Hypothalamic Areas Involved in Prostaglandin(PG)-Induced Gonadotropin Release. II: Effects of PGE2and PGF2αImplants on Follicle Stimulating Hormone Release1

Abstract

The effect of unilateral intrahypothalamic implants of PGE2 or PGF2.alpha. on FSH [follicle stimulating hormone] release in ovariectomized, estrogen-treated rats was studied. Both PG induced an equally small increase in plasma FSH following their implantation in the body of the arcuate nucleus-median eminence region (BARH-ME). Levels were maximally elevated 120 min post-implantation. PGE2 implanted in the caudal portion of the ARH-ME (TARH-post-ME) also induced a similar increase in plasma FSH, whereas its placement in the region of the ventromedial nucleus (VMH)-dorsomedial nucleus (DMH) did not significantly alter FSH titers. By contrast, PGE2 placed in the post-chiasmatic region (HARH-ME) clearly elevated plasma FSH as early as 40 min after implantation. Implants of PGF2.alpha. in this area were ineffective. PGE2 implants located more than 1 mm lateral from the midline or outside the hypothalamus were also ineffective. When PGE2 was placed in the preoptic area (POA) or anterior ventral portion of the anterior hypothalamic area (AHA), plasma FSH rose markedly showing the first significant increase between 40 and 60 min after implantation. PGE2 implants located in the dorsal portion of the AHA-paraventricular nucleus (DAHA-PVH) were also clearly more effective than implants in BARH-ME, but less effective than implants in the POA. PGF2.alpha. implanted in the POA evoked a smaller increase in plasma FSH than that induced by PGE2 implants in this region. Implantation of empty cannulae in the ARH-ME region or POA failed to increase plasma FSH levels significantly. Intrapituitary implants of PGE2 did not alter plasma FSH. PGE2 acts mainly on the POA-AHA region to induce FSH release. PGF2.alpha., although less effective, also stimulates FSH release in this area. The ARH-ME appears to be a less important site. The greater effectiveness in the POA-AHA region than in the ARH-ME may indicate that PGE2 is more effective in stimulating cell bodies of LHRH neurons than their axons. Although most of the sites at which PGE2 released FSH coincide with the distribution of LHRH, it is noteworthy that a relatively enhanced release of FSH took place from certain sites in the dorsal AHA-PVH and from sites in the post-ME, which suggests that PGE2 may act on neurons which secrete a specific FSH-RF and on neurons which release LHRH.