Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons

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Abstract
Activation of distinct classes of potassium channels can dramatically affect the frequency and the pattern of neuronal firing. In a subpopulation of vagal afferent neurons (nodose ganglion neurons), the pattern of impulse activity is effectively modulated by a Ca 2+ -dependent K + current. This current produces a post-spike hyperpolarization (AHP slow ) that plays a critical role in the regulation of membrane excitability and is responsible for spike-frequency accommodation in these neurons. Inhibition of the AHP slow by a number of endogenous autacoids (e.g., histamine, serotonin, prostanoids, and bradykinin) results in an increase in the firing frequency of vagal afferent neurons from 10 Hz. After a single action potential, the AHP slow in nodose neurons displays a slow rise time to peak (0.3–0.5 s) and a long duration (3–15 s). The slow kinetics of the AHP slow are due, in part, to Ca 2+ discharge from an intracellular Ca 2+ -induced Ca 2+ release (CICR) pool. Action potential-evoked Ca 2+ influx via either L or N type Ca 2+ channels triggers CICR. Surprisingly, although L type channels generate 60% of action potential-induced CICR, only Ca 2+ influx through N type Ca 2+ channels can trigger the CICR-dependent AHP slow . These observations suggest that a close physical proximity exists between endoplasmic reticulum ryanodine receptors and plasma membrane N type Ca 2+ channels and AHP slow potassium channels. Such an anatomical relation might be particularly beneficial for modulation of spike-frequency adaptation in vagal afferent neurons.

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