The Role of Excitatory Amino Acids and Intraneuronal Calcium in the Acute Intoxicational Effects of Ethanol

Nifedipine Alleviates Alterations in Hippocampal Kindling After Repeated Ethanol Withdrawal

“…Alterations in the L-type VOCC are consistent with ethanol-induced changes in overall calcium activity, with a doubling of the number of channels reported after longterm ethanol exposure, in both in vitro cell preparations and in intact animals (Deutsch et al, 1989;Ferrante and Triggle, 1990;Guppy and Littleton, 1994). Although one study of human alcoholics reported no differences in the number of these channels, the authors note that the long autolysis time (23 Ϯ 5 hr) before completion of the binding studies may have adversely impacted the results (Marks et al, 1989).…”

“…In synaptosomes, acute ethanol lowers intracellular calcium concentrations on a short-term basis (Daniell et al, 1987;Deitrich et al, 1989;Deutsch et al, 1989;Leslie et al, 1990). Significant increases in calcium binding from control levels have been observed during both ethanol intoxication (Dolin and Little, 1989;Guppy and Littleton, 1994;Guppy et al, 1995;Virmani et al, 1985;Whittington et al, 1978) and withdrawal (Perez-Velazquez et al, 1994;Virmani et al, 1985;Whittington et al, 1995), with the highest increases noted in the hippocampus (Virmani et al, 1985).…”

“…Ethanol administered acutely or on a chronic basis alters the function of a variety of neurotransmitter systems, in-cluding ␥-aminobutyric acid (Deutsch et al, 1989;Hoffman and Tabakoff, 1996;Nutt and Glue, 1990), NMDA (Deutsch et al, 1989;Hoffman and Tabakoff, 1996;Littleton, 1989), acetylcholine (Gonzalez and Sun, 1992), catecholamines (Hoffman and Tabakoff, 1996;Nutt and Glue, 1990), and peptidergic systems (Nutt and Glue, 1990). In fact, it is recognized that the cumulative effect of ethanol is the result of interactions among these as well as other systems (Nutt and Glue, 1990).…”

“…In fact, it is recognized that the cumulative effect of ethanol is the result of interactions among these as well as other systems (Nutt and Glue, 1990). Ethanol also alters calcium uptake (Deutsch et al, 1989;Leslie, 1987;Leslie et al, 1990;Mullikin-Kilpatrick and Treistman, 1995), calcium currents (Leslie, 1987;Mullikin-Kilpatrick and Treistman, 1995;Pozos and Oakes, 1987), and calcium-mediated neurotransmitter release (Leslie, 1987); and, voltage-operated calcium channels (VOCCs) are altered by ethanol exposure (Deutsch et al, 1989;Leslie, 1987;Mullikin-Kilpatrick and Treistman, 1995;Nutt and Glue, 1990). Further, some studies have suggested that treatment with calcium channel antagonists may reduce the severity of the acute withdrawal syndrome (Colombo et al, 1995;Dolin and Little, 1989;Little et al, 1986;Whittington et al, 1978).…”

Nifedipine Alleviates Alterations in Hippocampal Kindling After Repeated Ethanol Withdrawal

“…Calcium involvement in ethanol-induced effects is well recognized (Carlen et al, 1990;Greenberg et al, 1990;Leslie et al, 1990). In synaptosomes, acute ethanol lowers intracellular calcium concentrations on a short-term basis (Daniell et al, 1987;Deitrich et al, 1989;Deutsch et al, 1989;Leslie et al, 1990). Significant increases in calcium binding from control levels have been observed during both ethanol intoxication (Dolin and Little, 1989;Guppy and Littleton, 1994;Guppy et al, 1995;Virmani et al, 1985;Whittington et al, 1978) and withdrawal (Perez-Velazquez et al, 1994;Virmani et al, 1985;Whittington et al, 1995), with the highest increases noted in the hippocampus (Virmani et al, 1985).…”