POSSIBLE PARTICIPATION OF A NEUROTROPHIN RECEPTOR IN THE MECHANISM OF NEURONAL DEATH STATUS EPILEPTICUS-INDUCED

MONTROULL, LAURA ESTER; UNSAIN, NICOLÁS; MASCÓ, DANIEL HUGO

Hotel Casa Serrana, Huerta Grande, Córdoba

Congreso; Primera Reunión Conjunta de Sociedades de Biología de la República Argentina; 2007

Sociedades de Biología de la República Argentina

The interaction of Brain-Derived Neurotrophic Factor (BDNF) with the TrkB receptor has been implicated in neuronal survival, while the interaction of BDNF and/or its precursor (proBDNF) with p75ntr has been implicated in neuronal death (apoptosis). Severe and prolongated seizures (Status Epilepticus, SE) produce death in the hippocampus. SE can be studied in the lithium-pilocarpine model in rats. In this proyect we studied if SE induces changes in the protein levels of BDNF, proBDNF and their receptors. SE induced a remarkable decrease in TrkB levels determined by Western blot and this modification preceded the neuronal damage induced by SE. Interestingly, we found neither neuronal death nor TrkB decrease in animals that after being injected with pilocarpine showed mild, intermitent seizures but did not developed SE (NoSE). At the same time, the interaction of proBDNF with p75ntr, analized by co-inmunoprecipitation, significantly increased after SE, but also ocurred in the NoSE group. These results suggest that to produce neuronal injury, a decrease in TrkB receptor levels might be necessary, while proBDNF and p75ntr interaction would not be a determinant factor. The interaction of Brain-Derived Neurotrophic Factor (BDNF) with the TrkB receptor has been implicated in neuronal survival, while the interaction of BDNF and/or its precursor (proBDNF) with p75ntr has been implicated in neuronal death (apoptosis). Severe and prolongated seizures (Status Epilepticus, SE) produce death in the hippocampus. SE can be studied in the lithium-pilocarpine model in rats. In this proyect we studied if SE induces changes in the protein levels of BDNF, proBDNF and their receptors. SE induced a remarkable decrease in TrkB levels determined by Western blot and this modification preceded the neuronal damage induced by SE. Interestingly, we found neither neuronal death nor TrkB decrease in animals that after being injected with pilocarpine showed mild, intermitent seizures but did not developed SE (NoSE). At the same time, the interaction of proBDNF with p75ntr, analized by co-inmunoprecipitation, significantly increased after SE, but also ocurred in the NoSE group. These results suggest that to produce neuronal injury, a decrease in TrkB receptor levels might be necessary, while proBDNF and p75ntr interaction would not be a determinant factor.