OBJECTIVE: To investigate the effect of risperidone on the expression of brain-derived neurotrophic factor (BDNF) and its receptors, tyrosine kinase receptor (TrkB) and P75 neurotrophin receptor (P75NTR) in rat brain. METHODS: Sixteen SD rats were divided into two groups (n = 8 for each group). The rats in experimental group were treated with risperidone [0.25 mg/(kg · d)] for 14 d, while the control group was given placebo. Total RNA sample in prefrontal cortex, temporal cortex and hippocampus was extracted, and the expression of BDNF, TrkB and P75NTR mRNA were determined by quantitative real-time PCR. RESULTS: The treatment of risperidone significantly up-regulated the expressions of BDNF and TrkB in prefrontal cortex, temporal cortex and hippocampus, while the expression of P75NTR was not significantly changed. CONCLUSION: Risperidone upregulated BDNF-TrkB signaling, but not BDNF-P75NTR signaling, which may be helpful for the further pharmacological study of risperidone.
OBJECTIVE: To investigate the effect of risperidone on the expression of brain-derived neurotrophic factor (BDNF) and its receptors, tyrosine kinase receptor (TrkB) and P75 neurotrophin receptor (P75NTR) in rat brain. METHODS: Sixteen SD rats were divided into two groups (n = 8 for each group). The rats in experimental group were treated with risperidone [0.25 mg/(kg · d)] for 14 d, while the control group was given placebo. Total RNA sample in prefrontal cortex, temporal cortex and hippocampus was extracted, and the expression of BDNF, TrkB and P75NTR mRNA were determined by quantitative real-time PCR. RESULTS: The treatment of risperidone significantly up-regulated the expressions of BDNF and TrkB in prefrontal cortex, temporal cortex and hippocampus, while the expression of P75NTR was not significantly changed. CONCLUSION:Risperidone upregulated BDNF-TrkB signaling, but not BDNF-P75NTR signaling, which may be helpful for the further pharmacological study of risperidone.