M1 Muscarinic Receptors Boost Synaptic Potentials and Calcium Influx in Dendritic Spines by Inhibiting Postsynaptic SK Channels

摘要: Acetylcholine release and activation of muscarinic cholinergic receptors (mAChRs) enhance synaptic plasticity in vitro cognition memory in vivo. Within the hippocampus, mAChRs promote NMDA-type glutamate receptor-dependent forms long-term potentiation. Here, we use calcium (Ca) imaging combined with two-photon laser uncaging at apical spines CA1 pyramidal neurons to examine postsynaptic mechanisms modulation glutamatergic transmission. Uncaging-evoked excitatory potentials Ca transients are increased by stimulation; however, this is not due direct receptors. Instead, modulate a negative feedback loop in that normally suppresses signals. mAChR reduces sensitivity small conductance Ca-activated potassium (SK) channels found spine, resulting transients. These effects mediated M1-type occur casein kinase-2-dependent manner. Thus, regulates transmission tuning activity nonglutamatergic ion channels.