Noradrenaline-induced cation currents in isolated rat paratracheal ganglion neurons
Autor: | Yushi Ito, Norio Akaike, Chisato Umebayashi, Mari Umezu, Hitoshi Ishibashi |
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Rok vydání: | 2004 |
Předmět: |
Agonist
Adrenergic Antagonists medicine.medical_specialty Thapsigargin medicine.drug_class In Vitro Techniques Norepinephrine chemistry.chemical_compound Cations Internal medicine medicine Paratracheal Prazosin Animals Patch clamp Rats Wistar Molecular Biology Phenylephrine Neurons Dose-Response Relationship Drug Chemistry General Neuroscience Ganglia Parasympathetic Depolarization Adrenergic Agonists Rats Trachea Electrophysiology Endocrinology Biophysics Neurology (clinical) Developmental Biology medicine.drug |
Zdroj: | Brain Research. 1023:74-82 |
ISSN: | 0006-8993 |
Popis: | The actions of noradrenaline (NA) on the neurons acutely isolated from paratracheal ganglia of rats and the ionic mechanisms involved were studied with nystatin-perforated patch recording configuration. Under current-clamp conditions, application of 10 microM NA produced membrane depolarization followed by repetitive action potentials. NA evoked an inward cationic current under voltage-clamp conditions at a holding potential of -60 mV. Transient tail inward ('hump') current was also induced by washout of NA. The NA-induced current was reduced by extracellular Ca(2+) and Mg(2+), with half-maximal concentrations of 0.7 and 2.6 mM for Ca(2+) and Mg(2+), respectively. Phenylephrine, an alpha(1)-adrenoceptor agonist, mimicked the NA-induced current, but the 'hump' current did not occur upon washout of phenylephrine. The NA-induced current was inhibited by prazosin and WB-4101, alpha(1)-adrenoceptor antagonists. In contrast, in the presence of yohimbine, an alpha(2)-adrenoceptor antagonist, the NA-induced current was potentiated and the washout of NA failed to evoke the 'hump' current. The pretreatment of paratracheal neurons with pertussis toxin also potentiated the NA-induced current. The NA-induced inward current was inhibited by pretreatment with U73122, a phospholipase C inhibitor, and xestospongin-C, a membrane-permeable IP(3) receptor antagonist. On the other hand, thapsigargin, BAPTA-AM and calmidazolium had no effect on the NA-induced current, suggesting that release of Ca(2+) from intracellular Ca(2+) stores via IP(3) receptors is not involved in the NA action. The cationic channels activated by NA play an important physiological role in neuronal membrane depolarization in rat paratracheal ganglia. |
Databáze: | OpenAIRE |
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