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At least 343 records · Page 19Linked to original sources
PubMed1994

Drinking behavior and vasopressin responses to hyperosmolality in Alzheimer's disease.

Individuals with Alzheimer's disease (AD) have been shown to have abnormalities in response to fluid restriction. Twelve subjects with AD and ten elderly controls underwent overnight fluid restriction followed by measurement of plasma and urine vasopressin and serum osmolality. Estimates of "thirst" were determined after one hour of ad libitum water intake. All subjects were tested with a Mini-Mental State Examination (MMSE) and Global Deterioration Scale (GDS). Individuals with AD had a greater degree of overnight dehydration than the elderly control group (serum osmolality 310 +/- 1 vs. 305 +/- 1 mosmol/kg, p = 0.02). There was no difference between the groups in the plasma or urinary levels of vasopressin. There was a direct correlation (r = 0.45, p = 0.03) of the amount of water intake as a measure of "thirst" with the MMSE score as a measure of cognitive functioning. Individuals with advanced cognitive impairment may be at risk of dehydration due to loss of protective "thirst" responses with secondary complications of dehydration.

Aged↗
PubMed1982

The generality of the stimulus-binding hypothesis across drinking behavior and task performance in alcoholics.

This experiment investigated the validity of applying the stimulus-binding hypothesis of obesity to conceptualize drinking and task performance behaviors in alcoholics. Twenty alcoholics and 12 nonalcoholics participated in two counterbalanced experimental sessions. One session involved an assessment of subjects' voluntary consumption of preferred and nonpreferred nonalcoholic beverages. The other session involved their performance of four tasks that involved or manipulated the presence of salient external cues. The prediction of heightened externality in alcoholics was supported on the beverage consumption measures and was marginally supported on the task performance measures. The results are discussed in terms of their implications for models and treatments of alcohol problems.

Adult↗
PubMed2003

Cholinergic innervation to the upper esophageal sphincter muscle in the eel, with special reference to drinking behavior.

To elucidate innervation in the upper esophageal sphincter (UES) muscle of the eel, a key muscle in swallowing, repetitive electrical field stimulation (EFS; 30 mA, 40 V, 300 micros, 10 Hz, 10 trains) was employed. Anatomically, the eel UES muscle consists of striated fibers. The EFS-induced contraction of the UES was completely blocked by tetrodotoxin and curare, and abolished in Ca2+ -free Ringer solution. These results suggest that the EFS stimulates nerve fibers specifically and releases acetylcholine as a neurotransmitter. In fact, acetylcholine and carbachol constricted the UES in a concentration-dependent manner. Even after blocking neuronal firing with tetrodotoxin, acetylcholine constricted the UES muscle, suggesting the existence of acetylcholine receptors on the UES muscle cells. Both EFS- and carbachol-evoked contractions of the UES were blocked by curare at a lower concentration than by atropine or hexamethonium, suggesting that the acetylcholine receptor is nicotinic. Even in Ca2+ -free Ringer solution, a direct current stimulus (2 s duration) constricted the UES muscle to an extent similar to that in the presence of Ca2+, indicating that the muscle contraction itself does not need extracellular Ca2+, i.e., the muscle can be constricted by a release of Ca2+ from the sarcoplasmic reticulum.

Acetylcholine↗
PubMed2003

Central effects of various ligands on drinking behavior in eels acclimated to seawater.

Intracranial injection of eel angiotensin II (eANG II, 5x10(-13)-5x10(-8) mol), acetylcholine (ACh, 5x10(-12)-5x10(-9) mol), substance P (5x10(-10) mol) and isoproterenol (a beta-adrenoceptor agonist, 5x10(-11)-5x10(-9) mol) enhanced water intake in the seawater eel. The effects of eANG II, ACh and isoproterenol were dose-dependent. By contrast, water intake was inhibited by intracranial injection of eel atrial natriuretic peptide (eANP, 5x10(-13)-5x10(-10) mol), serotonin (5-HT, 5x10(-12)-5x10(-8) mol), ghrelin (5x10(-12)-5x10(-10) mol), gamma-amino butyric acid (GABA, 5x10(-11)-5x10(-8) mol), prolactin (PRL, 5x10(-10)-5x10(-9) mol), arginine vasotocin (AVT, 5x10(-12) mol), vasoactive intestinal peptide (VIP, 5x10(-11) mol), noradrenaline (5x10(-9) mol l(-1)) and phenylephrine (alpha-adrenoceptor agonist, 5x10(-11)-5x10(-9) mol). The inhibitory effects of eANP, 5-HT, ghrelin, GABA, PRL and phenylephrine were dose-dependent. The intracranial stimulatory effect of eANG II was relatively long-lasting compared with the intravenous effect. The stimulatory effect of intravenous eANG II disappeared immediately, and was followed by an inhibition, which could be well explained by an increase in eANP secretion from the atrium.

