Hideki Katakami

Effect of β-endorphin on pulsatile luteinizing hormone release in conscious castrated rats

Abstract The effect of intraventricular administration of β-endorphin on pulsatile LH release in castrated conscious rats was studied. The administration of 1 μg of β-endorphin into the lateral ventricle inhibited pulsatile discharge of LH secretion. Intravenous administration of naloxone blocked the suppressive effect of β-endorphin on LH release. These results suggest a possible role of β-endorphin, in addition to Met 5 -enkephalin, in the control of LH release in male rats.

Suppressive effect of dynorphin-(1–13) on luteinizing hormone release in conscious castrated rats

The effect of intraventricular administration of dynorphin-(1-13) on luteinizing hormone (LH) release was studied in castrated conscious rats. The administration of 5 micrograms of dynorphin-(1-13) into the lateral ventricle inhibited LH secretion. Intravenous administration of naloxone blocked this suppressive effect of dynorphin on LH release. These results suggest a possible role of dynorphin, in addition to beta-endorphin and Met5-enkephalin, in the control of LH release in male rats.

Effects of Neonatal Treatment with Monosodium Glutamate on Growth Hormone Release Induced by Clonidine and Prostaglandin E1 in Conscious Male Rats

Effects of the centrally acting alpha-adrenergic agonist, clonidine, on growth hormone (GH) secretion was studied in conscious male rats pretreated with monosodium glutamate (MSG) during the neonatal period. GH secretory profiles in individual adult rats were obtained by repeated blood samplings every 10-20 min from 10.00 to 17.00 h. GH secretion was pulsatile with mean peak values at around 12.40 and 15.20 h in control rats. When clonidine (15 micrograms/100 g body weight) was injected intravenously into control rats at 14.00 h in the interval between two anticipated spontaneous GH bursts, plasma GH was increased with a mean peak value 20 min after the injection, and the following anticipated spontaneous GH burst was not observed during the experiment. In the rats neonatally treated with MSG (4 mg/g body weight, s.c.), which causes selective destruction of the hypothalamic arcuate nucleus, plasma GH response to clonidine as well as the spontaneous GH bursts were considerably blunted, whereas prostaglandin E1 (5 micrograms/100 g body weight, i.v.) caused an abrupt increase in plasma GH levels in these animals. These results suggest that clonidine stimulates rat GH secretion, possibly by acting within the hypothalamus to stimulate GH releasing factor neurons.

Effects of VIP, TRH, GABA and dopamine on prolactin release from superfused rat anterior pituitary cells

Effects of VIP, TRH, dopamine and GABA on the secretion of prolactin (PRL) from rat pituitary cells were studied in vitro with a sensitive superfusion method. Dispersed anterior pituitary cells were placed on a Sephadex G-25 column and continuously eluted with KRBG buffer. Infusion of TRH (10(-11) - 10(-8)M) and VIP (10(-9) - 10(-6)M) resulted in a dose-related increase in PRL release. LHRH (10(-8) - 10(-5)M) had no effect on PRL release. On the other hand, infusion of dopamine (10(-9) - 10(-6)M) and GABA (10(-8) - 10(-4)M) suppressed not only the basal PRL release from dispersed pituitary cells but also the PRL response to TRH and VIP. The potency of TRH to stimulate PRL release is greater than that of VIP, and the potency of dopamine to inhibit PRL secretion is stronger than that of GABA on a molar basis. These results indicate that TRH and VIP have a stimulating role whereas dopamine and GABA have an inhibitory role in the regulation of PRL secretion at the pituitary level in the rat.

Involvement of Alpha-Adrenergic Mechanisms in Growth Hormone Release Induced by Opioid Peptides in Conscious Rats

