Apamin Reduces the Late Afterhyperpolarization of Lamprey Spinal Neurons, with Little Effect on Fictive Swimming
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The role of the late afterhyperpolarization (late AHP) in the firing properties of lamprey spinal neurons was tested by bath application of apamin, a selective blocker of the sk calcium-dependent potassium current. Intracellular recordings of identified motoneurons and interneurons were made with micropipette electrodes in the isolated lamprey spinal cord. Apamin reversibly reduced the amplitude of the late afterhyperpolarization without affecting other aspects of the action potential or the resting potential. The firing frequencies of the neurons were enhanced by apamin over a range of depolarizing current pulse injections. The effect of apamin was also tested on fictive swimming, which was induced in the isolated spinal cord by bath application of an excitatory amino acid (d-glutamate or ). A concentration of apamin (10 μM) sufficient to substantially reduce the late AHP had no significant effect on the ventral root burst rate, intensity, or phase lag during fictive swimming.