Effect of Amygdaloid Lesions on Hypothalamic Follicle-Stimulating Hormone-Releasing Factor in the Female Deermouse

Abstract

that lesions placed in the basolateral amygdaloid nuclear complex result in continuous release of luteinizing hormone (LH) from the hypophysis of the male and female deermouse. These changes in LH are accompanied by low levels of hypothalamic LH-releasing factor (Eleftheriou, 1967).The mechanism by which lesions in the amygdaloid complex affect changes in the hypophysial and plasma LH as well as in that of hypothalamic LH-RF is not established. The present report deals with the effects of lesions placed in the basolateral amygdala on the content of hypothalamic follicular-stimulating hormonereleasing factor (FSH-RF) in the female deermouse (Peromyscus maniculatus bairdii).Adult female deermice, weighing 15\p=n-\19 g., were lesioned bilaterally by thermocoagulation in the basolateral nuclear group of the amygdala according to the stereotaxic atlas for the species described previously (Eleftheriou & Zolovick, 1965;).Groups of 14 females each were killed 1, 2 and 3 weeks after the lesions had been produced. Two similar groups of sham-operated females were killed 1 and 2 weeks after the operation. In addition three similar groups were each killed at the dioestrous, pro-oestrous and oestrous stages of the cycle. The position of the lesions was confirmed by histological examination. Light and diet were not altered during the experiment and the body weight of operated animals did not change significantly.After the animals had been killed, the stalk-median eminence region and the adjacent ventral hypothalamus were dissected out (3-5 mg.) and pooled for each group of two animals. The pooled tissue was extracted according to Igarashi & McCann (19646). The extract was injected into male donor rats of the Holtzman strain (David, Fraschini & Martini, 1965) and the pituitary of each donor rat removed, weighed and homogenized in 0-9% NaCl solution (0-5 mg./0-l ml.). Extracts of control tissue (cortex) were also injected. The pituitaries were assayed for FSH content by the method of Igarashi & McCann (1964a). The recipient mice were females of the Charles-River (CD) strain, weighing 8-5-10-0 g. Pituitary preparations were injected as 0-5mg./0-l i.u. human chorionic gonadotrophin (HCG)/animal/day for 3 days. On the fourth day, the assay mice were killed, their uteri removed, cleaned

Effects of Amygdaloid Lesions on Hypothalamic--Hypophysial Luteinizing Hormone Activity

“…Thus, lesions in the medial amygdaloid nucleus result in increased secretion of adrenocorticotrophin and adrenal corticosterone (Mason, 1959;Eleftheriou, Zolovick & Pearse, 1966) while causing a transient inhibition of the secretion of thyrotrophin (Eleftheriou & Zolovick, 1968). In addition, lesions placed in the basolateral-lateral amygdaloid nuclear complex result in the continuous secretion of luteinizing hormone in both male and female deermice Eleftheriou, Zolovick & Norman, 1967) while affecting signi¬ ficantly the hypothalamic activity of both luteinizing hormone-releasing factor and follicular-stimulating hormone-releasing factor (Eleftheriou, 1967;Eleftheriou & Pattison, 1967). These data, combined with other data obtained previously, have given support to the theory that the amygdala exerts a modulating influence on the hypothalamic-hypophysial system for the secretion of certain trophic hormones (Koikegami, Yamada & Usui, 1953; Koikegami, Fuse,Yokoyama, Watanabe & Watanabe, 1955;Bunn & Everett, 1957;Shealy & Peele, 1957;Yamada & Greer, 1960;Taleisnik, Caligaris & DeOlmos, 1962).…”

Effects of Amygdaloid Lesions on Regional Brain Rna Base Ratios

“…Thus, lesions in the basolateral amygdaloid complex were found to in¬ crease pituitary and plasma levels of luteinizing hormone (LH), while producing a decline in the hypothalamic luteinizing hormone-releasing factor (LH-RF) Eleftheriou, Zolovick & Norman, 1967;Eleftheriou, 1967). Similar lesions produced a decline in hypothalamic follicular-stimulating hormone-releasing factor, FSH-RF (Eleftheriou & Pattison, 1967). In addition, lesions in the medial amygdaloid complex resulted in significant increases in pituitary and plasma adrenocorticotropine hormone (ACTH) accompanied by rises in plasma and adrenal cortico¬ sterone levels (Eleftheriou, Zolovick & Pearse, 1966) and a decline in plasma thyrotrophin (TSH) (Eleftheriou & Zolovick, 1968).…”