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TrkB is involved in the mechanism by which BDNF accelerates the glutamate-induced death of rat neuroblastoma B35 cells

Abstract Objective: Brain-derived neurotrophic factor (BDNF) binds to its high-affinity binding receptor, tropomyosin-related kinase (Trk) B, and can induce neuronal differentiation and survival. BDNF also accelerates neuronal cell death in a glutamate-induced model; however, it has been unknown whether the mechanism involves TrkB. In the current study, to determine the role of TrkB in neuronal cell death, we investigated TrkB involvement in BDNF acceleration of glutamate-induced neuronal death. Methods: A TrkB-stable transformant of rat neuroblastoma B35 (B35TrkB) cells was utilized to investigate whether TrkB is involved in BDNF acceleration of neuronal death. The cell viability of the B35TrkB cells was compared to that of mock vector-transgened B35 (B35mock) cells after treatment with/without BDNF and glutamate. Results: In both B35TrkB and B35mock cells, glutamate treatment decreased the cell viability. BDNF treatment further accelerated the decrease in the viability of B35TrkB cells, but not that in the viability of B35mock cells. At glutamate concentrations that did not significantly decrease cell viability, BDNF increased the cell viability of B35TrkB, but not that of B35mock. A mitogen-activated protein kinase (MAPK) inhibitor, U0126, suppressed BDNF’s accelerating effect on cell death. Although B35 parental cells endogenously express other neurotrophin receptors such as TrkA, nerve growth factor β (a ligand of TrkA and p75NTR) could not influence the viability of B35TrkB or B35mock cells. Conclusion: These results indicate that TrkB is an intermediator for the trophic and toxicity-exacerbating effects of BDNF against cell viabilities at non-cytotoxic and cytotoxic glutamate concentrations, respectively.