Stimulation of V1 axons engages glutamatergic and GABAergic synaptic transmission onto SPNs.

<p><b>A</b>. Representative high magnification view of the dorsomedial striatum in a <i>Rbp4</i>-Cre; <i>Drd2-</i>EGFP mouse virally injected in V1 with an AAV encoding Cre-dependent ChR2-mCherry. Axonal projections from V1 (red) are clearly seen within the DMS. The section is stained with DAPI (blue) to label cell bodies. iSPNs are easily identified using EGFP fluorescence (green). A presumptive dSPN (DAPI⁺; EGFP⁻) is also shown. <b>B</b>. Cell-attached recording from a SPN showing that a 1 ms 473 nm light flash (blue bar) reliably evokes a single action potential. Three consecutive extracellular waveforms are overlaid. <b>C</b>. As in <b>B</b> for another SPN recorded in the whole-cell current-clamp configuration. <b>D</b>. Whole-cell voltage-clamp traces from a SPN upon optogenetic stimulation (1 ms, blue bar) of ChR2-expressing V1 axons. EPSCs (black) were recorded at <i>E</i>_Cl = −70 mV, while IPSCs (red) were recorded at 0 mV (the reversal potential for ionotropic glutamate receptor mediated currents). Dashed gray lines mark the onset of both currents and highlight the delayed onset of IPSCs relative to EPSCs. Both EPSC and IPSC were eliminated after bath application of the glutamate receptor antagonists NBQX and CPP (both at 10 µM; gray and pink lines, respectively), confirming the disynaptic origin of IPSCs. <b>E</b>. Mean (± s.e.m) peak EPSC amplitude in dSPNs (blue) and iSPNs (green). <b>F</b>. Mean (± s.e.m) latency from flash onset to current onset of EPSCs (black) and IPSCs (red). <b>G</b>. Mean (± s.e.m) EPSC (black) and IPSC (red) amplitudes. Asterisk represents statistical significance, <i>P</i><0.05 vs. baseline amplitude. Data in E–G represent mean ± s.e.m. Number of recordings are indicated in parentheses.