Recent study also suggested that cholinergic activation exerts strong di-synaptic GABAA-mediated inhibition onto striatal MSNs, whereas cholinergic neuron inactivation increases firing of these MSNs in vivo [44]. While, the underlying circuit mechanism remains unknown, it is likely that fast-spiking interneurons are recruited by cholinergic activation. Fast-spiking parvalbumin expressing inhibitory interneurons are strongly excited by acetycholine through nAChRs, which are widely expressed on presynaptic terminals of these neurons [45]. Activation or inactivation of cholinergic interneurons can directly excite or suppress fast-spiking interneurons firing. These GABAergic interneurons in turn provide strong corticostriatal feed-forward inhibition [50,51].
