Wang et al. revealed an indirect mechanism where M1 receptor signaling reversibly enhances glutamatergic synaptic transmission[46]. The modulation is dependent on Cav1.3 channels and CB1 receptors. M1 receptor promotes excitatory glutamatergic transmission by reducing opening of postsynaptic Cav1.3 channels, which in turn diminishes endocannabinoid production and presynaptic CB1 receptor activation.