Acclimatization↗
PubMed1979

Effects of chronic intraventricular administration of angiotensin II on drinking behavior and blood pressure.

Angiotensin II was continuously infused into the lateral cerebral ventricle of rats, and the effects on daily food and water consumption, urine volume, and aortic blood pressure were studied. All was infused at a rate of 10 ng/hr for seven days, using subcutaneously implanted osmotic minipumps. An intraventricular (IVT) control group was infused with only the saline vehicle, while a third group received AII subcutaneously. IVT AII rats showed a four-fold increase in water consumption, to a mean of 171 ml/day during Days 2-4 of infusion, whereas water intake of the other groups did not change from preinfusion levels. Urine volume showed a similar pattern to water intake, increasing five-fold in the IVT AII group during Days 2-4. These measures declined during the final three days of AII infusion, but significant tolerance was not observed. Food intake decreased markedly in both saline and IVT AII groups after implantation of the pumps, but the latter resumed normal food intake more slowly than the former, and body weight remained below preinfusion levels throughout the AII period. Aortic blood pressure of the IVT AII rats showed a slight, but progressive, rise during the infusion period, but it did not significantly exceed that of the saline rats. These results indicate that continuous, low-level, intraventricular infusion of AII may markedly increase water intake without significantly increasing fluid retention or blood pressure.

Angiotensin II↗
PubMed2003

Drinking behavior elicited by central injection of angiotensin II: roles for protein kinase C and Ca2+/calmodulin-dependent protein kinase II.

Prior studies utilizing neurons cultured from the hypothalamus and brain stem of newborn rats have demonstrated that ANG II-induced modulation of neuronal firing involves activation of both protein kinase C (PKC) and Ca2+/calmodulin-dependent protein kinase II (CaMKII). The present studies were performed to determine whether these signaling molecules are also involved in physiological responses elicited by ANG II in the brain in vivo. Central injection of ANG II (10 ng/2 microl) into the lateral cerebroventricle (icv) of Sprague-Dawley rats increased water intake in a time-dependent manner. This ANG II-mediated dipsogenic response was attenuated by central injection of the PKC inhibitors chelerythrine chloride (0.5-50 microM, 2 microl) and Go-6976 (2.3 nM, 2 microl) and by the CaMKII inhibitor KN-93 (10 microM, 2 microl). Conversely, icv injection of chelerythrine chloride (50 microM, 2 microl) and KN-93 (10 microM, 2 microl) had no effect on the dipsogenic response elicited by central injection of carbachol (200 ng/2 microl). Furthermore, injection of ANG II (10 ng/2 microl) icv increases the activity of both PKC-alpha and CaMKII in rat septum and hypothalamus. These data suggest that signaling molecules involved in ANG II-induced responses in vitro are also relevant in physiological responses elicited by ANG II in the whole animal model.

Angiotensin II↗
PubMed2006

Using the Extrinsic Affective Simon Test as a measure of implicit attitudes towards alcohol: relationship with drinking behavior and alcohol problems.

In apparent contrast to the alleged importance of positive alcohol expectancies in alcohol (ab)use, a series of studies using the Implicit Association Test (IAT; [Greenwald, A. G., McGhee, D. E., & Schwartz, J.L.K. (1998). Measuring individual differences in implicit cognition: The Implicit Association Test. Journal of Personality and Social Psychology, 74, 1464-1480]), found that heavy and light drinkers display more negative implicit attitudes toward alcohol than toward sodas (e.g., [Wiers, R. W., van Woerden, N., Smulders, F. T. Y., & de Jong, P. J. (2002). Implicit and explicit alcohol-related cognitions in heavy and light drinkers. Journal of Abnormal Psychology, 111, 648-658]). One explanation for this might be that the negative-alcohol IAT effect reflects an artifact of the IAT procedure and are due to its relative nature and/or its sensitivity to task recoding strategies. Therefore, the present study used a non-relative measure that has been argued to be robust against participants' task recoding strategies (Extrinsic Affective Simon Test; EAST, [De Houwer, J. (2001). A structural and process analysis of the Implicit Association Test. Journal of Experimental Social Psychology, 37, 443-451]) to test heavy (n=16) and light (n=16) drinkers' automatic affective associations with alcohol and sodas. Heavy and light drinkers displayed clear positive associations with sodas and neutral (or ambivalent) automatic associations with alcohol. Importantly, positive automatic alcohol associations predicted unique variance of alcohol (mis)use and was the single best predictor of individuals' alcohol problems, underlining the idea that they do play a role in alcohol (mis)use.

Adult↗
PubMed1985

Regional depletion of central nervous system catecholamines: effects on blood pressure and drinking behavior.

