Resident Calmodulin Primes NMDA Receptors for Ca²⁺-Dependent Inactivation.

ABSTRACT: N-methyl-d-aspartate (NMDA) receptors are glutamate- and glycine-gated channels that flux Na⁺ and Ca²⁺ into postsynaptic neurons during synaptic transmission. The resulting intracellular Ca²⁺ transient is essential to physiological and pathological processes related to synaptic development, plasticity, and apoptosis. It also engages calmodulin (CaM) to reduce subsequent NMDA receptor activity in a process known as Ca²⁺-dependent inactivation (CDI). Here, we used whole-cell electrophysiology to measure CDI and computational modeling to dissect the sequence of events that underlies it. With these approaches, we estimate that CaM senses NMDA receptor Ca²⁺ influx at ∼9 nm from the channel pore. Further, when we controlled the frequency of

SUBMITTER: Iacobucci GJ 

PROVIDER: S-EPMC5700250 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature