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Control of tachykinin-evoked acetylcholine release from rat striatal slices by dopaminergic neurons

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Summary

The regulation of tachykinin-evoked acetylcholine release by the dopaminergic system in the neostriatum was examined. We studied the effect of selective and potent tachykinin agonists for each subtype of receptor ([Sar9,Met(O2)11]-Substance P for NK1; [Nle10]-Neurokinin A4−10 for NK2; and senktide for NK3) on endogenous acetylcholine release from rat striatal slices where the dopaminergic system was modified either by 6-hydroxydopamine lesion or by dopamine receptor antagonists. Unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway induced a decrease in senktide-evoked acetylcholine release and an increase in the effect of [Nle10]-Neurokinin A4–10 The same results were obtained after chronic haloperidol treatment, whereas SCH-23390 or clozapine treatment had no effect on tachykinin-evoked acetylcholine release, suggesting an involvement of D2 receptors. 6-hydroxydopamine lesion induced a diminution in the density of NK3 receptor, which could be related to the reduction in senktide-evoked acetylcholine release.

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Correspondence to: J. Marsal at the above address

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Alberch, J., Arenas, E., Pérez-Navarro, E. et al. Control of tachykinin-evoked acetylcholine release from rat striatal slices by dopaminergic neurons. Naunyn-Schmiedeberg's Arch Pharmacol 348, 445–449 (1993). https://doi.org/10.1007/BF00173201

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  • DOI: https://doi.org/10.1007/BF00173201

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