M1 receptor activation also regulates MSNs by modulating Cav channels. M1 receptor activation negatively regulates Cav1.3 by increased Ca2+ mobilization via phospholipase C (PLC) and phosphatase 2B (PP-2B) pathway [28,29,30]. While reducing currents through Cav2 channels inhibiting the AHP in MSNs in a pertussis-toxin-sensitive, Gβγ-mediated membrane delimited pathway [31,32]. Consistent with its effect on potassium channels, the inhibition of the AHP can increase firing frequency. Therefore, by coordinated modulation of these potassium and calcium channels, ACh can shape the synaptic integration and spiking activity in MSNs.
