Abstract

The effects of morphine administered intravenously and intracerebrally in the cortical amygdala and periaqueductal gray were examined on spontaneous neuronal activity in the hypothalamic ventromedial nucleus in both intact and castrated adult male rats. Spontaneous extracellular single unit activity in the ventromedial nucleus was significantly faster in chronically castrated (19–23 days) rats compared with intact control rats (6.0± 1.1 and2.5 ± 0.3 spikes s. respectively). Neurons in the ventromedial nucleus exhibited a significant attenuation of neuronal activity following the intravenous administration of morphine: the maximal per cent decrease (to 25% of the control unit activity) was the same in both castrated and intact rats, but cell firing in castrated rats was affected more at lower doses of morphine. When microinjected bilaterally in the cortical amygdala or periaqueductal gray (5μg/site). morphine produced the same maximal depression of unit activity in the ventromedial nucleus as when administered intravenously. The time required to significantly attenuate unit activity in the ventromedial nucleus was the same (3 min) whether morphine was administered intravenously or bilaterally in the periaqueductal gray. When microinjected bilaterally in the cortical amygdala, the depressant effect of morphine on cell tiring in the ventromedial nucleus was significant first at 10 min. These data correlate well with the time courses for depression of serum levels of luteinizing hormone produced by morphine microinjected in the same doses in the same extrahypothalamic sites in the rat. In view of the relatively high levels of specific opiate receptor binding in both the periaqueductal gray and amygdala, this report further supports a role for modulation by extrahypothalamic areas of opioid-induced changes in the functional activity of the hypothalamic-pituitary axis, perhaps via the ventromedial nucleus.

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