Nitrergic, glutamatergic and gabaergic systems in lithium toxicity
Author:
Affiliation:
1. Department of Medical Pharmacology, Istanbul Faculty of Medicine, Istanbul University, Turkey
2. Department of Biochemistry, Istanbul Faculty of Medicine, Istanbul University,Turkey
Publisher
Japanese Society of Toxicology
Subject
Toxicology
Link
https://www.jstage.jst.go.jp/article/jts/37/5/37_1017/_pdf
Reference50 articles.
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2. Antonelli, T., Ferioli, V., Lo Gallo, G., Tomasini, M.C., Fernandez, M., O’Connor, W.T., Glennon, J.C., Tanganelli, S. and Ferraro, L. (2000): Differential effects of acute and short-term lithium administration on dialysate glutamate and GABA levels in the frontal cortex of the conscious rat. Synapse, 38, 355-362.
3. Apte, S.N. and Langston, J.W. (1983): Permanent neurological deficits due to lithium toxicity. Ann. Neurol., 13, 453-455.
4. Bagetta, G., Massoud, R., Rodino, P., Federici, G. and Nistico, G. (1993): Systemic administration of lithium chloride and tacrine increases nitric oxide synthase activity in the hippocampus of rats. Eur. J. Pharmacol., 237, 61-64.
5. Bagetta, G., Rodino, P., Paoletti, A.M., Arabia, A., Massoud, R. and Nistico, G. (1995): Systemic administration of lithium chloride and tacrine but not kainic acid augments citrulline content of rat brain. Eur. J. Pharmacol., 294, 341-344.
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