Glutamate receptors also control DA release presynaptically (Desce et al., 1992; Krebs et al., 1991; Chéramy et al., 1986a, 1998, 1996) and CINs have recently been shown to release glutamate (Higley et al., 2011; Guzman et al., 2011). Moreover, several effects evoked by CIN activity are thought to be mediated by glutamate and not by ACh (Guzman et al., 2011). Because of our findings that endogenous cholinergic activity drives DA release in a nAChR-dependent fashion, we next examined if this occurred, at least in part, through activation of AMPA receptors. First, we confirmed that stimulation of CINs led to glutamate release. Under whole-cell voltage-clamp, single pulse optical stimulation of CINs evoked a single EPSC in medium spiny neurons (MSNs) (Fig. 3C). Furthermore, optical train stimulation failed to produce subsequent EPSCs following the initial pulse in the trains (5 pulses at 2 or 30 Hz; see supplemental material). Bath application of the AMPA receptor antagonist NBQX (5 μM) attenuated the EPSC amplitude to 18.6% ± 3.4% of the pretreatment value; p = 0.0002, n = 4. This confirms that selective optical
