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• W1526320980 abstract "OBJECTIVE: To assess the role of Tomosyn in kindling-induced epileptogenesis BACKGROUND: We have used the kindling model to evaluate whether altered presynaptic vesicular fusion is a driver of epileptogenesis. Neurotransmitter release requires fusion of vesicle and plasma membranes, mediated by the formation of a stable complex (7SC) of SNARE proteins. 7SC is composed of VAMP-2 (synaptic vesicle v-SNARE) and syntaxin 1 and SNAP-25 (neuronal active zone t-SNAREs). Tomosyn, as a place-holder for the v-SNARE, may be a negative regulator of neurotransmitter release. We previously showed that kindling in rodents leads to a permanent accumulation of 7SC in hippocampus ipsilateral to the stimulus. Compared to wild-type, mice deficient in VAMP-2 are kindling-resistant and demonstrate reduced ipsilateral hippocampal L-glutamate release. DESIGN/METHODS: Mice were genotyped by PCR using DNA prepared from distal tail and kindled to two successive stage 5 seizures by amygdala stimulation. Thirty days later, L-glutamate release was measured in bilateral hippocampal subfields using microelectrode arrays, and 7SC and SNARE proteins were quantified by western blotting. Data were analyzed by ANOVA and post hoc t -tests. RESULTS: Fewer stimuli led to Racine stage 5 seizures in Tomosyn -/- (4.9±0.6/n=15) and Tomosyn +/- (7.9±1.4/n=7) mice compared to Tomosyn +/+ mice (9.6±1.1/n=14); P=0.002. The after-discharge stimulus intensity was no different among groups (251±22μA/n=36). Kindling was associated with hippocampal 7SC asymmetry (ipsilateral vs . contralateral ratio: 1.11±0.002) in all 3 groups, as reported in VAMP-2-deficient mice (Matveeva et al . 2012; Neurosci 202:77) and rats (Matveeva et al . 2012; Epilepsia 53:157). KCl-evoked L-glutamate release was increased in dentate gyrus of Tomosyn -/- mice. CONCLUSIONS: Transgenic animals with altered levels of SNAREs/SNARE regulators are useful in determining if changes in neurosecretory machinery lead to changes in epileptogenesis and thus may identify molecular targets for future drug development to modulate seizure evolution. Study Supported by: Department of Veterans Affairs, DARPA, HL56652, HL091893, CTSA-LTR000117. Disclosure: Dr. Slevin has received personal compensation for activities with Teva Neuroscience and AbbVie, Inc. Dr. Slevin has received research support from Abbott Laboratories, BioTie, and Teva Neuroscience. Dr. Batten has nothing to disclose. Dr. Matveeva has nothing to disclose. Dr. Whiteheart has nothing to disclose. Dr. Vanaman has nothing to disclose. Dr. Gerhardt has received personal compensation for activities with Eli Lilly & Co., and Medtronic Inc. Dr. Gerhardt holds stock and/or stock options in Quanteon LLC, which sponsored research in which Dr. Gerhardt was involved as an investigator. Dr. Gerhardt has received research support from Eli Lilly & Co., and Medtronic Inc." @default.
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• W1526320980 date "2014-04-08" @default.
• W1526320980 modified "2023-09-26" @default.
• W1526320980 title "Reduction of Tomyson Expression Leads to a Kindling-Sensitive Phenotype in a Murine Model of Epilepsy (P1.267)" @default.
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