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Journal of Neuroscience, Vol 11, 2332-2338, Copyright © 1991 by Society for Neuroscience
Neurokinin receptors differentially mediate endogenous acetylcholine release evoked by tachykinins in the neostriatum
E Arenas, J Alberch, E Perez-Navarro, C Solsona and J Marsal
Departament de Biologia Cellular i Anatomia Patologica, Hospital de Bellvitge, Facultat de Medicina, Universitat de Barcelona, Spain.
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.(ABSTRACT TRUNCATED AT 250 WORDS)
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