Attenuation of Morphine’s Depression of Serum Luteinizing Hormone by Lesions in the Amygdala

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Abstract
The administration of morphine or opioid peptides produces alterations in the neuroendocrine regulation of anterior pituitary hormone secretion, including the depression of serum luteinizing hormone (LH) levels. CNS sites mediating the opioid-induced depression of serum LH levels 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 LH levels in the male rat. Lesions of the cortical amygdaloid nucleus, but not the medial, central or basolateral nuclei, significantly attenuated the depression of serum LH levels 60 min following acute morphine administration (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 serum LH levels. While morphine-treated subjects with bilateral lesions of the PAG exhibited significantly elevated serum LH levels compared to sham lesion control subjects, no attenuation of the morphine-induced depression of serum LH levels was observed 21 days following lesions of the PAG. The cortical nucleus of the amygdala, but not other amygdaloid nuclei or the PAG, apparently is an extrahypothalamic site involved in the mediation of narcotic-induced changes in gonadotropin secretion in the male rat.