Evidence for a Specific Neural Event That Controls the Estrous Release of Follicle-Stimulating Hormone in Golden Hamsters*

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Abstract
This study was designed to determine if the rostral hypothalamus (RH) exerts any control over the estrous (E) rise in serum FSH levels in golden hamsters. Proestrous (P) hamsters were subjected to two experimental techniques known to block the RH-dependent preovulatory gonadotropin release [phenobarbital (phen) administration and retrochiasmatic neural disconnection (RCD)]. After either treatment during P, the occurrence of the E FSH rise was examined. Phen administration at 1300 or 1400 h of P blocked the preovulatory LH/FSH rise, but did not inhibit the E FSH release. Phen administration at 1500, 1600, or 1700 h of P abolished neither the P nor the E gonadotropin releases. RCDs were made at hourly intervals from 1300-1800 h of P. The RCDs performed at 1300 and 1400 h of P blocked both the preovulatory rise in LH and FSH and the E rise in FSH that normally would have occurred. The RCDs performed at 1500 and 1600 h did not inhibit the P gonadotropin release but did block full expression of the E FSH rise. The RCDs performed at 1700 and 1800 h of P had no effect on the gonadotropin releases during P and E. Sham RCDs performed at 1300, 1400, and 1500 h of P did not alter the normal pattern of E FSH release. To determine whether the inhibitory effects of RCD at 1300 h of P on the E release of pituitary FSH were due to inhibition of the P LH release or ovulation, we performed RCDs at 1300 h of P on another group of hamsters. At 1400 h, purified LH was injected to elevate serum LH during P and to induce ovulation. In spite of this treatment, we observed no E FSH release. Thus, the inhibition of the E rise in serum FSH after RCD during P was due to actual neural disconnection. Results of this study suggest that a neural event that requires the integrity of the neural connection between the RH and medial basal hypothalamus occurs during P between 1300-1800 h. This event is necessary for full expression of the E FSH release and is not abolished by phen administration.