SK Channel Modulates Synaptic Plasticity by Tuning CaMKIIα/β Dynamics.

ABSTRACT: N-Methyl-D-Aspartate Receptor 1 (NMDAR)-linked Ca⁺⁺ current represents a significant percentage of post-synaptic transient that modulates synaptic strength and is pertinent to dendritic spine plasticity. In the hippocampus, Ca⁺⁺ transient produced by glutamatergic ionotropic neurotransmission facilitates Ca⁺⁺-Calmodulin-dependent kinase 2 (CaMKII) Thr286 phosphorylation and promote long-term potentiation (LTP) expression. At CA1 post-synaptic densities, Ca⁺⁺ transients equally activate small conductance (SK2) channel which regulates excitability by suppressing Ca⁺⁺ movement. Here, we demonstrate that upstream attenuation of GluN1 function in the hippocampus led to a decrease in Thr286 CaMKIIα phosphorylation, and increased SK2 expressi

SUBMITTER: Shrestha A 

PROVIDER: S-EPMC6834780 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature