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 (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 NK(1)R 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 NK(1)R antagonist response required the suppression of the enkephalin/MOR inhibitory control of acetylcholine release by betafunaltrexamine. The pharmacological profile of the tachykinin NK(1)R 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 NK(1)R implicated are the new NK(1)-sensitive receptor binding site. Therefore, in the limbic/PF territory of the dorsal striatum, endogenous tachykinin facilitates acetylcholine release via a tachykinin NK(1)R subtype. In the afternoon, the tachykinin/NK(1)R and the enkephalin/MOR transmissions interact to control cholinergic transmission.
Pérez
Sylvie
S
INSERM, Collège de France and University Pierre et Marie Curie, Paris, France.
Tierney
Adrienne
A
Deniau
Jean-Michel
JM
Kemel
Marie-Louise
ML
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001665:Binding Sites / Q000187:drug effects / Q000502:physiology; D001667:Binding, Competitive / Q000187:drug effects / Q000502:physiology; D002799:Cholinergic Fibers / Q000378:metabolism*; D002940:Circadian Rhythm / Q000187:drug effects / Q000502:physiology; D004745:Enkephalins / Q000378:metabolism; D008032:Limbic System / Q000378:metabolism; D008297:Male; D009025:Morpholines / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D017072:Neostriatum / Q000166:cytology / Q000378:metabolism*; D009434:Neural Pathways / Q000378:metabolism; D064729:Neurokinin-1 Receptor Antagonists; D009924:Organ Culture Techniques; D010880:Piperidines / Q000494:pharmacology; D017397:Prefrontal Cortex / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018040:Receptors, Neurokinin-1 / Q000819:agonists / Q000378:metabolism*; D017450:Receptors, Opioid, mu / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D015320:Tachykinins / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*
C469681:2-(1-(2-(4-(2-(3,5-bis(trifluoromethyl)phenyl)acetyl)-2-(3,4-dichlorophenyl)-2-morpholinyl)ethyl)-4-piperidinyl)-2-methylpropanamide; D004745:Enkephalins; D009025:Morpholines; D009292:Narcotic Antagonists; D064729:Neurokinin-1 Receptor Antagonists; D010880:Piperidines; D018040:Receptors, Neurokinin-1; D017450:Receptors, Opioid, mu; D015320:Tachykinins; D000109:Acetylcholine