Objective    To explore the role of transcription factor activator protein 2α (AP-2α) on the expression of tyrosine hydroxylase (TH) in noradrenergic neurons of locus ceruleus (LC) after traumatic brain injury.     Methods    Ninety rats were randomly divided into control group and injury group that comprised 5 subgroups. There were 15 rats in each group. The rat model of traumatic brain injury was established with Feeney’s methods. Brain stems were dissected from decapitated heads 1

3

6

24 and 72 h after traumatic injury and freeze-mounted for cryo-sectioning. TH and AP-2α expressions in noradrenergic neurons of LC were analyzed with double immunofluorescence.     Results    The number and fluorescence intensity of TH and AP-2α-positive neurons in LC at various intervals after injury significantly increased as compared with control group (P0.05). The expression of TH reached the peak 3 h after injury and decreased gradually

but still higher than control group 72 h after injury. The pattern of AP-2α expression was consistent with that of TH in LC

and AP-2α and TH could coexist in the same neurons.     Conclusion    The increase of TH expression in LC can synthesize more norepinephrine rapidly after brain injury. Norepinephrine plays an important role during the process of injury stress. AP-2α participates in the regulation of TH expression in noradrenergic neurons and its upregulation may be an important reason for increased TH expression in LC.