Zinc and water intake in rats: investigation of adrenergic and opiatergic central mechanisms

We have demonstrated that central administration of zinc in minute amounts induces a significant antidipsogenic action in dehydrated rats as well as in rats under central cholinergic and angiotensinergic stimulation. Here we show that acute third ventricle injections of zinc also block water intake induced by central ß-adrenergic stimulation in Wistar rats (190-250 g). Central inhibition of opioid pathways by naloxone reverses the zinc-induced antidipsogenic effect in dehydrated rats. After 120 min, rats receiving third ventricle injections of isoproterenol (160 nmol/rat) exhibited a significant increase in water intake (5.78 ± 0.54 ml/100 g body weight) compared to saline-treated controls (0.15 ± 0.07 ml/100 g body weight). Pretreatment with zinc (3.0, 30.0 and 300.0 pmol/rat, 45 min before isoproterenol injection) blocked water intake in a dose-dependent way. At the highest dose employed a complete blockade was demonstrable (0.54 ± 0.2 ml/100 g body weight). After 120 min, control (NaAc-treated) dehydrated rats, as expected, exhibited a high water intake (7.36 ± 0.39 ml/100 g body weight). Central administration of zinc blocked this response (2.5 ± 0.77 ml/100 g body weight). Naloxone pretreatment (82.5 nmol/rat, 30 min before zinc administration) reverted the water intake to the high levels observed in zinc-free dehydrated animals (7.04 ± 0.56 ml/100 g body weight). These data indicate that zinc is able to block water intake induced by central ß-adrenergic stimulation and that zinc-induced blockade of water intake in dehydrated rats may be, at least in part, due to stimulation of central opioid peptides

SDZ 216-525, a selective 5-Ht1A receptor antagonist, reverts zinc-induced inhibition of water intake in dehydrate rats

Zinc is found in many brain regions where it participates in important processes such as neurotransmission and neuromodulation. We previously demonstrated that acute third ventricle injection of zinc inhibits wather intake in dehydrated rats. The present study was undertaken to explore a possible link between zinc-induced inhibition of water intake in dehidrated rats and seotonergic systems in the brain. Adult, male Wistar rats had the third ventricle cannulated a week before the experiments. After an overnight period of water deprivation, the animals (N=12 per group) received acute intracerebroventricular injections (2µl) of Zn(Ac)2 (6.7, 67.1 and 67.6 ng/rat). Control animals (N = 12) receives NaAc (671.6 ng/rat). Zinc-treated animals displayed a significant after 120 min was 7.70 ñ 0.50 ml in control (NaAc-treated) dehydrated rats while animals treated with the highest dose of Zn(AC)2 drank 2.63 ñ 0.73 ml. Third ventricle injections of SDZ 216-525, a selective 5-HT1A receptor antagonist, 45 min before zinc administration, generated a dose-dependent reversal of zinc-induced thirst blockade in water-deprived rats. At the highest dose used (10µg/rat), the water intake of the animal after 120 min was 7.30 ñ 0.23 ml, a value equal to that of control animals. These data suggest that zinc may decrease water intake in dehydrated rats by activation of a 5-HT1A receptor-related mechanism

Acute effect of intracerebroventricular administration of zinc on the drinking behavior of rats induced by dehydration or central cholinergic and angiotensinergic stimulation

1. Zinc is a metal important for several biological functions including neuromodulation and neurotransmission in the central nervous system. 2. In the present paper we studied the acute effects of third ventricle injections (2 µl) of minute amounts of zinc acetate on the water intake of male, adult, Wistar rats (N = 7-14) under three conditions: water deprivation (14 h, overnight) and after third ventricle injections of carbachol (11 nmoles/rat in 2 µl) or angiotensin II (AII, 9.6 pmoles/rat in 2 µl). 3. Central injections of zinc acetate in different doses (0.3 and 3.0 nmoles/rat) induced a partial blockade of water intake of rats under all three conditions studied. Water intake after 120 min in control dehydrated rats (those receiving NaAc instead of Zn(Ac)2) was 7.89 + or - 0.47 ml while dehydrated animals receiving Zn(Ac)2 in the highest dose employed (3.0 nmoles/rat) animals receiving carbachol (2.41 + or - 0.84 ml). Angiotensin-treated animals exhibit a water intake of 3.85 + or - 0.48 ml after 45 min, a value reduced to 1.13 + or - 0.6 ml in those animals receiving angiotensin II plus zinc (3.0 nmoles/rat). 4. It is suggested that zinc alters the functional integrity of cholinergic and angiotensinergic systems in the central nervous system mediating water-intake behavior in rats

Drinking behavior in thyroidectomized rats: effects of central cholinergic stimulation and of water deprivation

Normally hydrated tytoidectomized (TX) rats stimulated intracerebroventricular with carbachol and delydrated TX rats drank significantly smaller volumes of water than their respective controls. This suggests lower central sensitivity to thirst and to drinking behavior induced by both cholinergic activation and extracellular fluid depletion. Dehydrated TX rats excreted a significantly larger urinary volume than the controls, suggesting the existence of changes in the renal mechanisms of water retention. Such changes could be related to a reduction in vasopressin binding sites

Desipramine blocks stress-induced prolactin release in rats: role of central beta-2 adrenoceptors

The present study was designed to examine the relationship between beta-adrenoceptors and the enhanced, sustained prolactin secretion induced by immobilization stress in rats. Chronic administration of desipramine (15 mg kg**-1 day**-1, intraperitoneally) for 7 days, a procedure that desensitizes central beta-adrenoceptors, partially inhibits stress-induced prolactin release. Intracerebroventricular adminsitration of the beta-2 adrenoceptor agonist salbutamol (1 microng/rat) to rats pretreated with desipramine for 7 days, 15 min before immobilization, significantly relieved the inhibition by desipramine 5 and 10 min after the initiation of stress but the effect was not demonstrable after 20 and 40 min. We conclude that beta-2 adrenoceptors play a role in the control prolactin release in response to stress

Evidence for interaction between central beta-2 adrenoceptors and epinephrine patways in the opioid-induced prolactin rise in the rat

1. The possible role of central beta-2 adrenoceptors and epinephrine pathways in opioid-prolactin (PRL) rise was investigated. 2. FK 33824, a synthetic opioid peptide injected into the third ventricle of Wistar male rats, generated a PRL rise that was significantly reduced by pretreatment with IPS 339, a potent and selective beta-2 antagonist. 3. inhibition of central epinephrine synthesis with SKF 64 139, which selectively blocks phenylethanolamine-N-methyltransferase, partially decreased the PRL release induced by FK 33824. 4. Proctolol, a selective beta-1 adrenoceptor blocker, did not modify the PRL secretion induced by FK 33824. 5 The results indicate that this FK 33824 - induced PRL rise depends in part on the functional integrity of central beta-2 adrenoceptors and that epinephrine pathways in the brain may play an important role in the mechanisms by which opioid peptides increase PRL secretion