CX3CR1 mutation alters synaptic and astrocytic protein expression, topographic gradients, and response latencies in the auditory brainstem.

ABSTRACT: The precise and specialized circuitry in the auditory brainstem develops through adaptations of cellular and molecular signaling. We previously showed that elimination of microglia during development impairs synaptic pruning that leads to maturation of the calyx of Held, a large encapsulating synapse that terminates on neurons of the medial nucleus of the trapezoid body (MNTB). Microglia depletion also led to a decrease in glial fibrillary acidic protein (GFAP), a marker for mature astrocytes. Here, we investigated the role of signaling through the fractalkine receptor (CX3CR1), which is expressed by microglia and mediates communication with neurons. CX3CR1^-/- and wild-type mice were studied before and after hearing onset and at 9 weeks of age. Levels of GFAP were significantly

SUBMITTER: Milinkeviciute G 

PROVIDER: S-EPMC8174095 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature