We show that selective optogenetic stimulation of CINs evokes DA release in a β2-containing nAChR-dependent manner. While electrophysiological studies have hypothesized that dopamine can be released in a manner that is not contingent upon ongoing activity in dopaminergic fibers (Ding et al., 2010), our data reveal previously unseen dynamics of this release process directly. Furthermore, we identify the convergence of different neurotransmitter systems participating in this phenomenon. Increased DA concentration during blockade of mAChRs suggests a critical role of these receptors in controlling ACh release. Consistent with recent reports demonstrating glutamate release from CIN terminals, interfering with AMPA receptor signaling weakens optically evoked DA release. More importantly, we determine that DA release can also be evoked by blue light activation of CINs in vivo.
