The role of endogenous serotonin in phasic LH release

Injection of the serotonin inhibitor, fluoxetine (75 micrograms) into the hypothalamus (IC) of ovariectomized (Ovx.) rats treated with 17beta-Estradiol (E2) and parachlorophenylalanine (PCPA 150 mg/kg) significantly increased the luteinizing hormone (LH) in these rats 24 hours later when PCPA had suppressed the LH surge in a parallel group of sham rats. There was a temporal delay in these changes of LH (and by implication serotonin metabolism), since there was no significant effect on the blocked LH surge within two hours of the injection. Since steroids play a major role in gonadotropin secretion and PCPA has been shown to depress LH release, it is interesting that E2 increased the rate of H-3 serotonin (1 X 10(-7) M) uptake in hypothalamic synaptosomes. This suggests a mechanism to increase the removal of synaptic serotonin and the low concentrations of serotonin used in these experiments suggest that uptake occurred in the high affinity serotonin uptake pump and can be influenced by ovarian steroids. This is in contrast to the saturation uptake of serotonin which was unaffected by steroids.