The Expressionof Syntaxin1B /GR33 mRNA IsEnhanced in theHippocampal KindlingModel of Epileptogenesis

Syntaxin, a protein required for the docking of synaptic vesicles, may be involved in the manifestation of synaptic plasticity . The possible involvement of syn- taxin in epileptogenesis was investigated by assessing the expression levelsof syntaxinl B/GR33 mRNA by in situhybridizationat differentstages of hippocampal kin- dling epileptogenesis and afterthe induction of general- ized seizures. Densitometric analysis of the autoradio- grams revealed that the expression was not changed in pyramidal and granular neurons of the hippocampal for- mation 24 h afterthe firstkindlingstimulation.However, the mRNA levelsinCA1, CA3, and fascia dentata neurons were bilaterallyenhanced after six afterdischarges and remained at this elevated levelduring the whole period along which afterdischarges were elicited.An immunoas- say was unable to reveal a clear significantincrease of syntaxinl B/GR33 protein levelsinhippocampus homog- enates of fullykindled animals .The use of syntaxinl 13- specificantibodies isnecessary to draw definiteconclu- sions on the changes at the protein level.At long term, 4 weeks after the last kindling-elicitedgeneralized sei- zure, no significantalterations in transcript levels could be detected . The results suggest that the induction of kindlingepileptogenesis isassociated with an enhanced expression of syntaxinl B/GR33, but this enhanced ex- pression is not necessary for persistence of kindling- induced synaptic plasticity. Key Words : Kindling- GR33-Syntaxinl B-Hippocampus-In situ hybridiza- tion-Epilepsy-Plasticity .