The effect of amygdaloid and hippocampal lesions on compensatory ovulation and pro-oestrous gonadotropin levels in the rat.
The purpose of this study was to examine the effects of limbic forebrain lesions in conjunction with unilateral ovariectomy (ULO) on compensatory ovulation. At metoestrus, cyclic rats were ULO and bilateral brain lesions were placed in either the cerebral cortex (CTX), dorsal hippocampus (DHPC), amygdaloid nucleus (ACO) or stria terminalis (ST). In addition, two control groups consisted of intact and ULO only rats. Plasma samples were obtained at the subsequent pro-oestrus and analyzed by radioimmunoassay for FSH and LH. All animals were killed at the next metoestrus and the number of eggs shed were determined. After ULO alone, twice as many ova as normal were shed from the remaining ovary. Ovulation was inhibited in 30% of the ACO- and ST-ULO animals and damage to either the DHPC, ACO or ST caused a delay in time to the post-lesioned ovulation. However, all animals in the four brain lesioned-ULO groups that did ovulate doubled the number of eggs shed. Pro-oestrus plasma levels of FSH and LH did not differ between animals in the six groups. Thus, while amygdaloid lesions may alter certain parameters of pituitary ovarian function, the limbic forebrain is not involved in the mechanism of compensatory ovulation.
D000679:Amygdala / Q000502:physiology*; D000818:Animals; D002369:Castration; D004971:Estrus; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006065:Gonadotropins, Pituitary / Q000097:blood*; D006624:Hippocampus / Q000502:physiology*; D007986:Luteinizing Hormone / Q000097:blood; D010060:Ovulation; D011247:Pregnancy; D011359:Proestrus; D051381:Rats
D006065:Gonadotropins, Pituitary; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone