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  • Title: Electrically evoked noradrenaline release from cultured chick sympathetic neurons: modulation via presynaptic alpha-adrenoceptors and lack of autoinhibition.
    Author: Böhm S, Huck S, Drobny H, Singer EA.
    Journal: Naunyn Schmiedebergs Arch Pharmacol; 1991 Jul; 344(1):130-2. PubMed ID: 1685556.
    Abstract:
    Sympathetic neurons from twelve day old chick embryos were plated on polystyrol discs and kept in culture for five days. After incubation with 3H-noradrenaline the discs were transferred to small chambers and superfused. Electrical field stimulation (36 pulses at 3 Hz) increased the outflow of tritium. The evoked overflow of tritium was abolished in the absence of extracellular calcium and was diminished by about 90% in the presence of tetrodotoxin (1 mumol/l). The alpha 2-adrenoceptor agonist 5-bromo-6-(2-imidazolin-2-ylamino)quinoxaline (UK-14,304) caused a concentration-dependent decrease in overflow, whereas the alpha 1-adrenoceptor agonist methoxamine was ineffective at up to 1 mumol/l. The concentration-response curve of UK-14,304 was shifted to the right by the alpha 2-adrenoceptor antagonist yohimbine (0.03 mumol/l). Yohimbine on its own caused no significant change. The noradrenaline reuptake inhibitor cocaine (10 mumol/l) caused a small (20%) increase in evoked overflow. The results indicate that cultured chick sympathetic neurons possess release-modulating alpha 2-adrenoceptors and that the electrically induced overflow of transmitter occurs under conditions virtually free of autoinhibition.
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