Brain-derived neurotrophic factor delays hippocampal kindling in the rat

摘要: Abstract Epileptic seizures increase the expression of brain-derived neurotrophic factor in hippocampus. Since this neurotrophin exerts modulatory effects on neuronal excitability structure, it may play an important role hippocampal epileptogenesis. This question was addressed by studying chronic infusions recombinant and antisense hippocampus during first seven days kindling. Infusion with (6–24 μg/day) significantly delayed progression standard kindling strongly suppressed induced rapid These suppressive were dose dependent, long lasting, not secondary to toxicity specific neurotrophin, as nerve growth accelerated progression. They also appeared be hippocampus, infusion (48 μg/day) amygdala only resulted a slight transient delay Conversely protective exogenous factor, oligodeoxynucleotides (12 nmol/day), resulting reduced endogenous aggravated Taken together, our results lead us suggest that seizure-induced constitute regulatory mechanism able restrain