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Biomedical subjects

E L Morrow

Publications and source records attributed to E L Morrow.

6 recordsLinked to original sources
PubMed1987

Calcium differentially alters behavioral and electrophysiological responses to ethanol in selectively bred mouse lines.

Sensitivity to the hypnotic action of ethanol has been found to increase in SS/Ibg (SS) but not in LS/Ibg (LS) mice after intracerebroventricular (icv) administration of calcium. In the present investigation, a correlation was found between calcium-induced changes in behavioral sensitivity and in the sensitivity of cerebellar Purkinje neurons to the depressant effects of locally applied ethanol. Cerebellar Purkinje neuron sensitivity was measured as the dose of ethanol pressure ejected from a multibarreled micropipette required to produce a 50% depression of spontaneous firing rate of single neurons. Administration of 0.2-0.4 mumol calcium chloride into the lateral ventricle of the brain increased the sensitivity of SS but not LS mice to the hypnotic behavioral effect of systemically administered ethanol. Similarly, Purkinje neuron sensitivity to locally applied ethanol was also enhanced in SS but not in LS mice 15 min following administration of calcium (0.25 mumol) icv. Furthermore, locally applied ethanol was more effective in depressing spontaneous Purkinje neuron discharge in SS mice when a 1 mM calcium solution was concomitantly pressure ejected with ethanol from the micropipette. Magnesium chloride did not mimic the effects of calcium on either behavioral or electrophysiological effects of ethanol, suggesting that the action of calcium is not a nonspecific effect of divalent cations. These data suggest that calcium-dependent processes may be involved in behavioral and electrophysiological effects associated with ethanol intoxication. Further research will be required to determine if the genetically selected difference in ethanol sensitivity expressed in LS and SS mice is regulated by calcium mechanisms.

Action Potentials↗
PubMed1987

Calcium influence on neurotensin and beta-endorphin enhancement of ethanol sensitivity in selectively bred mouse lines.

Intracerebroventricular (icv) administration of neurotensin produced a dose-dependent increase in ethanol sensitivity as measured by blood ethanol concentration at loss of righting reflex in SS/Ibg (SS) but not in LS/Ibg (LS) mice. Central administration of calcium also enhanced ethanol sensitivity of SS and to a lesser extent LS mice. Concurrent icv administration of calcium and neurotensin resulted in an additional enhancement of sensitivity to ethanol over that seen with either substance alone in both mouse lines. A dose-dependent increase in ethanol sensitivity was also produced in response to central administration of beta-endorphin in SS mice. No additional increase in sensitivity was noted following administration of beta-endorphin plus calcium. These results suggest a specific interaction of calcium and neurotensin may be involved in the mechanism through which ethanol elicits intoxication. The difference in response of LS and SS mice to neuropeptide and calcium-induced alterations in ethanol sensitivity may be related to the genetically selected differences to the acute narcotic actions of ethanol in these mice.

Alcoholic Intoxication↗
PubMed1986

Effects of ethanol and pentobarbital on neuronal hexose uptake in inbred mice.

The effect of ethanol and pentobarbital narcosis on 2-deoxyglucose uptake into brain synaptosomes prepared from inbred C57BL/6J and DBA/2J mice which exhibit differential central sensitivity to ethanol and heterogeneous ICR mice was examined. A reversible depression of synaptosomal uptake was exhibited in all strains administered ethanol acutely, occurring at 2 min in ICR and C57BL/6J mice and 15 min in DBA/2J. Uptake returned to control values in all strains at 30 min although the mice remained intoxicated. Brain glucose concentration was significantly elevated at this time. Pentobarbital administration was without effect on synaptosomal hexose transport in DBA/2J and C57BL/6J mice but increased it significantly in ICR mice at 30 min. Pentobarbital anesthesia did not alter brain glucose concentration. No correlation was apparent between synaptosomal 2-deoxyglucose uptake and differential CNS sensitivity to ethanol and pentobarbital. The effects of ethanol and pentobarbital on neuronal hexose transport is discussed with respect to reported changes in glycolytic metabolism produced by these agents.

Animals↗
PubMed1986

Calcium influence on neuronal sensitivity to ethanol in selectively bred mouse lines.

Sensitivity to ethanol, as measured by blood ethanol concentration at loss of righting reflex, was increased significantly in SS but not LS mice following intracerebroventricular (ICV) administration of calcium chloride or A23187, a calcium ionophore. Magnesium chloride or lanthanum chloride, ICV, did not alter sensitivity to ethanol in either SS or LS mice, further indicating a specificity for calcium cation. Calcium was without effect on sensitivity to halothane narcosis in LS or SS mice. Endogenous brain calcium content was similar in these mouse lines, and ethanol administration either in vivo or in vitro did not alter brain calcium concentration. These results indicate that differences in brain sensitivity to ethanol are mediated, in part, by genetic differences in calcium-related processes and support the hypothesis that ethanol-induced narcosis may be due to alterations in calcium metabolism in the CNS.

Animals↗