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Origin of 5‐hydroxytryptamine‐induced hyperpolarization of the rat superior cervical ganglion and vagus nerve
Author(s) -
Ireland S.J.
Publication year - 1987
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1987.tb11337.x
Subject(s) - hyperpolarization (physics) , depolarization , ouabain , superior cervical ganglion , membrane potential , chemistry , vagus nerve , biophysics , medicine , calcium , endocrinology , sodium , biology , stimulation , stereochemistry , organic chemistry , nuclear magnetic resonance spectroscopy
1 5‐Hydroxytryptamine (5‐HT)‐induced membrane potential changes were recorded extracellularly from rat superior cervical ganglia (SCG) and cervical vagus nerves in vitro.2 On the SCG, low concentrations of 5‐HT (1 × 10 −8 ‐3 × 10 −7 m ) induced concentration‐related hyperpolarization responses. Higher concentrations of 5‐HT (1 × 10 −6 ‐1 × 10 −4 m ) induced complex responses which typically consisted of an initial hyperpolarization, followed by a depolarization and subsequent after‐hyperpolarization. The depolarization, but not the initial hyperpolarization, was blocked by metoclopramide (3 × 10 −5 m ), quipazine (1 × 10 −6 m ) or MDL 72222 (1 × 10 −5 m ). 3 5‐HT‐induced hyperpolarization of the SCG was potentiated when the amount of calcium chloride added to the superfusion medium was reduced from 2.5 to 0.15 mmol l −1 . Hyperpolarization responses recorded from SCG preparations superfused with this low‐calcium medium were unaffected by the substitution of lithium chloride for sodium chloride and were potentiated by the omission of potassium ions. Ouabain (1 × 10 −3 m ) abolished both the hyperpolarization and the depolarization induced by 5‐HT. 4 On the vagus nerve, 5‐HT (1 × 10 −7 ‐3 × 10 −5 m ) did not induce initial hyperpolarization in either normal or low‐calcium Krebs‐Henseleit medium. However, in the latter solution only, depolarization responses induced by 5‐HT at concentrations of 1 × 10 −6 m or greater were followed by hyperpolarization. Both the depolarization and the post‐5‐HT hyperpolarization were blocked by metoclopramide (3 × 10 −5 m ) but were unaffected by spiperone (1 × 10 −7 m ). 5 On the vagus nerve, post‐5‐HT hyperpolarization responses were selectively and reversibly inhibited by ouabain, and by superfusion with Krebs‐Henseleit medium that was either potassium‐free or contained lithium chloride in place of sodium chloride. 7 These results demonstrate the generation in the rat SCG of a 5‐HT‐induced hyperpolarization response that is not mediated through 5‐HT 3 receptors and is unlikely to be a consequence of depolarization. In contrast, on the rat vagus nerve, the post‐5‐HT hyperpolarization observed in the present study had the characteristics expected of depolarization‐dependent activation of a sodium ion pump.