The results from our electrophysiological and morphological analyses learn more strongly suggest that proper strength of GABAA receptor-mediated inhibition onto the PC soma from molecular layer interneurons is crucial for CF synapse elimination from postnatal day 10 (P10) to around P16. Our results also suggest that the somatic inhibition influences the size of CF-induced Ca2+ transients and regulate Ca2+-dependent processes for the elimination of redundant CF inputs on the soma. To examine whether GABAergic transmission is reduced in the cerebellum of GAD67+/GFP mice, we recorded miniature inhibitory postsynaptic currents (mIPSCs) from PCs. In control mice, the amplitude

of mIPSCs changed during the first three postnatal weeks (Figures 1A and 1B), reaching maximum at P7–P9 and decreasing gradually thereafter. In GAD67+/GFP mice, there was only a modest change in the amplitude of

mIPSCs during postnatal development (Figures 1A and 1B). Consequently, the amplitude of mIPSCs in GAD67+/GFP PCs was significantly smaller than that of control mice at P7–P9 (control: 183 ± 20.2 pA, n = 11; GAD67+/GFP: 91 ± 10.2 pA, n = 11; p < 0.001), P10–P12 (control: 130 ± 15.7 pA, n = 13; GAD67+/GFP: 86 ± 4.5 pA, n = 11; p = 0.022), and P13–P15 (control: 111 ± 17.6 pA, n = 7; GAD67+/GFP: 60 ± 5.1 pA, n = 7; p = 0.017) (Figure 1B). In contrast, the frequency of mIPSCs was not different between the two mouse strains except at P10–P12 when the frequency was significantly higher in GAD67+/GFP PCs (control: 5.2 ± 0.5 Hz, n = 13; GAD67+/GFP: selleck compound 8.9 ± 0.9 Hz, n = 11; p = 0.002) (Figure 1C). Since GABAergic signaling has been reported to regulate interneuron’s axonal branching and synapse formation in the visual cortex (Chattopadhyaya et al., 2007), we examined whether GABAergic synapse formation is affected in GAD67+/GFP mice. We measured the density of GABAergic terminals on the soma

and dendrite of PCs by double immunofluorescence GBA3 confocal microscopic analysis for vesicular inhibitory amino acid transporter (VIAAT) and the PC marker calbindin (see Figure S1 available online). We found no significant differences between control and GAD67+/GFP mice at P10–P12 (Figure S1). Therefore, the higher mIPSC frequency in GAD67+/GFP mice at P10–P12 is considered to result from functional change rather than increased density of GABAergic terminals. It has been reported that GABA elicits depolarization and induces Ca2+ transients in immature rat PCs (Eilers et al., 2001). To examine whether GABA excites or inhibits PCs during postnatal development in mice, we monitored PC’s spontaneous activity with the cell-attached configuration and assessed the effect of ionophoretically applied muscimol, a GABAA receptor agonist (Figures 1D–1G).