Single pulse step depolarization (to 0mV, 10 ms) was used to evoke presynaptic Ca2+ currents and EPSCs. Experiments were made at room temperature (25°C–27°C) or at physiological temperature (35°C–37°C). Presynaptic pipette solutions containing MNI-caged-glutamate (10 mM, (S)-a-amino2,3-dihydro-4-methoxy-7-nitro-d-oxo-1H-indole-1-pentanoic acid, Tocris Cookson) were loaded into calyces through

whole-cell pipettes. MNI-glutamate was dissolved in the presynaptic pipette solution on the day of the experiment. A UV light flash was applied from a mercury lamp light source (100 μW) by opening a shutter (Uniblitz, Vincent Associate) for 1 s under the control of a shutter driver (JML Optical Industries). Data were analyzed using IGOR Pro 6.2J (WaveMatrics) and MS Excel 2003 (Microsoft) softwares. All values are given as mean ± SEM, and p < 0.05 was taken as a IOX1 mw significant difference in Student’s paired or unpaired t test. In figures, error bars indicate ± SEM. We thank Naoto Saitoh for technical advice, Takeshi Sakaba and Shigeo Takamori for their comments, Kevin Hunt for his

English editing, and Masahiro Kaneko for his collaboration in the early stages of this study. This study was supported by the Core Research for Evolutional Science and Technology of Japan Science and Technology Agency (to T.T.) and Grant-in-Aid for Young Trichostatin A order Scientists from the Japanese Ministry of Education, Culture, Sports, Science, and Technology (to T.H.). “
“Direction-selective retinal ganglion cells (DSGCs) respond strongly to an image moving in the preferred direction (PD) and weakly to an image moving in the opposite, or null, direction (ND). The primary circuit model for generating this direction selectivity in the retina claims that directional responses arise by asymmetric inhibition, i.e., that stimulation in the ND leads to stronger inhibition than

stimulation in the PD. This inhibition is thought to arise through starburst amacrine cells (SACs) already that release GABA onto and costratify with DSGC processes (Borst and Euler, 2011; Vaney et al., 2012; Wei and Feller, 2011). Consistent with this hypothesis, paired recordings from SACs and DSGCs reveal that depolarization of a SAC on the null side induces significantly larger GABAergic inhibitory currents in the DSGC than depolarization of a SAC on the preferred side (Fried et al., 2002; Vaney et al., 2012; Wei et al., 2011). Serial electron microscopy (EM) reconstructions of the SAC-DSGC circuit conclude that this asymmetry is due to a specific wiring of SAC processes that tend to form synapses onto a DSGC whose PD is oriented antiparallel to the SAC process (Briggman et al., 2011). Hence, the predominant model for retinal direction selectivity claims that the circuit is hard wired and that the wiring predicts the function.