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. Author manuscript; available in PMC: 2013 Sep 1.
Published in final edited form as: Cerebellum. 2012 Sep;11(3):666–680. doi: 10.1007/s12311-010-0210-9

Fig. 7.

Fig. 7

Hypothetical model of enhanced GABA release at synapses between cerebellar cortical interneurons and PCs in leaner mice. a In WT mice, Ca2+ influx through P/Q type Ca2+ channels in presynaptic terminals of inhibitory interneurons triggers a fast rise in intracellular Ca2+ concentration ([Ca2+]i) that causes synchronous GABA release, opening of postsynaptic chloride channels, and Cl efflux, which is detected as an inward postsynaptic current (symmetrical Cl, Vh=−75 mV). b If cytosolic Ca2+ buffering is weaker in leaner compared to WT GABAergic terminals, as has been reported for somatic Ca2+ buffering in leaner PCs [62, 63], evoked [Ca2+]i elevations may be large enough, in spite of reduced Ca2+ entry, to trigger regenerative CICR, leading to enhanced, asynchronous GABA release