PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Drinking Behavior”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1989

Drinking behavior and motor function in rat pups depleted of brain dopamine during development.

The ability of rat pups depleted of brain dopamine (DA) at either 3 or 15 days of age to increase fluid intake in response to intracellular dehydration was studied. Despite near-total depletions of striatal DA, animals depleted at either age ingested normal amounts of fluid even as soon as 3-7 days after incurring the brain damage. The effects of DA receptor blockade on ingestion and motor function were also studied. Haloperidol had markedly different effects as a function of the age at which the depletions were sustained. Weanlings that were depleted of DA at 3 days of age failed to exhibit the drug-induced adipsia, akinesia, and catalepsy seen in controls and animals that were depleted at 15 days of age. These findings suggest that the DA depletions were performed at different periods of brain organization. The resultant neural controls of ingestion and motor function are qualitatively different in the two groups of depleted animals. Rats depleted at 3 days of age utilize nondopaminergic mechanisms, whereas animals lesioned at 15 days of age continue to rely upon residual DA neurons for both behaviors.

Animals↗
PubMed1983

Minireview. Benzodiazepine-opiate antagonist interactions in relation to feeding and drinking behavior.

Benzodiazepines reliably produce overconsumption of food and fluids. Opiate antagonists, naloxone and naltrexone, block the benzodiazepine-induced hyperphagia and hyperdipsia at low doses. Hence, activation of endogenous opioid mechanisms may be closely involved in the benzodiazepine facilitatory effects on ingestional behavior. Evidence is reviewed that opiate antagonists diminish feeding and drinking responses, and may enhance satiety processes in feeding and drinking, in addition to selectively diminishing the palatability of attractive foods and fluids. It is proposed that a single mechanism of action of the opiate antagonists would be sufficient to account for both effects on feeding and drinking. Biochemical data confirm that acute benzodiazepine treatment in vivo is associated with a naloxone-reversible release of striatal enkephalin. It is possible therefore that there is a close association between the behavioral and biochemical data, which both show that acute benzodiazepine effects are reversed by opiate antagonists. The implied relationship between benzodiazepine and endogenous opioid mechanisms may be relevant to the question of concurrent opiate-benzodiazepine abuse.

Animals↗
PubMed1978

Striatal nondopaminergic neurons: possible involvement in feeding and drinking behavior.

Intracaudate injections of kainic acid destroy striatal neurons containing acetylcholine and gamma-aminobutyric acid but leave dopaminergic nerve terminals in this brain region intact. Rats injected with the drug are aphagic and adipsic, and have other behavioral abnormalities strikingly similar to those seen in animals with lesions in the dopaminergic nigrostriatal bundle.

Animals↗