Attenuation of morphine's depression of serum luteinizing hormone by lesions in the amygdala.

The administration of morphine or opioid peptides produces alterations in the neuroendocrine regulation of anterior pituitary hormone secretion, including the depression of serum levels of luteinizing hormone (LH). Central nervous system sites mediating the opioid-induced depression of serum levels of LH are not well understood. Discrete bilateral electrolytic lesions of amygdaloid nuclei or the periaqueductal central gray (PAG) were employed to investigate the role of these extrahypothalamic regions in the morphine-induced depression of serum levels of LH in the male rat. Lesions of the cortical amygdaloid nucleus, but not the medical, central or basolateral nuclei, significantly attenuated the depression of serum levels of LH 60 min following the acute administration of morphine (7.5 mg/kg). These results were independently replicated in different 10- and 22-day postlesion studies. Bilateral lesions of the medial region of the PAG, which did not encroach upon the dorsal raphe nucleus, elevated basal levels of serum LH. While morphine-treated subjects with bilateral lesions of the PGH exhibited significantly elevated serum levels of LH compared to sham lesion control subjects, no attenuation of the morphine-induced depression of serum levels of LH was observed 21 days following lesions of the PAG. These results indicate that the cortical nucleus of the amygdala, but not other amygdaloid nuclei or the PAG, is an extrahypothalamic site involved in the mediation of narcotic-induced changes in gonadotropin secretion in the male rat.