The purpose of the present study was to identify which catecholamine-containing neurons (norepinephrine (NE) or dopamine (DA)) and which central nervous system (CNS) region(s) innervated by them might participate in the pressor and drinking responses produced by central drug stimulation. Forebrain NE was reduced in rats by injecting 4 micrograms of 6-hydroxydopamine (6-OHDA) into the ascending noradrenergic bundles. Spinal cord NE was depleted by intracisternal injection of 50 micrograms 6-OHDA. Depletion of forebrain DA was produced by bilateral injection of 4 micrograms 6-OHDA into the substantia nigra of desipramine-pretreated rats. Pressor responses to various doses of angiotensin II (AII), carbachol or hyperosmolar NaCl injected into the lateral ventricles (LVT); and drinking responses to LVT AII and carbachol were examined. Injection of 6-OHDA into the noradrenergic bundles reduced telencephalic and hypothalamic NE by more than 80% without significantly affecting brain DA or spinal cord NE. Intracisternal 6-OHDA depleted spinal cord NE by 80% and forebrain NE by 20-25% without reducing brain DA. Injection of 6-OHDA into the substantia nigra reduced telencephalic DA by 86% and NE by 29% without significantly affecting NE in other CNS regions. Substantia nigra 6-OHDA injected animals evidenced attenuated drinking to both LVT AII and carbachol. Pressor responses to LVT AII, carbachol and hypertonic saline were largely unaffected. Almost complete depletion of brain and/or spinal cord NE failed to alter centrally mediated drinking or pressor responses. These data indicate that the integrity of brain DA neurons is required for the behavioral but not hypertensive responses produced by central drug stimulation.

Angiotensin II↗
PubMed1977

Antigen-antibody reactions in rat brain sites induce transient changes in drinking behavior.

The septum or hypothalamus of rat brain was injected through implanted cannulas with antibody against membrane antigens in the rat brain or with antibody against exogenous soluble antigens (such as ovalbumin) followed by the specific antigen. Both immunological systems produced a moderate but highly significant decrease in drinking by thirsty rats. This phenomenon is suggested as an experimental model for behavioral disorders resulting from nondegenerative, immunological processes in the brain.

Animals↗
PubMed1988

Effect of nimodipine on drinking behavior measured in the runway: comparison and interaction with (+/-)-amphetamine.

The aim of the present study was to evaluate the ability of the calcium channel blocker (CCE), nimodipine (NIM), to interact with (+/-)-amphetamine (AMPH) in modifying ingestive behavior. Rats performed in a water-reinforced runway paradigm with multiple trials. Water was available in sufficient quantity to produce satiety under control conditions as measured by a decline in response rate over the session. NIM and AMPH, given alone, did not produce significant effects on performance but produced behavioral changes when administered in combination. In particular, the combination of the highest doses (13 mg/kg i.p. NIM plus 0.56 mg/kg i.p. AMPH) initially depressed both running and drinking, whereas in later trials it increased running rate, without producing a parallel increase in water intake. These results suggest that NIM enhances AMPH-produced inhibition of drinking, whereas it first depresses and then enhances the AMPH-mediated runway performance, suggesting the rate dependency of this latter effect.

Amphetamine↗
PubMedDate not supplied

Septal destruction in infant rats and the ontogeny of drinking behaviors.

Male and female albino rat pups sustained septal destruction at 10 days of age and body weight and water intakes were measured daily throughout development until 200 days of age. During development the septal and control rats received a battery of drinking tests (e.g., cellular dehydration, hypovolemia, renin). Septal rats (males and females) were hyperdipsic for daily water intakes as early as 31 days of age and the daily hyperdipsia persisted through 200 days of age. On the battery of drinking tests, septal rats consumed water at control volumes on all tests except water deprivation (following which females were hyperdipsic) and food deprivation (during which both males and females were hyperdipsic). Urine output-water intake relationships were determined, and a series of food deprivation tests were conducted during development to determine the etiology of the developmental septal hyperdipsia. All results suggest that hyperdipsia associated with septal destruction during the preweaning period is a primary condition and not secondary to altered output mechanisms, abnormal feeding-drinking patterns, or displacement behavior.

Animals↗
PubMed1996

Performance in the cross-maze and slip funnel tests of four pairs of rat lines selectively bred for divergent alcohol drinking behavior.

Alcohol naive rats from lines genetically selected for high and low alcohol drinking and founded on either Wistar (P/NP lines) and distinct heterogeneous stocks (AA/ANA and replicate HAD/LAD lines) were tested in the explorative cross-maze and the inescapable slip funnel. Rats of the low alcohol-consuming ANA, NP, LAD1 and LAD2 lines all exhibited a shorter latency before initiating exploration of the maze than did their high alcohol-consuming counterparts (66, 51, 33 and 51% of the values for AA, P, HAD1 and HAD2 lines, respectively). Significant line differences were also found with the slip funnel test (AA > ANA for time in a sprawling posture; P > NP but HAD1 < LAD1 and HAD2 < LAD2 for time escaping), but the directions of line differences were not consistently related to those in alcohol drinking.

Journal Article↗