Effects of caffeine on the excitability and intracellular Ca(2+) transients of neonatal rat hypoglossal motoneurons in vitro.

Abstract

Since constitutively-high intracellular Ca(2+) ([Ca(2+)](i)) may confer hypoglossal motoneurons special vulnerability to excitoxic damage, we investigated the spatiotemporal dynamics of [Ca(2+)](i) and its relation to spike firing of rat hypoglossal motoneurons recorded under whole-cell patch clamp coupled with high resolution [Ca(2+)](i) imaging. A rise in [Ca(2+)](i), appearing in conjunction with single action potentials and becoming larger during spike trains, was first detected immediately beneath the cell membrane area, peaked 10-20 ms after each spike, and propagated to the cell core with slow decay time. Depletion of ryanodine-sensitive [Ca(2+)](i) stores by caffeine increased background [Ca(2+)](i), augmented the spike medium afterhyperpolarization, slowed down the action potential firing rate and depolarized cells (after an early hyperpolarization). The decay time constant of [Ca(2+)](i) transients was more than doubled by caffeine, although peak [Ca(2+)](i) remained unchanged. It is suggested that the main role of caffeine-sensitive stores was to buffer [Ca(2+)](i) elevated by sustained firing and to control spike accommodation.

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