Genetic background regulates semaphorin gene expression and epileptogenesis in mouse brain after kainic acid status epilepticus

The host response to neural injury, which can include axonal sprouting and synaptic reorganization is likely to be under tight genetic regulatory control at the level of the genome and may be implicated in epileptogenesis. Despite its importance, however, the molecular basis of synaptic reorganizati...

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Bibliographic Details
Published in:Neuroscience 2005, Vol.131 (4), p.853-869
Main Authors: Yang, J., Houk, B., Shah, J., Hauser, K.F., Luo, Y., Smith, G., Schauwecker, E., Barnes, G.N.
Format: Article
Language:English
Subjects:
Animals
Axons - metabolism
Biological and medical sciences
Blotting, Northern
Brain Chemistry - genetics
Cell Count
Cloning, Molecular
Dentate Gyrus - metabolism
Deoxyglucose - metabolism
epilepsy
Excitatory Amino Acid Agonists
Fundamental and applied biological sciences. Psychology
GAP-43 Protein - metabolism
Gene Expression Regulation - physiology
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
hippocampus
Immunoblotting
Immunohistochemistry
In Situ Hybridization
Kainic Acid
Male
Medical sciences
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
mouse
Nervous system (semeiology, syndromes)
Neurology
Pyramidal Tracts - metabolism
RNA Probes
semaphorin
Semaphorins - biosynthesis
Semaphorins - genetics
Species Specificity
Status Epilepticus - chemically induced
Status Epilepticus - genetics
Status Epilepticus - metabolism
Synapses - physiology
synaptic reorganization
Vertebrates: nervous system and sense organs
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Summary:The host response to neural injury, which can include axonal sprouting and synaptic reorganization is likely to be under tight genetic regulatory control at the level of the genome and may be implicated in epileptogenesis. Despite its importance, however, the molecular basis of synaptic reorganization is unclear. We have studied the development of synaptic reorganization, semaphorin gene expression, and epileptogenesis in hippocampus of epileptogenic sensitive (FVB/NJ) and epileptogenic resistant (C57BL/6J) mice (i.e. distinct genetic backgrounds) after kainic acid-induced status epilepticus. Our results support the hypothesis that disruption of transcriptional regulation of axon guidance genes leads to a differential loss of tonic neuropilin-2 dependent activation of semaphorin 3F receptors on hippocampal neurons on distinct genetic backgrounds. This results in rearranged synaptic circuitry and thus promotes epileptogenesis. These findings may define biologic principles underlying the role of semaphorin signaling which may broadly apply to other systems undergoing neural regeneration.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2004.09.064