Calcium currents in striatal fast-spiking interneurons: dopaminergic modulation of Ca(V)1 channels

BACKGROUND: Striatal fast-spiking interneurons (FSI) are a subset of GABAergic cells that express calcium-binding protein parvalbumin (PV). They provide feed-forward inhibition to striatal projection neurons (SPNs), receive cortical, thalamic and dopaminergic inputs and are coupled together by electrical and chemical synapses, being important components of the striatal circuitry. It is known that dopamine (DA) depolarizes FSI via D(1)-class DA receptors, but no studies about the ionic mechanism of this action have been reported. Here we ask about the ion channels that are the effectors of DA actions. This work studies their Ca(2+) currents. RESULTS: Whole-cell recordings in acutely dissociated and identified FSI from PV-Cre transgenic mice were used to show that FSI express an array of voltage gated Ca(2+) channel classes: Ca(V)1, Ca(V)2.1, Ca(V)2.2, Ca(V)2.3 and Ca(V)3. However, Ca(V)1 Ca(2+) channel carries most of the whole-cell Ca(2+) current in FSI. Activation of D(1)-like class of DA receptors by the D(1)-receptor selective agonist SKF-81297 (SKF) enhances whole-cell Ca(2+) currents through Ca(V)1 channels modulation. A previous block of Ca(V)1 channels with nicardipine occludes the action of the DA-agonist, suggesting that no other Ca(2+) channel is modulated by D(1)-receptor activation. Bath application of SKF in brain slices increases the firing rate and activity of FSI as measured with both whole-cell and Ca(2+) imaging recordings. These actions are reduced by nicardipine. CONCLUSIONS: The present work discloses one final effector of DA modulation in FSI. We conclude that the facilitatory action of DA in FSI is in part due to Ca(V)1 Ca(2+) channels positive modulation.