Inward rectification in response to FMRFamide in Aplysia neuron L2: summation with transient K current.
The response of Aplysia abdominal ganglion neuron L2 to the molluscan neuroactive peptide Phe-Met-Arg-Phe-NH2 (FMRFamide) was studied in voltage-clamp experiments. In all of the experiments, focal application of the peptide to the soma activated an inward rectifier current and reduced the apparent amplitude of the transient K current, IA. In a few cells, Na and K currents were activated in addition to these effects. Voltage-jump experiments were performed to study the ionic dependence, kinetics, and voltage dependence of the inward rectifier. Inward rectification increased exponentially during hyperpolarizing pulses and recovered exponentially on return to the resting potential. The reversal potential was variable, but was near -40 mV at the beginning of experiments. Inward rectification was insensitive to changes in external Na, Ca, or K concentration, but lowering the external Cl concentration had complicated effects on current amplitude. When KCl microelectrodes were used, perfusion with low-Cl external saline increased the amplitude of the peptide-dependent inward rectifier and shifted its reversal potential to a more positive voltage. With KAc microelectrodes, perfusion with low-Cl saline reduced the amplitude of the current. Inward rectification increased when a KAc microelectrode was withdrawn and replaced with a low-resistance KCl electrode, even when there was no measurable change in reversal potential. These results suggest that the FMRFamide-dependent inward rectifier is a Cl current that, like the current described by Chesnoy-Marchais (1982, 1983), is modulated by intracellular Cl. FMRFamide reduced the apparent amplitude of IA without affecting the voltage dependence of IA activation or inactivation.(ABSTRACT TRUNCATED AT 250 WORDS)
Thompson
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S
Hopkins Marine Station of Stanford University, Pacific Grove, California 93950.
Ruben
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P
D000818:Animals; D001048:Aplysia / Q000502:physiology*; D002712:Chlorides / Q000502:physiology; D004594:Electrophysiology; D019835:FMRFamide; D007700:Kinetics; D009474:Neurons / Q000502:physiology*; D009479:Neuropeptides / Q000494:pharmacology*; D011188:Potassium / Q000502:physiology*
D002712:Chlorides; D009479:Neuropeptides; D019835:FMRFamide; D011188:Potassium