Journal
JOURNAL OF NEUROCHEMISTRY
Volume 103, Issue 6, Pages 2153-2163Publisher
BLACKWELL PUBLISHING
DOI: 10.1111/j.1471-4159.2007.04944.x
Keywords
acetylcholine; Mu opioid receptor; striatum; tachykinin; tachykinin NK1 receptor subtypes
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The tachykinin neurokinin 1 receptors (NK(1)Rs) 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 NK(1)Rs 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 beta funaltrexamine. The pharmacological profile of the tachykinin NK1R regulation tested by application of the receptor agonists [[Pro(9)]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.
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