The effects of synthetic enkephalin analog (KF 33-824) and beta-endorphin on growth hormone (GH) secretion and their interaction with brain monoamines were investigated in unanesthetized male rats. Blood samples (0.4 ml each) were withdrawn every 10-20 min for 6 h from a catheter chronically implanted in the right atrium. In all control rats, immunoreactive GH secretion was pulsatile in nature and two major GH bursts were found to occur around 12.00 and 15.30. The opioid peptides were injected between bursts at 14.00. Following an intravenous administration of FK 33-824 (10 microgram/100 g b.w.), there was an abrupt increase in plasma GH, which was significantly suppressed by naloxone (125 microgram/100 g b.w., i.v.), a specific opiate antagonist. Pretreatment with reserpine (1 mg/100 g b.w., i.p.) abolished not only the natural GH burst but also the GH response to FK 33-824. Pretreatment with dopamine-beta-hydroxylase inhibitors, diethyldithiocarbamate (DDC, 100 mg/100 g b.w., i.v.) and fusarate (10 mg/100 g b.w., i.v.) also inhibited the natural GH burst and GH rise induced by FK 33-824. Intravenous injection of clonidine (15 microgram/100 g b.w.), an alpha-adrenergic stimulant, resulted in an increase in plasma GH in the rats pretreated with reserpine, DDC or fusarate. Phenoxybenzamine (1 mg/100 g b.w., i.v.), an alpha-adrenergic blocking agent, inhibited the GH response to KF 33-824. On the other hand, GH release induced by FK 33-824 was not influenced by propranolol (1 mg/100 g b.w., i.v.), a beta-adrenergic blocking agent, nor pimozide (0.1 mg/100 g b.w., i.v.), a dopamine antagonist. Intraventricular administration of beta-endorphin (5 microgram/rat) also increased the plasma GH levels which were lowered by phenoxybenzamine. These findings suggest that alpha-adrenergic mechanisms are involved in GH release induced by opioid peptides in the rat.

Serotonin stimulates vasoactive intestinal polypeptide release from rat hypothalamus in vitro

Abstract The effect of serotonin (5-HT) on the release of immunoreactive vasoactive intestinal polypeptide (VIP) from rat hypothalamus was examined in vitro with a perifusion system. 5-HT (10 −6 M) and high potassium (56 mM) stimulated VIP release in a calcium-dependent manner. VIP release induced by 5-HT was blunted by cyproheptadine (10 −5 M). These findings suggest that 5-HT has a stimulating effect on VIP release from the hypothalamus.

Stimulation of prolactin secretion in the rat by α-neo-endorphin, β-neo-endorphin and dynorphin

Abstract Intraventricular injections of α-neo-endorphin, β-neo-endorphin and dynorphins (dynorphin[1–13], dynorphin[1–17], dynorphin[1–8]) resulted in an increase in plasma prolactin levels in urethane-anesthetized rats. Dynorphin [1–13] was the most potent to stimulate prolactin release among these opioid peptides. Plasma prolactin responses to these stimuli were blunted by naloxone, an opiate antagonist. In in vitro studies, prolactin release from perfused pituitary cells was stimulated by α-neo-endorphin, and the effect was blunted by naloxone, whereas neither β-neo-endorphin nor dynorphin[1–13] affected prolactin release. These results suggest that newly identified “big” Leu-enkephalins in the brain stimulate prolactin secretion in the rat and that α-neo-endorphin has a possible direct action on the pituitary.

Stimulation by dynorphin of prolactin and growth hormone secretion in the rat

The intraventricular injection of synthetic dynorphin-(1–13) resulted in a significant and dose-related increase in plasma prolactin (PRL) and growth hormone (GH) levels in urethane-anesthetized rats. The potency of dynorphin was much greater than that of [Leu5]-enkephalin. Plasma PRL and GH responses to dynorphin were blunted by naloxone, an opiate receptor antagonist. These results suggest a possible role of dynorphin in stimulating the secretion of PRL and GH in the rat.

Inhibition of Prolactin Secretion by Gastrin Releasing Peptide (GRP)in the Rat

Abstract Synthetic gastrin releasing peptide (GRP) injected intraventricularly (1μg/rat), but not intravenously, suppressed rat prolactin (PRL) release induced by a Met-enkephalin analog, FK33-824 (10 μg/100 g body wt., iv). GRP also blunted PRL release induced by a dopamine antagonist, domperidone(l μg/100 g body wt., iv). In contrast, GRP did not suppress elevated plasma PRL levels sustained by a large dose of domperidone (10μg/100 g body wt., iv). GRP (10-5M) had no effect on PRL release from super fused pituitary cells in vitro. These results suggest that GRP inhibits PRL secretion in the rat by acting through the brain to stimulate the dopaminergic mechanism

Inhibition by Naloxone of Prolactin Release Induced by L-5-Hydroxytryptophan in Rats

Abstract Intravenous injection of l-5-hydroxytryptophan (l-5-HTP), but not l-5-HTP, resulted in an increase in plasma prolactin (PRL) levels in anesthetized rats. l-5-HTP-induced PRL release was blunted by naloxone, a specific opiate antagonist. In rats pretreated with either reserpine or α-methyl-p-tyrosine (α-MT), basal plasma PRL levels were elevated and l-5-HTP injection caused a further increase in plasma PRL concentrations. However, PRL release induced by l-5-HTP was not blunted by naloxone in these animals pretreated with reserpine and α-MT. These results suggest that PRL release induced by serotonin is modulated, at least in part, by opioid peptidergic mechanisms, which are closely related to brain catecholamines.