GM1 ganglioside treatment promotes recovery of electrically-stimulated [3H]dopamine release in striatal slices from rats lesioned with kainic acid.
The electrically-evoked release of [3H]dopamine ([3H]DA) from rat striatal slices was studied after a monolateral intrastriatal injection of kainic acid (KA). The release in the KA-lesioned striatum measured 4 days after the lesion was largely reduced (by 80%) with respect to the contralateral striatum. Administration of GM1 ganglioside (GM1) beginning on the day of the lesion resulted in restoration of the catecholamine release. Significant recovery was observed when GM1 was administered i.p. daily at the dose of 3 mg/kg for 6 days. The ganglioside given for 6 days at 30 mg/kg restored to near normal the electrically-evoked [3H]DA release. Similar recovery from the KA-induced injury occurred spontaneously but required 50 days.
Raiteri
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Istituto di Farmacologia e Farmacognosia, Università degli Studi di Genova, Italy.
Bonanno
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Pende
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D000818:Animals; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D003714:Denervation; D004298:Dopamine / Q000378:metabolism*; D004558:Electric Stimulation; D005677:G(M1) Ganglioside / Q000494:pharmacology*; D007608:Kainic Acid / Q000633:toxicity*; D008297:Male; D009474:Neurons / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D018092:Kainic Acid Receptors; D017981:Receptors, Neurotransmitter / Q000502:physiology
D004298:Dopamine; D005677:G(M1) Ganglioside; D007608:Kainic Acid; D018092:Kainic Acid Receptors; D017981:Receptors, Neurotransmitter