Targeting Neuronal GPR65 With Delayed BTB09089 Treatment Improves Neurorehabilitation Following Ischemic Stroke.

ABSTRACT:

Background

GPR65 (G protein-coupled receptor 65) can sense extracellular acidic environment to regulate pathophysiological processes. Pretreatment with the GPR65 agonist BTB09089 has been proven to produce neuroprotection in acute ischemic stroke. However, whether delayed BTB09089 treatment and neuronal GPR65 activation promote neurorestoration remains unknown.

Methods

Ischemic stroke was induced in wild-type (WT) or GPR65 knockout (GPR65^-/-) mice by photothrombotic ischemia. Male mice were injected intraperitoneally with BTB09089 every other day at days 3, 7, or 14 poststroke. AAV-Syn-GPR65 (adenoassociated virus-synapsin-GPR65) was utilized to overexpress GPR65 in the peri-infarct cortical neurons of GPR65^-/- and WT mice. Motor function was monitored

SUBMITTER: Chen R 

PROVIDER: S-EPMC11259240 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature