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The effect of reserpine on peptide histidine isoleucine amide (PHI)-like immunoreactive terminals in the rat median eminence was examined by immunocytochemistry using an antiserum that recognizes the amidated C-terminal portion of PHI. Acute reserpine treatment induced marked depletion ofPHI-like immunoreactivity in the external layer of the median eminence. Pretreatment with a monoamine oxidase inhibitor, nialamide, prevented the depletion. These results suggest the inhibitory role of monoamines, particularly catecholamines, on the release of PHI into the portal capillaries. Tatemoto and Mutt have isolated peptide histidine isoleucine amide (PHI) from the porcine intestine (12) and suggested that this peptide has a marked sequence homology to vasoactive intestinal peptide (VIP). Recent nucleotide sequence analysis has shown that VIP and PHM (a human counterpart of PHI) are derived from a common precursor molecule (4). Hokfelt et al. (3) reported the presence of PHI-like immunoreactive perikarya in the hypothalamic paraventricular nucleus that send axons to the external layer of the median eminence. PHI exists in the rat hypophysial portal blood (11) and may participate in the control of prolactin secretion (5, 6, 8, 14). Although several actions of PHI on the anterior pituitary have been reported, regulatory mechanism of PHI secretion at the hypothalamic level is still obscure. We examined the effect of monoamines on the release of PHI into the portal vessels by using reserpine. Seybold er al. (10) and Bugnon et al. (1) have reported by immunocytochemistry that reserpine depletes vasopressin-like and corticotropin-releasing factor (CRF)-like immunoreactive terminals in the external layer of the median eminence. By using an antiserum specific for the amidated PHI-C terminal portion, which is suspected to be important for biological activity of PHI (12), we have found in this study that reserpine also depletes PHI-like immunoreactive terminals in the external layer of the median eminence. The depletion was inhibited by pretreatment with a monoamine oxidase inhibitor, nialamide, suggesting that monoamines regulate the release of PHI as well as of vasopressin and CRF into the portal vessels. We adopted the experimental design described by Seybold et al. (10) with some modifications. Experiments were performed using male Wister rats each weighing 200230 g. Animals.were housed in 3-5 animals per cage, fed ad libizum and kept at 24°C with controlled lighting (lights on from 6:00 to 18 :00). Rats (n=20) were injected intraperitoneally with 5 or 10 mg/kg reserpine at 12 :00 to eliminate the effect of the circadian rhythm. Animals were sacrificed 2, 8, 24 h

biomedical research

&lt;b&gt;Reserpine depletes peptide histidine isoleucine amide-like immunoreactivity in the external layer of the rat median &lt;/b&gt;&lt;b&gt;eminence &lt;/b&gt;