title: Participation of a pure neuronal mechanism in the control of gonadal functions.
abstract: The present review summarizes the data on the existence of a neural connection between the gonads and the central nervous system. As an experimental model the development of compensatory ovarian hypertrophy following unilateral ovariectomy was studied. Unilateral ovariectomy or orchidectomy resulted in a higher cellular activity in the hypothalamic arcuate neurons contralateral to hemigonadectomy and an increased luteinizing hormone-releasing hormone content in the medio-basal hypothalamus ipsilateral to the removed gonad. Local treatment of the remaining ovary with 6-hydroxy-dopamine prevented the development of compensatory ovarian hypertrophy after unilateral ovariectomy. Hemitransection of the spinal cord contralateral to hemigonadectomy, different unilateral hypothalamic deafferentations of the medio-basal hypothalamus as well as unilateral lesion of the medial preoptic area or of the arcuate nucleus blocked the compensatory ovarian growth when the brain surgery was on the same side as ovariectomy. Furthermore, in hypophysectomized + unilaterally ovariectomized rats a less severe ovarian atrophy occurred than in animals solely with hypophysectomy. All these data favour the view that - besides the hormonal control - a pure neuronal mechanism is also involved in the regulation of gonadal functions.
mesh_terms: D000818:Animals; D001921:Brain / Q000502:physiology*; D002369:Castration; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000032:analysis; D007031:Hypothalamus / Q000032:analysis / Q000502:physiology; D008297:Male; D009474:Neurons / Q000502:physiology*; D010053:Ovary / Q000502:physiology*; D012313:RNA / Q000096:biosynthesis; D051381:Rats; D013737:Testis / Q000502:physiology*
chemical_list: D007987:Gonadotropin-Releasing Hormone; D012313:RNA