The influx of Ca2+ and the release of noradrenaline evoked by the stimulation of presynaptic nicotinic receptors of chick sympathetic neurons in culture are not mediated via L-, N-, or P-type calcium channels
| Autor: | Georg Hertting, Angelika Schobert, Ken Lee, Vladimir Dolezˇal |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
medicine.medical_specialty
Sympathetic Nervous System Nifedipine Dimethylphenylpiperazinium Chick Embryo Receptors Nicotinic Norepinephrine Ganglion type nicotinic receptor Internal medicine medicine Animals Channel blocker Nicotinic Antagonist Molecular Biology Cells Cultured Voltage-dependent calcium channel Chemistry General Neuroscience Calcium channel 3-Pyridinecarboxylic acid 1 4-dihydro-2 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl ester Electric Stimulation Endocrinology Nicotinic agonist Calcium Calcium Channels Neurology (clinical) Alpha-4 beta-2 nicotinic receptor Developmental Biology medicine.drug |
| Zdroj: | Brain Research. 740:75-80 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/s0006-8993(96)00876-1 |
| Popis: | We have shown earlier that nicotinic agonists induce the release of noradrenaline from chick sympathetic neurons in culture in two ways: (a) by activating the postsynaptic nicotinic receptors on nerve cell bodies, giving rise to spreading electrical activity and opening of voltage operated calcium channels in neuronal processes; (b) by activating the presynaptic nicotinic receptors on neuronal processes. In the present work, we investigated the contribution of various pathways to the observed Ca 2+ influx and subsequent noradrenaline release. Sympathetic neurons in culture were stimulated either by the nicotinic agonist dimethylphenylpiperazinium or electrically, in the presence or absence of tetrodotoxin and of specific blockers of calcium or nicotinic channels, and the effects on [Ca 2+ ] i in the area of neuronal processes and on noradrenaline release were measured. Under control conditions, the N-type channel blocker ω-conotoxin (0.1 μmol/1) diminished the release of noradrenaline and the increase of intraterminal Ca 2+ by 48% and 55%, respectively, whereas the L-type channel blocker (+)Bay k 8644 (1 μmol/1) diminished the release of noradrenaline by 25% and the increase of [Ca 2+ ] i by 39%. The P-type channel blocker ω-agatoxin (0.3 μmol/1) had no effect. The effects of the L-type channel ligands were complex and could only be explained on the assumption that, at high concentrations, these drugs also act as nicotinic antagonists. Tetrodotoxin blocked the Ca 2+ response evoked by electrical stimulation whereas DMPP applied in the presence of tetrodotoxin still evoked an increase of [Ca 2+ ] i and the release of noradrenaline (27% and 30% of control without tetrodotoxin, respectively). These residual responses were not blocked by any of the calcium channel blockers used or by their combination. Apparently, a substantial part of the influx of Ca 2+ induced by the activation of presynaptic nicotinic receptors is not carried by the N-, L- or P-type channels and probably occurs directly via the open channels of nicotinic receptors. |
| Databáze: | OpenAIRE |
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