BACKGROUND: Exogenous brain-derived neurotrophic factor (BDNF) promotes retinal ganglion cell survival. However, the protective mechanisms remain unclear. OBJECTIVE: To investigate changes in retinal tyrosine kinase receptor B (trkB) expression and effects of exogenous BDNF on trkB activation in a rat model of acute high intraocular pressure (HIOP). DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Department of Anatomy and Neurobiology, Xiangya Medical School, Central South University from January 2004 to August 2006. MATERIALS: Rabbit anti-BDNF and anti-trkB.FL(full-length) polyclonal antibodies were purchased from Santa Cruz Biotechnology, USA; rabbit anti-p-trkB polyclonal antibodies were purchased from Cellsignal, USA.METHODS: A total of 48 healthy, adult, Sprague Dawley rats were randomly assigned to acute HIOP (without BDNF pre-treatment) and BDNF pre-treated groups, with 24 animals in each group. In the BDNF pre-treated group, the left eyes were intravitreally injected with 3 μg/kg BDNF 2 days prior to HIOP. Rats in the acute HIOP group were not pre-treated with BDNF. HIOP models were established by increased intraocular pressure in the left eyes until the b-wave of flash electroretinogragh disappeared and pressure was maintained for 60 minutes. The right eyes of all rats were not treated and served as the normal controls. MAIN OUTCOME MEASURES: Retinal structure and cell numbers in the ganglion cell layer (GCL) were detected by Nissl staining; expression of trkB and phosphorylated trkB in the rat retina were determined by immunohistochemistry.RESULTS: A greater number of GCL neurons were observed in the pre-treated group compared to the acute HIOP group (P < 0.05). TrkB expression was significantly increased following HIOP at days 1 and 3 (P < 0.05), but expression varied between retinal areas. Although trkB expression decreased at 7 days, phosphorylated trkB dramatically decreased with increasing time (P < 0.05). TrkB expression in BDNF pre-treated rats was similar to the acute HIOP group at early injury time points. Nevertheless, trkB expression was significantly decreased compared to the acute HIOP group at 7 days (P < 0.05), and phosphorylated trkB expression was significantly greater compared to the acute HIOP group at each time point (P < 0.05). CONCLUSION: TrkB expression displayed temporal and spatial changes in the rat retina following acute HIOP, and trkB up-regulation suggested that more BDNF was required for treating the injured retina. Exogenous BDNF partially ameliorated decreased expression of phosphorylated trkB and provided protection to the injured retina, to a certain degree, following HIOP.