Developmental alcohol exposure impairs synaptic plasticity without overtly altering microglial function in mouse visual cortex.

ABSTRACT: Fetal alcohol spectrum disorder (FASD), caused by gestational ethanol (EtOH) exposure, is one of the most common causes of non-heritable and life-long mental disability worldwide, with no standard treatment or therapy available. While EtOH exposure can alter the function of both neurons and glia, it is still unclear how EtOH influences brain development to cause deficits in sensory and cognitive processing later in life. Microglia play an important role in shaping synaptic function and plasticity during neural circuit development and have been shown to mount an acute immunological response to EtOH exposure in certain brain regions. Therefore, we hypothesized that microglial roles in the healthy brain could be permanently altered by early EtOH exposure leading to deficits in experience-depe

SUBMITTER: Wong EL 

PROVIDER: S-EPMC5696045 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature