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At least 883 records · Page 49Linked to original sources

PubMed2003

Brain muscarinic receptor subtypes mediating water intake and Fos following cerebroventricular administration of bethanecol in rats.

RATIONALE: The brain regions and receptor subtypes involved in water intake following central cholinergic stimulation have been incompletely characterized. OBJECTIVES: To examine whether drinking and brain Fos-immunoreactivity (ir) induced in rats by central administration of bethanecol is reversed by either the preferential M1 antagonist pirenzepine, the M3 antagonist 4-DAMP, or their combination. METHODS: Male Sprague-Dawley rats were surgically implanted with cerebroventricular cannulae. The muscarinic agonist, bethanecol was used as the dipsogenic agent. Either nonselective (atropine) or selective muscarinic receptor antagonists were injected together with bethanecol to determine blockade of drinking. In parallel studies, Fos-ir was assessed in discrete brain regions. RESULTS: Bethanecol-induced drinking was completely blocked by atropine or by a combination of pirenzepine and 4-DAMP; these latter antagonists alone produced sub-total inhibition of drinking. In contrast, water intake induced by angiotensin II was unaffected by combination of pirenzepine and 4-DAMP. Fos-ir was induced by bethanecol in many brain regions previously implicated in body fluid regulation, including subfornical organ and the magnocellular supraoptic and paraventricular hypothalamic nuclei. Induced Fos-ir was substantially but not completely prevented by co-injection of either pirenzepine or 4-DAMP, but their combination did not seem markedly more effective than either alone. CONCLUSIONS: Drinking induced by brain muscarinic receptor stimulation seems to proceed by a combination of M1 and M3 receptor subtypes. Drinking induced by angiotensin II occurs independently of this mechanism. Fos-ir induced in fluid-related brain regions by bethanecol either uses additional receptor type(s) or is less easily blocked than drinking behavior.

Animals↗

PubMed1999

Limited access alcohol drinking in high- and low-alcohol preferring selected lines of mice.

BACKGROUND: Selection studies and genetic analyses of drinking behavior in rodents often involved unlimited access to alcohol over a period of weeks, with water and food freely available. Most studies investigating the pharmacology of alcohol drinking, on the other hand, use procedures in which access to alcohol is limited to a particular time each day. Reconciliation of findings between these two conditions likely depends on their sharing common genetic mechanisms as indicated, for example, by covariation in response to selection. To this end, high- and low-alcohol preferring (HAP and LAP, respectively) mice, selected for differences in 24-hr access alcohol drinking over a 4-week period, were subjected to a limited access alcohol drinking protocol. METHODS: During 2-hr sessions, mice had access to various concentrations of alcohol (7-15%, v/v) in the home cage for 2 hr a day, with ad libitum access to food and water. Additional sessions were conducted with no food present. RESULTS: Although both strains consumed alcohol and water during these sessions, HAP mice drank far more alcohol than did LAP mice. HAP but not LAP mice drank alcohol at a high rate early in the session compared with later in the session. Additionally, HAP mice responded to changes in alcohol concentration, whereas LAP mice did not. Removal of food did not influence alcohol drinking, although water drinking decreased following food removal. HAP mice reached appreciable blood alcohol concentrations after limited access. CONCLUSIONS: These findings indicate that in these selectively bred mice, alcohol drinking during limited and unlimited access may be genetically related, and that drinking during limited access sessions in HAP mice is likely for the pharmacological properties of alcohol.

Alcohol Drinking↗

PubMed2006

College binge drinking: deviant versus mainstream behavior.

College binge drinking is examined from the perspectives of two cultures. The traditional culture views binging as deviant; the second culture promotes it. In this context, logit regression is used to explore the effects of various factors, including student employment and parental education. Employed students are less likely to binge than are students who are not employed. Also, students whose mother is a college graduate, but whose father is not, are more likely to binge than other students. The prescriptions for reducing binge drinking are different when the behavior is perceived as mainstream rather than deviant. The research calls for the development of a process for promoting cultural change in an environment of continually changing student leadership.

Adolescent↗

PubMed1986

Fetal noradrenergic transplants into amine-depleted basal forebrain nuclei restore drinking to angiotensin.

