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Galanin‐induced hyperpolarization and decreased membrane excitability of neurones in mudpuppy cardiac ganglia.
Author(s) -
Konopka L M,
McKeon T W,
Parsons R L
Publication year - 1989
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1989.sp017523
Subject(s) - galanin , hyperpolarization (physics) , depolarization , medicine , membrane potential , endocrinology , chemistry , inhibitory postsynaptic potential , neuropeptide , biophysics , biology , biochemistry , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
1. Membrane hyperpolarization and decreased excitability produced by galanin were investigated in vitro on parasympathetic postganglionic neurones in the cardiac ganglion of the mudpuppy, Necturus maculosus. 2. Galanin produced a slowly developing hyperpolarization which, in 2.5 mM‐KCl, reversed at ‐105.4 +/‐ 2.7 mV. The reversal potential was shifted by 38.7 +/‐ 4.9 mV following a fourfold elevation of the extracellular potassium concentration. 3. Galanin inhibited action potential firing in spontaneously active neurones and decreased the number of spikes in a train produced by long (500‐680 ms) depolarizing current pulses. Both effects were independent of the galanin‐induced hyperpolarization. 4. Galanin increased the threshold for spike generation, prolonged the spike hyperpolarizing after‐potential and decreased the maximum rate of rise, amplitude and maximum rate of fall of the sodium spike. These effects occurred independently of the galanin‐induced hyperpolarization. 5. Galanin decreased the amplitude and duration of TTX‐insensitive spikes initiated in cells maintained in a solution containing 9 mM‐calcium, 20 mM‐TEA and 1.5 microM‐TTX. 6. These results suggest that a galanin‐like peptide may act as an inhibitory transmitter in the mudpuppy cardiac ganglion.