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Pharmacological Characterization of Tachykinin Receptors Controlling Acetylcholine Release from Rat Striatum: An In Vivo Microdialysis Study
Author(s) -
Steinberg R.,
Rodier D.,
Souilhac J.,
Bougault I.,
EmondsAlt X.,
Soubrié P.,
Le Fur G.
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.65062543.x
Subject(s) - substance p , tachykinin receptor , microdialysis , agonist , acetylcholine , endocrinology , medicine , receptor , chemistry , stimulation , neurokinin a , neurokinin b , cholinergic , neurotransmitter , neuropeptide , biology , dopamine
The regulation of striatal cholinergic function by tachykinins was examined in urethane‐anesthetized rats by using microdialysis. Substance P (0.01–1 µ M ), [Sar 9 ,Met(O 2 ) 11 ]substance P (1–10 µ M ), septide (0.1–3 µ M ), neurokinin (NK) A (0.1–10 µ M ), and senktide (0.1–10 µ M ) produced concentration‐dependent increases in striatal acetylcholine (ACh) release. Septide was the most potent agonist for inducing release of ACh, whereas the stimulating effect of senktide was less pronounced and more progressive in onset. The response to septide was prevented by intraperitoneal administration of the nonpeptide NK 1 antagonist SR 140333 (1–3 mg/kg) but not by the nonpeptide NK 2 receptor antagonist SR 48968, indicating that the effect was mediated specifically by NK 1 receptors. ACh release caused by NKA was reduced by SR 48968 (1–3 mg/kg) and slightly affected by SR 140333, indicating a principal role for NK 2 receptors in the peptide response. The similar efficacy of SR 140333 and SR 48968 in blocking substance P‐induced ACh release suggested that the effect of this peptide involves the stimulation of both NK 1 and NK 2 receptors. Finally, our results indicate that the increase in striatal ACh release induced by the D 1 agonist (+)‐SKF‐38393 (3 µ M ) may be mediated indirectly through local release of NKA or substance P acting at NK 2 receptors.