6-Hydroxydopamine-induced catecholamine denervations in the organum vasculosum of the lamina terminalis and the median preoptic nucleus attenuate drinking responses to systemic angiotensin II (ANG II) injections. Transplanting catecholamines in these nuclei using fetal noradrenergic (NE) cell suspension restores ANG II-elicited thirst. These results emphasize the functional importance of NE neuronal systems in nuclei of the anteroventral third ventricle (AV3V) in mediating ANG II-induced drinking behaviors.

Angiotensin II↗

PubMed1980

Effects of isoproterenol and chlordiazepoxide on drinking and conflict behaviors in rats.

Isoproterenol, a beta-adrenergic agents, induced drinking in water-satiated rats. Isopropeternol exhibited significant anti-conflict activity on water-deprived rats in the Shock-induced Suppression of Drinking (SSD) procedure. Chlordiazepoxide (CDP), at the highest dose tested, also increased drinking in non-deprived naive rats. As expected, CDP demonstrated highly significant anti-conflict activity in thirsty rats (SSD test). These results suggest that in conflict procedures, where food or water is used as a reward, agents that affect the consumatory drive mechanisms could show up as "false positives." Moreover, agents that affect primary drives (e.g., CDP), in addition to their anti-anxiety activity, could show additive activity in such conflict procedures.

Animals↗

PubMed1989

Reducing alcohol consumption through television advertising.

Regular drinkers from the general public whose drinking behavior was known to be unaffected by a previous antidrug advertising campaign were involved in a field experiment to assess the impact of a television commercial based on controlled-drinking principles. In a 2 x 2 factorial arrangement of exposure to the advertising campaign (advertisement, no advertisement) and exposure to a letter announcing the campaign (letter, no letter), 96 subjects from two cities in tropical North Queensland provided baseline and posttreatment details of alcohol consumption and alcohol-related attitudes. Baseline measures were taken approximately 12 months prior to the start of the campaign, and posttesting occurred 3 weeks after the campaign. Results were consistent with the proposition that the advertisement reduced intake provided that subjects also received the standard letter alerting them to the start of the campaign.

Adolescent↗

PubMed1988

Neonatal diethylstilbestrol alters blood pressure and CNS drinking response in SHR and WKY rats.

Neonatal SHR and WKY rats were treated with diethylstilbestrol or propylene glycol (controls). Control SHR had higher blood pressures than WKY rats. Neonatal diethylstilbestrol treatment delayed the onset and full expression of hypertension in the male SHR but had no effect on blood pressure in the other animals. Neonatal diethylstilbestrol treatment had an adverse effect on body weights of male SHR and WKY rats through 98 days of age (not statistically decreased thereafter). Adult female SHR and WKY rats treated neonatally with diethylstilbestrol had body weights significantly greater than the control females. Neonatal treatment with diethylstilbestrol resulted in precocious puberty in female SHR and WKY rats. Control female SHR and WKY rats and female SHR treated neonatally with diethylstilbestrol had attenuated angiotensin - II induced drinking response from the central administration of estrogen in adulthood. The angiotensin II - induced drinking response was not significantly attenuated by central estrogen in adult WKY females exposed neonatally to diethylstilbestrol. Neonatal diethylstilbestrol treatment of WKY female rats appears to have altered neuroendocrine secretions that control CNS drinking behavior.

Angiotensin II↗

PubMed2002

Rats made cirrhotic by chronic CCl4 treatment still exhibit anticipatory activity to a restricted feeding schedule.

Food entrainment of clock genes in the liver suggests that this organ may underlie a food entrained oscillator (FEO), which manifests under restricted feeding schedule (RFS). In order to test the importance of a functional liver for the expression of FEO, chronic CCl4-treated cirrhotic rats and oil-treated controls were entrained to RFS and drinking behavior was continuously monitored. After 20 d of free-running conditions, food access was restricted to 2 h, followed by a refeeding-fasting protocol to test persistence of anticipatory drinking. Present data show no differences between groups for the onset and intensity of anticipation during RFS. After RFS, however, cirrhotic rats exhibited a significantly longer free-running period and a delay and lower intensity of the persistence of activity under fasting conditions. Histology confirmed injury of the liver chronically treated with CCl4. Present data indicate that a dysfunctional liver due to chronic CCl4 does not prevent animals from exhibiting anticipatory activity but may promote metabolic derangement of the clock mechanisms of the suprachiasmatic nucleus and the FEO.

Animals↗

PubMed1986

Reduced ethanol consumption during cyproheptadine administration in rats from a long-term alcohol-treated colony.

The influence of cyproheptadine (CPH) on forced and voluntary ethanol intake was studied in long-term alcohol-treated rats. Wistar rats from a colony (WAC) that have been drinking alcohol as their only liquid fluid for the 25 previous generations and from a genetically related colony (WN) that had never been given alcohol were used. In the first experiment, daily IP doses of 15 mg/kg CPH were found to reduce forced ethanol consumption during CPH treatment in both WAC and WN rats which had been drinking ethanol for six months. In two additional groups of WAC and WN rats which were not given ethanol, water intake was not affected by CPH administration. In a second experiment, alcohol preference was reduced both during and after CPH, but total fluid intake (ethanol + water) was not affected. These findings suggest that the effect of CPH could be specific to ethanol. The decrease in ethanol consumption was associated with a significant body weight loss; this result may support the hypothesis of a link between the serotoninergic system, food intake, and alcohol drinking behavior that has been considered by earlier investigators.

Alcohol Drinking↗

PubMed1976

Coffee consumption among psychiatric inpatients.

Of 135 patients on an acute psychiatric ward, 34 were "high users" of coffee. The high users tended to be older, single, and have diagnoses of psychosis. They showed significantly more state anxiety than other patients, but there were no differences in trait anxiety or MMPI scores. Further research is suggested to determine whether high caffeine consumption among inpatients may be related to staff coffee-drinking behavior and/or treatment with anticholinergic drugs.

Adult↗

PubMed2001

Dipsogenic response induced by angiotensinergic pathways from the lateral hypothalamic area to the subfornical organ in rats.

Experimental observations in several species have suggested that angiotensinergic neural circuits from the lateral hypothalamic area (LHA) to the subfornical organ (SFO) may participate in the control of drinking behavior in the rat. In an attempt to verify this possibility, experiments were undertaken to investigate whether activation of LHA neurons following microinjection of angiotensin II (ANG II) into the LHA elicits drinking. Injections of ANG II (10(-11) mol) into the LHA caused drinking in 25 out of 36 rats having the tips of cannulas in the LHA. The efficacy of ANG II was potentiated by increasing the dose of the drug. To clarify the contribution of angiotensinergic neurons in the LHA with efferent projections to the SFO to the drinking induced by ANG II, the effects of pretreatment with saralasin (Sar), a specific ANG II antagonist, in the SFO or its surrounding region on the drinking to ANG II were examined. Previous injections of Sar into the SFO significantly reduced the water intake caused by ANG II injected into the LHA, whereas treatment with Sar in the ventral hippocampal commissure (VHC) or third ventricle (3V) was without effect. These findings provide the evidence for the involvement of the angiotensinergic pathways from the LHA to the SFO in the dipsogenic action.

Angiotensin II↗

PubMed1977

Electric shock produced drinking in the squirrel monkey.

Squirrel monkeys were periodically exposed to brief electric tail shocks in a test environment containing a rubber hose, response lever, and a water spout. Shock delivery produced preshock lever pressing and postshock hose biting. Additionally, all subjects displayed licking responses following postshock biting-attack episodes. Further experiments showed that licking was: (1) influenced by hours of water deprivation; (2) drinking behavior; (3) the direct result of shock delivery; and (4) developed spontaneously in naive subjects with or without opportunities for hose biting or lever pressing. Removing the opportunity to attack increased postshock drinking. A noxious environmental stimulus that causes aggression can also produce drinking.

Aggression↗

PubMed2005

"Blood-contacting neurons" in the brain of the Japanese eel Anguilla japonica.

To discriminate "blood-contacting neurons" within the brain of the eel, Evans blue (EB) was injected intraperitoneally. After five days, six brain areas were externally stained blue with the dye; the saccus dorsalis (SD), the epiphysis (E), the area postrema (AP), the posterior part of the magnocellular preoptic nucleus (PM), the pituitary (Pit), and the saccus vasculosus (SV). Among the EB-positive area, some cells in the PM, the anterior tuberal nucleus (NAT) and the AP were discriminated as the "blood-contacting neurons" histologically, whereas EB-positive neurons were not detected in the SD, the E, the Pit and the SV regions. In the PM, most EB-positive neurons (90 %) were immunoreactive to vasotocin (AVT) antibody, indicating that these neurons are vasotocinergic. The remaining EB-positive neurons (10 %) were not immunoreactive to ANG II and tyrosine hydroxylase (TH) antibodies. Although some neurons in the PM were immunoreactive to ANG II antibody, they were EB-negative. In contrast, almost all EB-positive neurons in the AP showed TH-like immunoreactivity (-lir), indicating that these neurons utilize catecholamine(s) as a neurotransmitter. The EB-positive neurons in the NAT were not immunoreactive to AVT, ANG II and TH antibodies, whereas some neurons without EB-staining showed ANG II-lir. Possible roles of these neurons in regulating drinking behavior in eels are discussed.

Angiotensin II↗

PubMed1995

Histamine H3 receptors contribute to drinking elicited by eating in rats.

A role for endogenous histamine and its H3 receptor subtype for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats. The i.p. injection of the H3 agonist R-alpha-methylhistamine (Ramh, 2.5 mg/kg) shortened the latency to initiate drinking and increased 1-h water intake in nondeprived rats freely eating pellets and drinking water. The ICV injection (through a surgically implanted chronic cannula) of 10 micrograms Ramh increased water intake; this Ramh-induced drinking was abolished by previous ICV injection of the H3 antagonist thioperamide (Th, 60 micrograms). For rats drinking and eating after 24-h food deprivation, s.c. Th inhibited drinking behavior: for example, 10 mg/kg Th s.c. delayed the latency to initiate drinking and inhibited 1-h water intake without inhibition of food intake. In contrast, 60 micrograms Th ICV failed to inhibit food-related drinking in rats eating after food deprivation. For nondeprived rats eating a small cracker, 10 mg/kg Th s.c. delayed the latency to initiate drinking and abolished water intake without effect of eating, and 60 micrograms Th ICV had similar effects upon drinking elicited by ingestion of cracker. The IG infusion (through a surgically implanted gastric catheter) of 2 ml 600 or 900 mOsm/kg NaCl, a treatment that is subthreshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was abolished by 10 mg/kg Th s.c. and attenuated by 60 micrograms Th ICV. The IG infusion of 2 ml 1800 mOsm/kg NaCl, a treatment that is above threshold for increase in systemic plasma osmolality, elicited drinking that was attenuated by 10 mg/kg s.c. or 60 micrograms Th ICV. These results demonstrate that peripheral and central H3 receptors for histamine have a role in drinking elicited by eating and the postprandial gastrointestinal osmotic consequences of eating. These findings extend the evidence demonstrating a histaminergic contribution to food-related drinking in rats.

Animals↗

PubMed1999

The influence of parental drinking and closeness on adolescent drinking.

OBJECTIVE: This study examines the relationship of parental drinking and adolescent's closeness to parents to adolescent drinking behavior by focusing on three related issues: (1) the independent effects of parental drinking and closeness to parents on adolescent drinking, (2) the mediating role of closeness to parents for the effect of parental drinking, and (3) their interactive effects. METHOD: The issues were addressed with use of data from 378 respondents in a random-digit dialing sample of 625 male adolescents at age range 16 to 19 in the Buffalo area. Mother's and father's drinking and adolescent's closeness to mother and father were measured separately. Regression analyses were used to assess the effects of these measures on adolescent drinking regarding the three related issues. RESULTS: Only father's drinking has a direct effect on adolescent drinking. Although closeness to mother is a significant protection against adolescent drinking, mother's drinking has no effect on closeness to mother. In contrast, father's drinking has a significant effect on closeness to father, but closeness to father has no direct effect on adolescent drinking. Therefore, there is no mediating role of closeness to parents for the effect of parental drinking. Finally, there is an interaction between mother's drinking and closeness to mother, which indicates that adolescents whose mothers are heavy drinkers and who have low closeness to their mothers drink more heavily. CONCLUSIONS: Findings suggest that for the mother and the father there are different patterns of the relationship between parental drinking and closeness at work in explaining adolescent drinking.

Adolescent↗

PubMed1999

The effect of peers' alcohol consumption on parental influence: a cognitive mediational model.

OBJECTIVE: The current study was designed to elucidate familial and social influences on adolescent alcohol consumption by testing three hypotheses derived from the prototype/willingness model of adolescent risk behavior: (1) parents' prototypes of adolescent drinkers affect adolescent consumption through their impact on adolescents' prototypes, (2) strong parent-child relationships are associated with acceptance of parental influence regarding drinking and thus with less adolescent drinking and (3) association with peers who drink dilutes parental influence over adolescents' alcohol consumption. METHOD: Two hundred sixty-six rural adolescents, ages 15 through 17 at Time 1, and their parents and siblings completed questionnaires about drinking behavior and drinking-related cognitions at 1-year intervals for 3 years. RESULTS: Structural equation models provided evidence of transmission of prototypes of adolescent drinkers from parents to adolescents and evidence that these prototypes mediate adolescent alcohol consumption. They also provide evidence that although parents' prototypes and parent-adolescent relationships are important in shaping the adolescents' drinking, association with peers who drink significantly attenuates this influence. CONCLUSIONS: These data suggest that parents can influence their children's drinking, but that this influence has more of an impact if the adolescent is not involved in a drinking-conducive peer environment. The current analyses also suggest that the process of becoming an adolescent drinker involves an active rejection of parents' influence rather than a passive movement away from parents' attitudes and beliefs-a process that is accelerated by association with peers who drink.

Adolescent↗

PubMed1983

A microcomputer-based data acquisition system for continuous recording of feeding and drinking by rats.

A monitoring system to continuously record the daily pattern of drinking and eating of rats is described. This system, based on a North Star microcomputer, can record the amount of food ingested with a temporal resolution of +/- 1.0 second and quantitative accuracy within +/- 5%. Drinking behavior is detected using a drinkometer which also has a temporal resolution of +/- 1.0 second. Data are analyzed by computer to determine absolute amounts of consumption and patterns of intake. The patterns of feeding and drinking recorded by this system are similar to those observed using other monitoring devices.

Animals↗

PubMed2000

Pharmacogenetics of responses to alcohol and genes that influence alcohol drinking.

OBJECTIVE: There is now compelling evidence for genetic influence on susceptibility to alcoholism. This article presents results from studies qualifying alcoholism as a pharmacogenetic disorder of the brain. METHOD: Studies from the author's research group and other investigators, of human subjects and experimental animal models, are reviewed. Included are experiments on the pharmacogenetics (elimination and metabolism) and pharmacodynamics (initial response, tolerance and dependence) of ethanol. RESULTS: Studies in humans have reliably shown that the genes for the principal enzymes of alcohol metabolism influence drinking behavior and alcoholism risk. Notably, the functional genetic variants of alcohol dehydrogenase that exhibit high alcohol oxidizing activity, and the genetic variant of aldehyde dehydrogenase that exhibits low acetaldehyde oxidizing activity, protect against heavy drinking and alcoholism. Extensive studies of inbred and selectively bred experimental rodent models with alcohol drinking preference, tolerance development and alcohol withdrawal susceptibility have shown strong genetic influence on these responses to ethanol. Neuroanatomical, neurochemical and genetic studies have shown the involvement of serotonin, dopamine, glutamate, gamma-aminobutyric acid and opioid pathways in these actions of ethanol. Genetic studies, including association and genome-wide survey studies in both humans and rodents, implicate serotonin 1b receptor, dopamine D2 receptor, tryptophan hydroxylase and neuropeptide Y as candidate targets of genetic susceptibility in these pharmacodynamic actions of ethanol. CONCLUSIONS: There are genetic predisposing factors for alcoholism. Nonspecific susceptibility factors include personality traits characterized by behavioral inhibition (e.g., novelty-seeking and impulsivity). These genetically influenced traits interact with other, also genetically influenced, traits involved in the metabolism and pharmacodynamic effects of alcohol, and this interaction forms the basis for nominating alcoholism as a pharmacogenetic disease. Clearly, there are also many environmental factors that influence drinking behavior. Individuals have different sets of susceptibility genes and experience different kinds of environmental provocation. These factors underlie the heterogeneity and complexity of the clinical phenotype of alcoholism.

Alcohol Dehydrogenase↗