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Tachykinin regulation of cholinergic transmission in the limbic/prefrontal territory of the rat dorsal striatum: implication of new neurokinine 1‐sensitive receptor binding site and interaction with enkephalin/mu opioid receptor transmission

The tachykinin neurokinin 1 receptors (NK1Rs) regulation of acetylcholine release and its interaction with the enkephalin/mu opioid receptors (MORs) transmission was investigated in the limbic/prefrontal (PF) territory of the dorsal striatum. Using double immunohistochemistry, we first showed that in this territory, cholinergic interneurons contain tachykinin NK1Rs and co‐express MORs in the last part of the light period (afternoon). In slices of the striatal limbic/PF territory, following suppression of the dopaminergic inhibitory control of acetylcholine release, application of the tachykinin NK1R antagonist, SSR240600, markedly reduced the NMDA‐induced acetylcholine release in the morning but not in the afternoon when the enkephalin/MOR regulation is operational. In the afternoon, the NK1R antagonist response required the suppression of the enkephalin/MOR inhibitory control of acetylcholine release by βfunaltrexamine. The pharmacological profile of the tachykinin NK1R regulation tested by application of the receptor agonists [[Pro9]substance P, neurokinin A, neuropeptide K, and substance P(6–11)] and antagonists (SSR240600, GR205171, GR82334, and RP67580) indicated that the subtype of tachykinin NK1R implicated are the new NK1‐sensitive receptor binding site. Therefore, in the limbic/PF territory of the dorsal striatum, endogenous tachykinin facilitates acetylcholine release via a tachykinin NK1R subtype. In the afternoon, the tachykinin/NK1R and the enkephalin/MOR transmissions interact to control cholinergic transmission.