Connexin43 in neonatal excitatory neurons is important for short-term motor learning.

ABSTRACT

In the neocortex, gap junctions are expressed at very early developmental stages, and they are involved in many processes such as neurogenesis, neuronal migration and synapse formation. Connexin43 (Cx43), a gap junction protein, has been found to be abundantly expressed in radial glial cells, excitatory neurons and astrocytes. Although accumulating evidence suggests that Cx43-mediated gap-junctional coupling between astrocytes plays an important role in the central nervous system, the function of Cx43 in early excitatory neurons remains elusive. To investigate the impact of Cx43 deficiency in excitatory neurons at early postnatal stages, we conditionally knocked out Cx43 in excitatory neurons under the Emx1 promoter by tamoxifen induction. We found that deletion of Cx43 around birth did not impair the laminar distribution of excitatory neurons in the neocortex. Moreover, mice with Cx43 deletion during the early postnatal stages had normal anxiety-like behaviors, depression-related behaviors, learning and memory-associated behaviors at adolescent stages. However, Cx43 conditional knockout mice exhibited impaired motor-learning behavior. These results suggested that Cx43 expression in excitatory neurons at early postnatal stages contributes to short-term motor learning capacity.