Dopamine release and dopaminergic inhibition of acetylcholine release in rat striatal slices after nigro-striatal hemitransection and parenteral ganglioside administration.

Hemitransection of the nigro-striatal bundle in adult rats reduced [3H]dopamine ([3H]DA) uptake into striatal slices from the lesioned side to about 20% of that in the contralateral side 5 days after surgery. Spontaneous recovery of [3H]DA uptake was observed at days 8 and 15 post-lesion (42 and 67% of the unoperated side, respectively). After a short treatment (3 days) with the GM1 ganglioside inner ester (AGF2, 30 mg/kg i.p., daily, starting on day 2 after surgery) [3H]DA uptake amounted to 52% of that in the unoperated side. The electrically evoked fractional overflow of [3H]DA was increased by 500% in slices prepared from the lesioned side 5 days after injury, largely due to the reduced re-uptake by the DA axon terminals. The increase on day 5 was only about 350% in AGF2-treated animals. The DA D2 receptor antagonist, (-)-sulpiride, potentiated the stimulus-evoked overflow of [14C]acetylcholine in slices from the unoperated side prelabelled with [14C]choline. The effect of (-)-sulpiride was much reduced (by about 80%) in the lesioned striata at days 5 and 8 after surgery. Partial recovery was seen at day 15. The lesion did not modify the (-)-sulpiride effect in animals treated with AGF2 from the 2nd to the 5th day post-lesion. Thus early ganglioside administration slows the loss of endogenous dopaminergic control of acetylcholine release caused by partial hemitransection of the nigro-striatal bundle.