Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/25862
Title: Neurokinin receptors differentially mediate endogenous acetylcholine release evoked by tachykinins in the neostriatum.
Author: Arenas, Ernest
Alberch i Vié, Jordi
Pérez Navarro, Esther
Solsona Sancho, Carles
Marsal Tebé, Jordi
Keywords: Receptors colinèrgics
Neuropèptids
Ganglis basals
Acetylcholine receptors
Neuropeptides
Basal ganglia
Issue Date: 1991
Publisher: Society for Neuroscience
Abstract: The regulation of neostriatal cholinergic function by tachykinins (TKs) has been studied by measuring endogenous ACh released from rat neostriatal slices. Septide (SEP; a highly selective substance P analog), neurokinin A (NKA), and neurokinin B (NKB) elicited endogenous ACh release in a concentration-dependent manner. The rank order in potency was the following: NKB (EC50 approximately 0.5 nM) greater than NKA (EC50 approximately 7 nM) greater than SEP (EC50 approximately 12 nM). Spantide (SPA) was less effective (39% inhibition) than [D-Arg6, D- Trp7,9, N-Methyl-Phe8]-substance P fragment 6–11 (53% inhibition) at antagonizing ACh release evoked by SEP and NKA. Smaller doses of the antagonists inhibited the effects of SEP compared to NKA, and the effects of NKB could only be antagonized by SPA. These findings suggest the involvement of the three neurokinin (NK) receptors in ACh release evoked by TKs with the following rank order: NK3 greater than NK2 greater than NK1. 6-Hydroxydopamine lesions of nigrostriatal neurons and tetrodotoxin (TTX) intoxication of striatal tissue revealed two different patterns of regulation of cholinergic function by TKs. On the one hand, SEP and NKA evoked ACh release, independently of the nigrostriatal dopaminergic system, by acting on NK1 and NK2 receptors that are probably localized on the somatodendritic field of cholinergic neurons receiving substance P terminals. On the other hand, dopaminergic terminals seem to regulate NKB neurons that modulate cholinergic neurons, because NKB-evoked ACh release decreased by 24% in the denervated striata. In addition, TTX partially blocked (50%) ACh release evoked by NKB, suggesting that NKB acts on NK3 receptors at both the nerve terminals and the somatodendritic field of cholinergic neurons.
Note: Reproducció del document publicat a: https://doi.org/10.1523/JNEUROSCI.11-08-02332.1991
It is part of: Journal of Neuroscience, 1991, vol. 11, num. 8, p. 2332-2338
Related resource: https://doi.org/10.1523/JNEUROSCI.11-08-02332.1991
URI: http://hdl.handle.net/2445/25862
ISSN: 0270-6474
Appears in Collections:Articles publicats en revistes (Patologia i Terapèutica Experimental)
Articles publicats en revistes (Biomedicina)

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