Effects of methylphenidate on oxytocin and vasopressin levels in pinealectomized rats during light-dark cycle.

Although previous reports have shown that methylphenidate (MPH), in addition to its known behavioral effect, can influence the hypothalamo-pituitary-adrenal axis by increasing the plasma ACTH, the pineal gland seems to be involved in neuroendocrinological processes too, e.g., in hypothalamic synthesis and release of oxytocin (OXY) and vasopressin (AVP). Therefore, a study was performed to measure the OXY and AVP content of the hypothalamus, neurohypophysis, and plasma after application of MPH in the morning and evening in pinealectomized (PE) as well as sham-operated control (SO) rats. Pinealectomy influenced both the daily pattern (reversed in the neurohypophysis) and the levels of OXY and AVP. Starting from this different situation, application of MPH produced diverse effects. Hypothalamus: PE, increase in both hormones in the morning and evening; SO, decrease in morning OXY level. Neurohypophysis: PE, increase in morning OXY level; SO, decrease in both hormones even though in the morning only. Plasma: PE, decrease in morning OXY concentration; SO, increase in both hormones in the morning and decrease in the evening. The present results indicate that MPH application influences the hypothalamo-neurohypophysial system. Furthermore, the hypothesis has been supported that this influence may be dependent on the circadian activity of the pineal gland as well.

The effect of melatonin on suckling-induced oxytocin and prolactin release in the rat.

There is growing evidence that melatonin (MEL) inhibits oxytocin (OT) release when used in a low dose, while higher doses stimulate the release of the hormone in the rat. In the present study we investigated the effect of exogenous MEL, administered intracerebroventricularly (ICV), on suckling-induced OT and prolactin (PRL) release in the urethane-anesthetized rat. Lactating rats suckled by 8-12 pups were studied on days 8-12 of postpartum, and lactating pups-deprived rats on the same days of postpartum served as a control. Plasma OT and PRL levels as well as hypothalamic and neurohypophyseal OT contents were measured by RIA. Suckling stimulated the secretion of both OT and PRL. The ICV injection of 1 ng/ml MEL produced a significant inhibition of suckling-induced OT as well as PRL secretion. Melatonin in doses of 100 ng/ml or 10 micrograms/ml did not modify the OT release but significantly inhibited PRL release brought about by suckling; 10 pg/ml of MEL was not effective in this regard. Thus, exogenous MEL seems to inhibit suckling-induced OT as well as PRL secretion when applied at doses regarded to be in the range of the physiological level; when applied in higher doses, it was shown not to influence the release of OT following physiological stimulation such as suckling.

Thyrotropin-releasing hormone (TRH) modifies oxytocin release from the hypothalamo-neurohypophysial system in salt-loaded rats.

Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), for three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly decreased hypothalamic oxytocin content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats drinking tap water, neurohypophysial oxytocin content decreased. Plasma oxytocin concentration was distinctly elevated under TRH treatment in rats euhydrated but, on the contrary, decreased in salt-loaded rats as compared with animals similarly drinking hypertonic saline but not TRH-treated. The present data suggest that TRH may be involved in some regulatory processes related to oxytocin biosynthesis and release from the rat hypothalamo-neurohypophysial system.

Insulin-like immunoreactivity (IRI) in the rat hypothalamo-neurohypophysial system: effect of dehydration and haemorrhage.

Hypothalamic IRI was not affected in haemorrhaged rats, but diminished considerably in the dehydrated ones. In the neurohypohysis, IRI was distinctly higher both in dehydrated and haemorrhaged rats, i.e., under disorders which stimulated vasopressin and/or oxytocin release. It is suggested that insulin-like substance(s) may be someway involved in regulation of vasopressin or oxytocin secretion.

Thyrotropin-releasing hormone (TRH) inhibits vasopressin release from hypothalamo-neurohypophysial system of rats drinking hypertonic saline.

Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.) for three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly increased hypothalamic vasopressin content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats given hypertonic saline, neurohypophysial vasopressin content increased. Plasma vasopressin concentration was distinctly diminished under TRH treatment, the respective difference being significant, however, barely in salt-loaded rats. The present data suggest that TRH may be involved in some regulatory processes related to vasopressin biosynthesis and release from the rat hypothalamo-neurohypophysial system.

