strychnine and Alcoholic-Intoxication

Elevated dopamine levels are believed to contribute to the rewarding sensation of ethanol (EtOH), and previous research has shown that strychnine-sensitive glycine receptors in the nucleus accumbens (nAc) are involved in regulating dopamine release and in mediating the reinforcing effects of EtOH. Furthermore, the osmoregulator taurine, which is released from astrocytes treated with EtOH, can act as an endogenous ligand for the glycine receptor, and increase extracellular dopamine levels. The aim of this study was to address if EtOH-induced swelling of astrocytes could contribute to elevated dopamine levels by increasing the extracellular concentration of taurine. Cell swelling was estimated by optical sectioning of fluorescently labeled astrocytes in primary cultures from rat, and showed that EtOH (25-150 mM) increased astrocyte cell volumes in a concentration- and ion-dependent manner. The EtOH-induced cell swelling was inhibited in cultures treated with the Na(+) /K(+) /2Cl⁻ cotransporter blocker furosemide (1 mM), Na(+) /K(+) -ATPase inhibitor ouabain (0.1 mM), potassium channel inhibitor BaCl₂ (50 µM) and in cultures containing low extracellular sodium concentration (3 mM). In vivo microdialysis performed in the nAc of awake and freely moving rats showed that local treatment with EtOH enhanced the concentrations of dopamine and taurine in the microdialysate, while glycine and β-alanine levels were not significantly modulated. EtOH-induced dopamine release was antagonized by local treatment with the glycine receptor antagonist strychnine (20 µM) or furosemide (100 µM or 1 mM). Furosemide also prevented EtOH-induced taurine release in the nAc. In conclusion, our data suggest that extracellular concentrations of dopamine and taurine are interconnected and that swelling of astrocytes contributes to the acute rewarding sensation of EtOH.

Topics: Alcoholic Intoxication; Animals; Astrocytes; Dopamine; Ethanol; Furosemide; Glycine Agents; Male; Neural Pathways; Nucleus Accumbens; Rats; Rats, Wistar; Receptors, Glycine; Sodium Potassium Chloride Symporter Inhibitors; Strychnine; Taurine; Ventral Tegmental Area; Water-Electrolyte Balance

The authors describe a patient presenting with both ethanol intoxication and important strychnine poisoning. The diagnosis and treatment of strychnine poisoning are discussed. The authors emphasize the need of careful urine screening for drugs and toxic products in all ethanol-intoxicated patients.

Topics: Aged; Alcoholic Intoxication; Humans; Male; Poisoning; Strychnine; Suicide, Attempted

In this paper we describe new data and review some studies on the mechanisms of alcohol-induced motor impairment in rats. Habituation to handling did not affect the naive behavioural differences between the alcohol sensitive and alcohol insensitive rat lines. Nor was there any effect on the differential sensitivities of the lines to the motor impairing and hypnotic effects of alcohol. Peripheral mechanisms may be involved in the differential behaviours of these lines, as the plasma corticosterone response was much weaker in the alcohol sensitive animals, suggesting a limited capacity to react to stress and alcohol. A similar blunted response to acute ethanol exposure was found in the uptake of the benzodiazepine antagonist [3H]Ro 15-1788 in vivo by the cerebellum of alcohol sensitive rats. The finding that these rat lines do not have any general differences in their brain inhibitory GABAergic receptors was extended to the spinal cord inhibitory glycinergic receptors, which showed only a modest line difference in their dissociation constant. The apparent localisation of the two main receptor differences (high-affinity [3H]muscimol binding and diazepam sensitivity of [3H]Ro 15-4513 binding) to the cerebellar granule layer suggests a genetic modification in the granule cells of alcohol-sensitive rats. In conclusion, our studies on acute intoxication by moderate alcohol doses show that several central nervous and peripheral factors may be involved in this behaviour. As many of these factors mitigate the effects of alcohol, alcohol antagonistic treatments should be aimed at activating and supporting multiple adaptive phenomena.

Topics: Adrenal Glands; Alcoholic Intoxication; Animals; Behavior, Animal; Benzodiazepinones; Brain; Convulsants; Cortisone; Disease Models, Animal; Drug Tolerance; Ethanol; Habituation, Psychophysiologic; Kidney; Male; Rats; Strychnine

Topics: Alcoholic Intoxication; Animals; Caffeine; Cats; Dextroamphetamine; Disease Models, Animal; Dogs; Ethanol; gamma-Aminobutyric Acid; Humans; Maleates; Naloxone; Pentylenetetrazole; Rabbits; Strychnine

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Alcoholic Intoxication; Animals; Anticonvulsants; Blood Pressure; Body Temperature; Bronchi; Catatonia; Dibenzocycloheptenes; Drug Antagonism; Drug Synergism; Electroshock; Gastrointestinal Motility; Heart; Histamine H1 Antagonists; Humans; Knee; Male; Methionine Sulfoximine; Mice; Motor Activity; Nervous System; Neuromuscular Junction; Pentylenetetrazole; Reaction Time; Reflex; Reticular Formation; Spasm; Strychnine; Tremor

Topics: Agaricales; Alcoholic Intoxication; Benzene; Carbon Monoxide Poisoning; Morphine; Nitrites; Oxygen; Oxygen Inhalation Therapy; Phosgene; Poisoning; Strychnine; Toxicology; Vegetables