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