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Serotonin Induces a Cyclic AMP‐Mediated Outwardly Rectifying Slow K + Current in a Single Identified Snail Neuron
Author(s) -
PaupardinTritsch Danièle,
Gerschenfeld H. M.
Publication year - 1990
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1990.tb00392.x
Subject(s) - tetraethylammonium , extracellular , biophysics , neuron , reversal potential , forskolin , intracellular , chemistry , iontophoresis , medicine , endocrinology , stimulation , patch clamp , biochemistry , neuroscience , biology , receptor , potassium , organic chemistry
In the F2 neuron of the parietal ganglion of the snail Helix aspersa either bath or iontophoretic application of serotonin (5‐HT) induces an outward current. This current has a long latency (10–60 s) and a slow time course, a 500 ms iontophoretic application of 5‐HT evoking a response lasting 3–5 min. This slow outward current reverses at ‐80 mV, a value equal to E K . After doubling the extracellular K + concentration the reversal potential of the 5‐HT response is shifted by 19 mV, as predicted by the Nernst equation. The I‐V curves reveal that the 5‐HT‐induced slow outward current is outwardly rectifying. This 5‐HT response is blocked by intracellular Cs + and tetraethylammonium (TEA + ) and by extracellular TEA + and Ba 2+ , but is not affected by the removal of extracellular Ca 2+ or the intracellular injection of ethyleneglycol‐bis‐(β‐amino‐ethylether)‐N,N,N′,N′‐tetra‐acetic acid (EGTA). These results indicate that the outwardly rectifying slow outward current induced by 5‐HT in the F2 neuron is carried by K + and is Ca 2+ ‐independent. In the single isolated F2 neuron, 5‐HT induces a 2.5‐fold stimulation of the adenylate cyclase activity. In addition, both the intracellular injection of 3′,5′‐adenosine monophosphate (cAMP) and the application of forskolin mimic the effect of 5‐HT on the F2 neuron. The phosphodiesterase inhibitor isobutylmethylxanthine also induces a slow outward current and potentiates the 5‐HT response. The intracellular injection of a synthetic 20‐residue peptide inhibitor of the cAMP‐dependent protein kinase blocks the slow outward K + current induced by 5‐HT. These results show that in the F2 neuron, 5‐HT elicits a slow K + current via the stimulation of adenylate cyclase, an increase in intracellular cAMP and the activation of the cAMP‐dependent kinase which probably phosphorylates a population of outwardly rectifying K + channels or some protein/s associated with these channels.