Journal
EPILEPSY RESEARCH
Volume 73, Issue 3, Pages 266-274Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.eplepsyres.2006.11.003
Keywords
epilepsy; neurotransmission; NSF; SNARE; SV2
Categories
Funding
- NHLBI NIH HHS [HL56652, R01 HL056652] Funding Source: Medline
- NINDS NIH HHS [R01 NS046242] Funding Source: Medline
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Modifications of neurotransmission may contribute to the synchronization of neuronal networks that are a hallmark of epileptic seizures. In this study we examine the synaptosomal. proteins involved in neurotransmitter release to determine if alterations in their interactions correlate with the chronic epileptic state. Using quantitative western blotting, we measured the levels of 7S SNARE complexes and SNARE effectors in the effected hippocampi from animals that were electrically kindled through stimulation from one of three different foci. All three kindling paradigms, amygdalar, entorhinal, and septal, were associated with an accumulation of 7S SNARE complexes in the ipsitaterat hippocampus, measured 1 month after completion of kindling. Of the eight SNARE effectors examined (alpha-SNAP, NSF, SV2A/B, Munc18a/nSec1, Munc13-1, Complexins 1 and 2, and synaptotagmin I), there was a statistically significant bihemispheric increase of hippocampat SV2 and decrease of NSF upon kindling; neither by itself would be expected to account for the asymmetry of SNARE complex distribution. These data suggest that an ipsilateral. hippocampal. accumulation of SNARE complexes is a permanent alteration of kindling-induced epilepsy, regardless of stimulation pathway. The significance of these findings toward a molecular understanding of epilepsy will be discussed. (c) 2006 Elsevier B.V. All rights reserved.
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