PMID- 11886452
OWN - NLM
STAT- MEDLINE
DCOM- 20020510
LR  - 20220408
IS  - 0953-816X (Print)
IS  - 0953-816X (Linking)
VI  - 15
IP  - 4
DP  - 2002 Feb
TI  - Decreased BDNF signalling in transgenic mice reduces epileptogenesis.
PG  - 721-34
AB  - 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.
FAU - Lahteinen, Sari
AU  - Lahteinen S
AD  - Laboratory of Molecular Pharmacology, A.I.Virtanen Institute, University of 
      Kuopio, Kuopio, Finland.
FAU - Pitkanen, Asla
AU  - Pitkanen A
FAU - Saarelainen, Tommi
AU  - Saarelainen T
FAU - Nissinen, Jari
AU  - Nissinen J
FAU - Koponen, Eija
AU  - Koponen E
FAU - Castren, Eero
AU  - Castren E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Neuropeptide Y)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Action Potentials/genetics
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Dentate Gyrus/*metabolism/pathology/physiopathology
MH  - Down-Regulation/*genetics
MH  - Epilepsy/chemically induced/metabolism/pathology
MH  - Epilepsy, Temporal Lobe/*genetics/metabolism/physiopathology
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Female
MH  - Growth Cones/metabolism/ultrastructure
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Mossy Fibers, Hippocampal/metabolism/ultrastructure
MH  - Nerve Degeneration/etiology/*metabolism/pathology
MH  - Neuronal Plasticity/*genetics
MH  - Neuropeptide Y/metabolism
MH  - Receptor, trkB/*genetics/metabolism
MH  - Signal Transduction/genetics
EDAT- 2002/03/12 10:00
MHDA- 2002/05/11 10:01
CRDT- 2002/03/12 10:00
PHST- 2002/03/12 10:00 [pubmed]
PHST- 2002/05/11 10:01 [medline]
PHST- 2002/03/12 10:00 [entrez]
AID - 10.1046/j.1460-9568.2002.01897.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 2002 Feb;15(4):721-34. doi: 10.1046/j.1460-9568.2002.01897.x.