Biochemical changes in the rat cerebellar cortex elicited by chronic treatment with methyl mercury.
Long-term (20 days) treatment with methyl mercury (MeHg) increases the total number of benzodiazepine binding sites and decreases essentially the content of cyclic GMP in the cerebellar cortex. In contrast, this treatment fails to modify the content of GABA and cyclic AMP, GAD activity and GABA binding sites in the same brain area. The changes in cyclic GMP and benzodiazepine binding sites in the cerebellar cortex are discussed in relation to the motor disturbances associated with MeHg intoxication.
D000818:Animals; D002531:Cerebellum / Q000032:analysis / Q000187:drug effects*; D006152:Cyclic GMP / Q000032:analysis; D005968:Glutamate Decarboxylase / Q000032:analysis; D008297:Male; D008767:Methylmercury Compounds / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D011956:Receptors, Cell Surface / Q000187:drug effects; D011963:Receptors, GABA-A
D008767:Methylmercury Compounds; D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D005968:Glutamate Decarboxylase; D006152:Cyclic GMP