Hypothalamic and neurohypophysial vasopressin and oxytocin content as influenced by haemorrhage in melatonin-treated male rats.

The effect of haemorrhage (1 ml per 100 g b. w.) on the vasopressin and oxytocin storage in the hypothalamus and neurohypophysis of melatonin-treated male rats was determined. Melatonin treatment (100 micrograms/100 g b. w., once daily over 8 days) resulted in a known decrease of vasopressin as well as oxytocin content both in the hypothalamus and neurohypophysis. Haemorrhage decreased the neurohypophysial vasopressin and oxytocin storage in animals injected with vehicle solution or otherwise not treated. In melatonin-treated rats, however, bleeding did not affect the actual (i.e., decreased by melatonin) vasopressin and oxytocin content in the hypothalamo-neurohypophysial system. The results demonstrate that melatonin may be involved in mechanisms determining the rate of the response of vasopressinergic and oxytocinergic neurones to bleeding.

The effect of intracerebroventricular insulin on the hypothalamic and neurohypophysial oxytocin activity in euhydrated or dehydrated rats.

Rats dehydrated up to four days were given intracerebroventricularly insulin in a daily dose of 100 ng. Insulin decreased significantly the hypothalamic and neurohypophysial oxytocin content in euhydrated rats. In dehydrated animals the oxytocin activity in the hypothalamo-neurohypophysial system, markedly depleted after deprivation of water, could be further reduced by intracerebroventricular treatment with insulin. These results seem to suggest a possible regulatory role of brain insulin in the mechanisms of oxytocin release.

The hypothalamic and neurohypophysial vasopressor and oxytocic activities in stressed rats treated with haloperidol.

A decrease of oxytocin and vasopressin content was observed in the hypothalamus and neurohypophysis of immobilized rats but not of those exposed to cold. In rats otherwise not treated, dopaminergic blockade due to haloperidol was followed by an increase of the vasopressin content in the neurohypophysis. In immobilized animals, the hypothalamic and neurohypophysial content of oxytocin decreased and could be further reduced by haloperidol. In contrast haloperidol prevented the decrease of the hypothalamic and neurohypophysial vasopressin under conditions of stress owing to immobilization. In cold-exposed animals, however, haloperidol did not affect the storage of neurohypophysial vasopressin and oxytocin. Thus, it may be supposed that the response of oxytocinergic and vasopressinergic neurones to stress is dependent on the kind of stressor; furthermore, the dopaminergic transmission seems to be involved in the functional regulation of these neurones under conditions of stress due to immobilization.

The effects of prostaglandin synthetase inhibitor indomethacin on the hypothalamic and neurohypophysial oxytocin content in euhydrated and dehydrated male white rats.

Rats euhydrated or dehydrated up to eight days were given intraperitoneally indomethacin (IM) twice daily in a dose of 0.2 mg/100 g of initial body weight. A single dose of IM injected to euhydrated animals did not affect the neurohypophysial oxytocic activity but decreased that potency in the hypothalamus. When IM was administered repeatedly during four or eight days, the hypothalamic oxytocic activity did not differ from the respective controls; under such conditions the oxytocic activity in the neurohypophysis increased progressively. Under conditions of dehydration the known depletion of hypothalamic and neurohypophysial oxytocin storage was not affected by indomethacin. It is therefore suggested that impulses of osmoreceptor origin are of distinct importance in determining the function of oxytocinergic neurones under conditions of inhibited prostaglandin synthesis.

The hypothalamic and neurohypophysial oxytocic activities in stressed rats: independence from beta-adrenergic blockade.

A distinct decrease of oxytocin was found in the hypothalamus of immobilized rats but not of those exposed to cold. Similarly, the content of oxytocin was lower in the neurohypophysis of rats immobilized for 24 hr but, on the contrary, increased in animals exposed to cold for 24 hr. Propranolol did not modify the mentioned changes brought about by immobilization or exposure to cold.