par Dethy, Sophie 
;Manto, Mario ;Bastianelli, Enrico;Gangji, Valérie ;Laute, Marie-Aline;Goldman, Serge ;Hildebrand, Jerzy
Référence Neuroscience letters, 224, 1, page (25-28)
Publication Publié, 1997-03
;Manto, Mario ;Bastianelli, Enrico;Gangji, Valérie ;Laute, Marie-Aline;Goldman, Serge ;Hildebrand, Jerzy Référence Neuroscience letters, 224, 1, page (25-28)
Publication Publié, 1997-03
Article révisé par les pairs
| Résumé : | Cerebellar syndrome has been described after acute lithium intoxication in human. Neuropathological studies have demonstrated neuronal loss and spongiosis in the cerebellum. We describe an animal model of acute lithium-induced cerebellar degeneration. Five hours following administration of lithium chloride (250 mg/kg, i.p.), the cerebellar white matter of seven rats out 14 exhibited extensive spongiform changes. Microdialysis study in the rat cerebellar cortex demonstrated basal concentrations of dopamine (DA), hydroxy-3-methoxyphenylacetic acid (HVA) and 5-hydroxy-3-indolacetic acid (5-HIAA). These metabolites were unaffected by acute lithium intoxication suggesting that the cerebellar toxicity is not due to a modification of dopaminergic or serotoninergic neurotransmission. |
