PubMed Health⌕ Search

Biomedical subjects

C K Erickson

Publications and source records attributed to C K Erickson.

At least 73 records · Page 4Linked to original sources
PubMed1978

Sustained release of alcohol: subcutaneous silastic implants in mice.

A sustained-release device for use in ethanol dependence studies in mice is described. The Silastic device, dubbed SERT (sustained ethanol release tube), holds 0.35 milliliter of 95 percent ethanol (by volume) and is implanted under the skin of the back where it releases ethanol for up to 12 hours, with no observable tissue damage. The device may be adaptable to the release of other volatile liquids or drugs, in other animals.

Alcoholic Intoxication↗
PubMed1978

Ethanol: modifications of acute intoxication by divalent cations.

Calcium, other divalent cations, and calcium antagonists were tested for their ability to alter ethanol-induced sleeping time, hypothermia, and behavioral intoxication in mice and rats. Calcium given intraventricularly significantly enhanced sleeping time and behavioral intoxication in a dose-related manner. The ionophores X537A and A23187 accentuated the effect of a low dose of calcium, whereas the calcium chelators EDTA and EGTA decreased sleeping time. Calcium also enhanced tertiary butanol- and chloral hydrate-induced sleeping time. The effects of cations on ethanol-induced hypothermia were less significant. The results suggest the existence of a central calcium pool that is involved in ethanol intoxication in rodents.

Alcoholic Intoxication↗
PubMed1977

Alteration of ethanol-induced changes in locomotor activity by adrenergic blockers in mice.

The effects of various doses of ethanol (ETOH) on spontaneous locomotor activity (SLMA) in mice were measured using photocell activity chambers. Of the 4 i.p. doses injected, the 2 lowest doses (0.5 and 1.0 g/kg) stimulated SLMA, the next higher dose (2.0 g/kg) produced a biphasic effect of depression followed by stimulation, and the highest dose (4.0 g/kg) depressed SLMA. The mechanism of the biphasic effect of the 2.0 g/kg dose was studied in tests with central catecholamine antagonists at various doses 30 min before ETOH. Doses of 5, 10, and 20 mg/kg of propranolol, a beta-receptor blocker, significantly antagonized the depressant effect of ETOH but had no influence on the stimulant effect. High doses (10 and 20 mg/kg) of phentolamine, an alpha-receptor blocker, significantly antagonized the stimulant phase of ETOH action but had no significant effect on the depressant phase. All doses (0.062-0.250 mg/kg) of spiroperidol, a dopaminergic blocking drug, significantly enhanced the SLMA depression produced by ETOH. These results indicate that the SLMA-depressant effect of ETOH may be mediated by central "beta-type" receptors, that the SLMA-stimulant effect of ETOH may be mediated by central "alpha-type" receptors, and that at least part of ETOH's action may be due to dopaminergic mechanisms.

Animals↗