Premium
Decreased BDNF signalling in transgenic mice reduces epileptogenesis
Author(s) -
Lähteinen Sari,
Pitkänen Asla,
Saarelainen Tommi,
Nissinen Jari,
Koponen Eija,
Castrén Eero
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2002.01897.x
Subject(s) - epileptogenesis , tropomyosin receptor kinase b , status epilepticus , pentylenetetrazol , neuroscience , neurotrophic factors , transgene , genetically modified mouse , epilepsy , biology , brain derived neurotrophic factor , kainic acid , tropomyosin receptor kinase a , endocrinology , neurotrophin , medicine , receptor , glutamate receptor , genetics , gene , anticonvulsant
Brain derived neurotrophic factor (BDNF) has been suggested to be involved in epileptogenesis. Both pro‐ and antiepileptogenic effects have been reported, but the exact physiological role is still unclear. Here, we investigated the role of endogenous BDNF in epileptogenesis by using transgenic mice overexpressing truncated trkB, a dominant negative receptor of BDNF. After induction of status epilepticus (SE) by kainic acid, the development of spontaneous seizures was monitored by video‐EEG system. Hilar cell loss, and the number of neuropeptide Y immunoreactive cells were studied as markers of cellular damage, and mossy fibre sprouting was investigated as a plasticity marker. Our results show that transgenic mice had significantly less frequent interictal spiking than wild‐type mice, and the frequency of spontaneous seizures was lower. Furthermore, compared to wild‐type animals, transgenic mice had less severe seizures with later onset and mortality was lower. In contrast, no differences between genotypes were observed in any of the cellular or plasticity markers. Our results suggest that transgenic mice with decreased BDNF signalling have reduced epileptogenesis.