Sexual hormones terminate in the rat: the significantly enhanced catecholaminergic/serotoninergic tone in the brain characteristic to the post-weaning period.
The amount of dopamine released from the striatum, substantia nigra and tuberculum olfactorium, noradrenaline from locus coeruleus and serotonin from the raphe, was significantly higher in four and five weeks old rats than in three month old ones, proving that the catecholaminergic/serotoninergic activity enhancer (CAE/SAE) regulation works unrestrained during developmental longevity and is restricted thereafter. As the dampening of the CAE/SAE regulation (end to the second month of age) coincided temporally with the appearance of sexual hormones, we castrated three weeks old male and female rats and measured at the end of the third month of their life the release of catecholamines and serotonin from selected discrete brain regions. The amount of catecholamines and serotonin released from the neurons was significantly higher in castrated than in untreated or sham operated rats, signalting that sexual hormones inhibit the CAE/SAE regulation in the brain. We therefore treated male and female rats s.c. with oil (0.1 ml/rat), testosterone, (0.1 mg/rat), estrone (0.01 mg/rat) and progesterone (0.5 mg/rat), respectively, and measured their effect on the CAE/SAE regulation. Twenty-four hours after a single injection with the hormones, the release of noradrenaline, dopamine and serotonin was significantly inhibited in the testosterone or estrone treated rats, but remained unchanged after progesteron treatment. In rats treated with a single hormone injection, testosterone in the male and estrone in the female was the significantly more effective inhibitor. Remarkably, the reverse order of potency was found in rats treated with daily hormone injections for 7 or 14 days. After two-week treatment with the hormones estrone was in the male and testosterone in the female the significantly more potent inhibitor of the CAE/SAE regulation. The data indicate that sexual hormones terminate the hyperactive phase of adolescence by dampening the impulse propagation mediated release of catecholamines and serotonin in the brain.
Knoll
J
J
Department of Pharmacology, Semmelweis University, Budapest, Hungary. jozsefknoll@hotmail.com
Miklya
I
I
Knoll
B
B
Dalló
J
J
D000818:Animals; D001921:Brain / Q000254:growth & development / Q000378:metabolism / Q000502:physiology*; D002369:Castration; D004298:Dopamine / Q000378:metabolism / Q000502:physiology*; D004970:Estrone / Q000494:pharmacology / Q000502:physiology; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology*; D006128:Growth / Q000502:physiology; D008136:Longevity / Q000502:physiology; D008297:Male; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology*; D011374:Progesterone / Q000494:pharmacology / Q000502:physiology; D051381:Rats; D012701:Serotonin / Q000378:metabolism / Q000502:physiology*; D012741:Sexual Maturation / Q000502:physiology; D013739:Testosterone / Q000494:pharmacology / Q000502:physiology; D014886:Weaning
D012739:Gonadal Steroid Hormones; D004970:Estrone; D012701:Serotonin; D013739:Testosterone; D011374:Progesterone; D004298:Dopamine; D009638:Norepinephrine