Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0278080 (physical dependence)
 1,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of several drugs on the kinetics of 14C-dopamine were studied in slices of rat striata in vitro. While morphine (35 muM) did not affect the uptake of 14C-dopamine into the slices, d-amphetamine (50muM) and imipramine (100 muM) strongly inhibited it. Morphine significantly slowed the K+ -induced release of the labelled dopamine; imipramine almost completely blocked it, while amphetamine h had no clear effect. The effect of morphine was dose-dependent and could be inhibited by the narcotic antagonist naloxone. The results demonstrate that each of the drug had a characteristic pattern of effects in our system studied. The inhibitory action of morphine on the dopamine release in vitro probably reflects in vivo symptoms of a central dopamine deficiency in rats (catalepsy, akinesia, muscular rigidity) after morphine application. In further series of experiments, it was studied if the sensitivity of brain dopamine receptors increased after repeated applications of morphine, which induced clear signs of physical dependence. Since chronic morphine treatment did not increase the potency of apomorphine (which directly stimulates dopamine receptors) in inducing stereotyped behavior, it is concluded that an increased sensitivity of dopamine receptors is not necessarily involved in morphine tolerance and dependence.
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PMID:Studies on dopamine kinetics in rat brain tissue under the influence of morphine. 117 89

This paper reports findings relative to a simple, rapid and reproducible technique for the induction of physical dependence upon ethanol in the rat. The dependence was induced by intragastric intubation of 20% (w/v) ethanol solutions at 9-15 g/kg in 3-5 fractional doses daily for 4 days, maintaining blood ethanol concentrations above a threshold level sufficient to sustain observable sedation throughout the entire period of intubation. Two phases were distinguished during the withdrawal period: 1. Prodromal detoxication, characterized by a spectrum of signs and responses of diminishing severity, related to the decline in blood ethanol concentrations (mg/dl): death, greater than 640; coma, 780-460; loss of righting reflex, 640-400; ataxia 3-1, 570-250; sedation 340-190; neutrality, 220-130; 2. Ethanol dependence, characterized by a spectrum of withdrawal signs and reactions of progressively increasing severity as blood ehtanol concentration approached 100 mg/dl: hyperactivity, tremors, akinesia, spastic rigidity, and induced and spontaneous convulsions. A rapid sucession of two diverse clusters of signs and reactions represents a reversal of the central nervous system function from the extremes of ethanol intoxication (CNS depression) to the extremes of ethanol dependence (CNS hyperexcitability) during the withdrawal period. Both extremes may terminate in death.
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PMID:Induction of physical dependence upon ethanol and the associated behavioral changes in rats. 123 14