Erythropoietin attenuates loss of potassium chloride co-transporters following prenatal brain injury.

ABSTRACT: Therapeutic agents that restore the inhibitory actions of γ-amino butyric acid (GABA) by modulating intracellular chloride concentrations will provide novel avenues to treat stroke, chronic pain, epilepsy, autism, and neurodegenerative and cognitive disorders. During development, upregulation of the potassium-chloride co-transporter KCC2, and the resultant switch from excitatory to inhibitory responses to GABA guide the formation of essential inhibitory circuits. Importantly, maturation of inhibitory mechanisms is also central to the development of excitatory circuits and proper balance between excitatory and inhibitory networks in the developing brain. Loss of KCC2 expression occurs in postmortem samples from human preterm infant brains with white matter lesions. Here we show that late ge

SUBMITTER: Jantzie LL 

PROVIDER: S-EPMC4134983 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature