Inhibition of endoplasmic reticulum stress reverses synaptic plasticity deficits in striatum of DYT1 dystonia mice.

ABSTRACT:

Background and objective

Striatal plasticity alterations caused by endoplasmic reticulum (ER) stress is supposed to be critically involved in the mechanism of DYT1 dystonia. In the current study, we expanded this research field by investigating the critical role of ER stress underlying synaptic plasticity impairment imposed by mutant heterozygous Tor1a^+/- in a DYT1 dystonia mouse model.

Methods

Heterozygous Tor1a^+/- mouse model for DYT1 dystonia was established. Wild-type (Tor1a^+/+, N=10) and mutant (Tor1a^+/-, N=10) mice from post-natal day P25 to P35 were randomly distributed to experimental and control groups. Patch-clamp and current-clamp recordings of SPNs were conducted with intracellular electrodes for electrophysiological an

SUBMITTER: Cai H 

PROVIDER: S-EPMC8436893 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature