Cumulative effect of prostaglandin E2(PGE2) injections on electroencephalographic activity in male monkeys (Macaca mulatta).

Bipolar stainless steel electrodes were stereotaxically implanted in hypothalamic and cerebral cortical regions of 24 adult male gonadally intact monkeys. Electrical activity of these regions was recorded before and after the first, second, third, thirteenth, fourteenth and fifteenth day of intravenous (I. V.) injection of PGE2 (400 mikrogramm/kg body weight). The inferences drawn from the EEG record were: (i), the immediate response was a tendency towards spindle formation (ii), high voltage spindles appeared at regular intervals in all sites i.e., preoptic area, posterior hypothalamus, ventromedial nucleus and cerebral cortex (iii), the changes observed. in EEG were progressive with time and transitional with respect to various regions of the brain (iv), these changes were synchronized whenever and wherever they were present, but the generalized showing in the form of overall inhibition could never be seen (v), the dose showed a cumulative effect after repeated daily injections of PGE2.

Possible effects of prostaglandin (PGE2) on hypothalamo-hypophyseal-gonadal axis in male rhesus monkeys (Macaca mulatta).

The effect of hypothalamo-hypophyseal-gonadal axis of prostaglandin E2 (PGE2) administered in a dose of 500 micrograms/kg body weight/day for 15 days to adult monkeys is reported. It altered the functional integrity of the testis and accessory sex organs as reflected by the changes in the estimations of the alkaline phosphatase, acid phosphatase, succinic dehydrogenase in the testis, sialic acids in caput and cauda epididymis, citric acid in the seminal vesicles, and fructose in the prostate and seminal vesicles. Histologically, PGE2 produced a marked decrease in the sperm count and an increase in the number of and size of exfoliated granulocytes was observed, which might have been due to the stimulatory effect of PGE2 on gonadotrophin release. The alterations induced in the electroencephalograph also suggest an involvement of hypothalamic mechanisms for gonadotrophin release, for which certain plausible explanations have been provided. The results suggest that the changes in reproductive parameters might be a consequence of endocrinological and functional disturbance induced by PGE2 and there is a strong likelihood of involvement of hypothalamo-pituitary integration in this complex.