury to the central serotonin system without any significant damage to the central catecholamine fiber systems. This treatment produced a 60–75% drop in forebrain 5-HT, a 65–80% reduction in hypothalamic [3H]5-HT uptake, and a 65–75% reduction in the hypothalamic synthesis of [3H]5-HT from [3H]tryptophan in vitro, at 4–12 days after injection. Forebrain 5-HT levels remained low up to 55 days (the latest time point studied) whereas the [3H]5-HT uptake and the serotonin forming capacity in the hypothalamus showed a gradual recovery within two months after injection. In the DMI-5,7-DHT treated rats, there was a significant reduction in serum LH, but not FSH, lasting for 26 days after low dose (100 μg) and for 69 days after a higher one (150 μg). The time course of recovery of serum LH levels seemed to correlate well with the regrowth of sprouting serotonin fibers in the hypothalamus (as indicated by the recovery of [3H]5-HT uptake and [3H]5-HT synthesis). Stress-induced prolactin release (exposure to ether vapour) was not affected by the DMI-5,7-DHT treatment. The results indicate that the serotoninergic neuron system has a facilitatory role in the regulation of pituitary LH secretion in the male rat. They further indicate that stress-induced prolactin release is unimpaired in animals with a damaged serotoninergic system. Moreover, our data lend support to the idea that the recovery of the neuroendocrine regulatory mechanisms is caused by an actual regeneration of the drug-lesioned serotonin axons.