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• W2095281061 abstract "While it had no effect on the resting tension of mouse tracheal segments, 5-HT (10−8–10−4 M) potentiated concentration dependently the contractions induced by electrical field stimulation (EFS). The maximal potentiation was 105 ± 38% and the EC50 value was 1.4 ± 0.6 × 10−6 M (n = 6). The responsiveness of mouse trachea to acetylcholine was not altered by 5-HT (10−5 M). The 5-HT1A,B antagonist pindolol (10−6 M), the combined 5-HT2 and 5-HT1C receptor antagonist, ketanserin (10−6 M), or the combined 5-HT1 and 5-HT2 receptor antagonist, methysergide (10−6 M), all partially inhibited the effect of 5-HT on the twitch responses. Blockade of 5-HT3 receptors by GR 38032F (10−6 M) did not affect the potentiation by 5-HT. Antagonism of 5-HT3 and 5-HT4 receptors by ICS 205,930 (3 × 10−6 M) increased the potentiation of the twitch responses by 5-HT, this was probably due to a decrease of the baseline EFS-induced twitch response by ICS 205,930. Alkylation of the 5-HT2 receptor by phenoxybenzamine (3 × 10−7 M) treatment did not significantly affect the potentiation of the twitch responses by 5-HT. The β-adrenoceptor antagonist, timolol (10−6 M), and the α-adrenoceptor antagonist, phentolamine (10−6 M), did not influence the potentiation of the twitch responses by 5-HT, excluding the involvement of the adrenergic system. The 5-HT2 and 5-HT1C receptor agonist, α-methyl-5-HT, and the 5-HT1A,B,D receptor agonist, 5-CT, induced a concentration dependent potentiation of the twitch responses. The 5-HT3 receptor agonist, 2-methyl-5-HT, did not affect the twitch responses up to 10−5 M. These results indicate that presynaptic 5-HT1-like receptors facilitate cholinergic neurotransmission in mouse trachea." @default.
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• W2095281061 date "1991-12-01" @default.
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• W2095281061 title "5-HT1-like receptors mediate potentiation of cholinergic nerve-mediated contraction of isolated mouse trachea" @default.
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• W2095281061 doi "https://doi.org/10.1016/0014-2999(91)90175-p" @default.
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