| First Author | He XP | Year | 2004 |
| Journal | Neuron | Volume | 43 |
| Issue | 1 | Pages | 31-42 |
| PubMed ID | 15233915 | Mgi Jnum | J:91467 |
| Mgi Id | MGI:3047172 | Doi | 10.1016/j.neuron.2004.06.019 |
| Citation | He XP, et al. (2004) Conditional deletion of TrkB but not BDNF prevents epileptogenesis in the kindling model. Neuron 43(1):31-42 |
| abstractText | Epileptogenesis is the process whereby a normal brain becomes epileptic. We hypothesized that the neurotrophin brain-derived neurotrophic factor (BDNF) activates its receptor, TrkB, in the hippocampus during epileptogenesis and that BDNF-mediated activation of TrkB is required for epileptogenesis. We tested these hypotheses in Synapsin-Cre conditional BDNF(-/-) and TrkB(-/-) mice using the kindling model. Despite marked reductions of BDNF expression, only a modest impairment of epileptogenesis and increased hippocampal TrkB activation were detected in BDNF(-/-) mice. In contrast, reductions of electrophysiological measures and no behavioral evidence of epileptogenesis were detected in TrkB(-/-) mice. Importantly, TrkB(-/-) mice exhibited behavioral endpoints of epileptogenesis, tonic-clonic seizures. Whereas TrkB can be activated, and epileptogenesis develops in BDNF(-/-) mice, the plasticity of epileptogenesis is eliminated in TrkB(-/-) mice. Its requirement for epileptogenesis in kindling implicates TrkB and downstream signaling pathways as attractive molecular targets for drugs for preventing epilepsy. |
