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

1999; National Academy of Sciences; Volume: 96; Issue: 14 Linguagem: Inglês

10.1073/pnas.96.14.7650

1091-6490

Ruth Cordoba-Rodriguez, Kimberly A. Moore, Joseph P. Y. Kao, Daniel Weinreich,

Receptor Mechanisms and Signaling

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 <0.1 to >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.