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A. Akopian, M. Cristofanilli; Reciprocal Relationship Between Ca2+ Influx and Actin Cytoskeleton Organization in the Salamander Retina . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1513.
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© ARVO (1962-2015); The Authors (2016-present)
In a variety type of cells Ca2+ is involved in actin reorganization, resulting either in actin polymerization or depolymerization. Very little is known about the relationship between Ca2+ and the actin cytoskeleton organization in retinal neurons. Here we studied the effect of high K+–induced depolarization on F–actin organization in third–order neurons of the salamander retina.
Isolated neurons were stained under various experimental conditions with Alexa–Fluor488–phalloidin, a compound that permits visualization and quantification of polymerized actin. Fluorescence images were obtained with a Nikon Eclipse C–1 confocal microscope. Whole–cell light–evoked EPSCs were recorded from On–Off ganglion cells in slice preparation with the patch pipette containing latrunculin B, an actin depolymeryzing agent.
Depolarization–induced Ca2+ influx through voltage–gated L–type channels causes actin depolymerization, as assessed by ∼53 % reduction in the intensity of Alexa–Fluor488–phalloidin staining. Calcium–induced F–actin disruption was attenuated in the presence of PKC antagonists, chelerythrine, or GF 109203X. In addition, phorbol 12–myristate 13–acetate (PMA), but not 4αPMA, mimicked the effect of Ca2+ influx on F–actin. Activation of ionotropic glutamate receptors by AMPA and NMDA also caused a reduction in F–actin. No effect was observed by caffeine or thapsigargin, agents that stimulate Ca2+ release from internal stores. In a slice preparation whole–cell recordings of light–evoked EPSCs from ON–OFF ganglion cells revealed a significant reduction in OFF– but not ON–EPSCs by latrunculin B. A qualitatively similar reduction in OFF–EPSPs was observed when recordings were made in current clamp mode.
We showed earlier that F–actin disruption results in a reduction in Ca2+ influx through both voltage– and glutamate–activated channels. Together these data suggest that elevation of intracellular Ca2+ during excitatory synaptic activity provides the molecular basis for activity–dependent actin remodeling, which in turn may serve as a feedback mechanism to attenuate excitotoxic Ca2+ accumulation induced by synaptic depolarization.
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