Connexins, gap junction proteins, have short half-lives of only a few hours; therefore, degradation of these proteins can rapidly modulate their function. Autophagy is a type of degradation pathway that has been implicated in several diseases and was reported to be induced following traumatic brain injury (TBI). The aim of the present study was to investigate the involvement of neuronic autophagy in proteolysis of phosphorylated connexin 43 (p-Cx43) in hippocampal astrocytes following TBI in rats. Western blot analysis and immunofluorescence showed a TBI-induced increase in levels of astrocytic p-Cx43 following treatment with 3-methyladenine, an inhibitor of autophagy, in the hippocampus. Internalized gap junctions were observed in the neuronic cytoplasm using transmission electron microscopy. These results demonstrated that neuronic autophagy may regulate cellular levels of p-Cx43 in hippocampal astrocytes following TBI. This therefore indicated that the persistence of p-Cx43 accumulation was due to insufficient degradation capacity of constitutive autophagy.