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The Expression of Syntaxin1B/GR33 mRNA Is Enhanced in the Hippocampal Kindling Model of Epileptogenesis
Author(s) -
Kamphuis W.,
Smirnova T.,
Hicks A.,
Hendriksen H.,
Mallet J.,
Lopes da Silva F. H.
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.65051974.x
Subject(s) - epileptogenesis , kindling , fascia dentata , hippocampal formation , kindling model , neuroscience , syntaxin , stimulation , hippocampus , synaptic plasticity , chemistry , in situ hybridization , messenger rna , biology , dentate gyrus , biochemistry , vesicle , receptor , gene , membrane
Syntaxin, a protein required for the docking of synaptic vesicles, may be involved in the manifestation of synaptic plasticity. The possible involvement of syntaxin in epileptogenesis was investigated by assessing the expression levels of syntaxin1B/GR33 mRNA by in situ hybridization at different stages of hippocampal kindling epileptogenesis and after the induction of generalized seizures. Densitometric analysis of the autoradiograms revealed that the expression was not changed in pyramidal and granular neurons of the hippocampal formation 24 h after the first kindling stimulation. However, the mRNA levels in CA1, CA3, and fascia dentata neurons were bilaterally enhanced after six afterdischarges and remained at this elevated level during the whole period along which afterdischarges were elicited. An immunoassay was unable to reveal a clear significant increase of syntaxin1B/GR33 protein levels in hippocampus homogenates of fully kindled animals. The use of syntaxin1B‐specific antibodies is necessary to draw definite conclusions on the changes at the protein level. At long term, 4 weeks after the last kindling‐elicited generalized seizure, no significant alterations in transcript levels could be detected. The results suggest that the induction of kindling epileptogenesis is associated with an enhanced expression of syntaxin1B/GR33, but this enhanced expression is not necessary for persistence of kindling‐induced synaptic plasticity.