This study aims to investigate the potential effects of anticonvulsant drugs on neuropeptides (galanin and neuropeptide Y) and neurotrophic factors (BDNF and NGF) in pentylenetetrazol (PTZ)-kindled seizures in the rat.
However, the beneficial or detrimental consequences of CREB-BDNF activation on the induction and/or progression of seizures depend specifically on the region of brain involved and the time of activation.
Here we report that male offspring of socially isolated parents showed decreased agonistic behaviour and social transmission of flavour preference, impairment in reversal learning, increased seizure susceptibility, reduced plasma oxytocin levels, and increased plasma and brain levels of BDNF, all features resembling an ASD-like phenotype.
We could not find a relation between the Val/Met polymorphism of the BDNF and the development of the seizure threshold during the course of the ECT sessions.
Given the long postulated role of BDNF in epileptogenesis, TRPC3 channels may be a critical component in the underlying pathophysiology of seizure and epilepsy.
BDNF-tg mice also displayed reduced breeding efficiency, higher anxiety-like scores, high self-grooming, impaired prepulse inhibition, and higher susceptibility to seizures when placed in a new empty cage, as compared with wild-type (WT) littermate controls.
Individuals with the p.R168X mutation and heterozygous for the BDNF polymorphism were also at an increased risk of seizure onset (hazard ratio 5.3, 95% confidence interval 1.6-17.7) compared with those homozygous for the wild-type BDNF allele.
PRI-2191 alone had no effect on gene expression, but it enhanced the seizure-evoked expression of HSP-70, had an opposite effect on BDNF mRNA level and did not affect prepro-TRH mRNA level.
Furthermore, BDNF hyperactivity may be associated with early brain outgrowth, increased prevalence of seizures in autism, and similar behaviors observed in autism and fragile X syndrome.
PRI-2191 alone had no effect on gene expression, but it enhanced the seizure-evoked expression of HSP-70, had an opposite effect on BDNF mRNA level and did not affect prepro-TRH mRNA level.
Several studies suggest that brain-derived neurotrophic factor (BDNF) can exacerbate seizure development during status epilepticus (S.E.) and subsequent epileptogenesis in the adult brain.
Our results suggest that the 240T allele in the BDNF gene may be a genetic marker that indicates an enhanced susceptibility to seizures, setting up a cascade leading eventually to chronic partial epilepsy in patients with such a genetic predisposition.
As nerve growth factor and brain derived neurotrophic factor are the best-studied proteins of this class, we begin by discussing the evidence linking these neurotrophins to epilepsy and seizure.
Furthermore, neuronal electrical activity and seizures stimulate the transcription of specific messenger RNAs coding for neurotrophic factors like nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF).