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Accumulation of 7S SNARE complexes in hippocampal synaptosomes from chronically kindled rats
Author(s) -
Matveeva E. A.,
Whiteheart S. W.,
Slevin J. T.
Publication year - 2003
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.1471-4159.2003.01589.x
Subject(s) - kindling , epileptogenesis , hippocampal formation , neuroscience , kindling model , neurotransmitter , stimulation , glutamate receptor , entorhinal cortex , epilepsy , limbic system , hippocampus , chemistry , snare complex , psychology , receptor , central nervous system , vesicle , membrane , biochemistry
Kindling is a model of complex partial epilepsy wherein periodic application of an initially subconvulsive stimulus leads to first limbic and then generalized tonic‐clonic seizures. Several laboratories have reported that augmented neurotransmitter release of l ‐glutamate is associated with the chronically kindled state. Neurotransmitter release requires membrane proteins called SNAREs, which form transmembrane complexes that participate in vesicle docking and are required for membrane fusion. We show here that kindling by entorhinal stimulation is associated with an accumulation of 7S SNARE complexes in the ipsilateral hippocampus. This increase of 7S SNARE complexes appears to begin early in the kindling process, achieves a peak with full kindling, and remains at this level for at least a month following cessation of further kindling stimuli. The increase is focal and permanently limited to the ipsilateral hippocampus despite progression to generalized electrographic and behavioral seizures. It is not seen in animals that receive electroconvulsive seizures, suggesting it is related to the kindling process itself. The duration and focality of increased 7S SNARE complexes with entorhinal kindling suggest that this is an altered molecular process associated with epileptogenesis.