SNAP-25, enSNAREd in neurotransmission and regulation of behaviour

Wilson, Michael C.; Mehta, Priya; Hess, Ellen J.

doi:10.1042/bst0240670

Cited by 14 publications

(8 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SNAP‐25 undergoes changes in expression during early fetal development and aging (Shimohama et al, 1997). SNAP‐25 is expressed as two isoforms, both of which can be induced by stimuli producing long‐term potentiation (LTP) in the hippocampus (Roberts et al, 1998; Genoud et al, 1999) and is integral to the process of Ca‐sensitive, stimulus‐evoked transmitter vesicle exocytosis (Mehta et al, 1996; Wilson et al, 1996; Ferrer et al, 1998; Washbourne et al, 2002). Moreover, SNAP‐25 has been shown to be related to behavioral regulation in a mouse mutant (Hess et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…SNAP‐25 has been proved to be critical to Ca‐sensitive, stimulus‐evoked transmitter release (Wilson et al, 1996; Washbourne et al, 2002) and is involved in production of LTP (Roberts et al, 1998; Steffensen et al, 1999), which is critical to learning and memory. The fact that this protein is found to be markedly reduced in hippocampus in young Tg(+/+) animals prior to their development of amyloid plaques, as shown in this study, may account for the physiologic observations of behavioral deficits and reductions in evoked potentials within hippocampal slices from young transgenic PDGF‐APP (V717F) animals, as demonstrated by Hsia et al (1999).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Reversal of amyloid β toxicity in Alzheimer's disease model Tg2576 by intraventricular antiamyloid β antibody

Chauhan

Siegel

2002

J of Neuroscience Research

View full text Add to dashboard Cite

There are considerable data on synaptic dysfunction in Alzheimer's disease (AD). However, the precise molecular basis for synaptotoxicity in AD is not known. We tested the hypothesis that amyloid beta (Abeta), as produced in Tg2576 mice overexpressing a mutant form of amyloid precursor protein, leads to changes in SNAP-25, a molecule required for Ca-sensitive neurotransmitter vesicle exocytosis. Anti-Abeta antibody was injected into the third ventricle (icv) of 10-month-old Tg2576 mice, preceding formation of plaques. Immunodensity of glial fibrillary acidic protein (GFAP) and SNAP-25 were quantitated in the hippocampus 1 month later. SNAP-25 was reduced by 96% in the inner molecular layer (SMi) of dentate gyrus, by 95% in the hilum, and by 75-76% in stratum lucidum (SL), stratum oriens (SO), and stratum radiatum (SR) of CA1-CA3 of the Tg2576 mice. GFAP was increased by more than 50-fold, specifically within the neuropil of CA1-CA3, and by twofold in portions of fimbria. One injection of 10 microg of anti-Abeta antibody into the third ventricle at 10 months completely prevented or restored changes in GFAP at 11 months of age. The restoration of SNAP-25 by anti-Abeta antibody compared with wild type was 69% in CA1-SO, 93% in CA1-SR, 85% in CA3-SL, 77% in SMi, and 60-73% in hilum. In addition, whereas control injections of saline or IgG produced greatly increased GFAP diffusely in the hippocampus of Tg2576 animals, there was no increase in GFAP after anti-Abeta injection, suggesting a synergistic interaction of nonspecific trauma with Abeta in the transgenic mice. This is the first report of depleted SNAP-25 immunoreactivity in Tg models and the first report of icv injection of anti-Abeta antibody in this model of AD. The largest reductions of the SNAP-25 are in hilum and SMi, so either reduction in the septal-hilum-SMi path is primary or reduction in this path begins at an earlier age than in CA3-CA1 fields. A single icv injection of anti-Abeta antibody is potent in reversing Abeta effects and, therefore, represents a suitable model for investigating early Abeta toxicity. In addition, intrathecal or icv antibody may be an efficient means of treating or preventing toxicity in AD, particularly under conditions of immune hyporesponsivity.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Reversal of amyloid β toxicity in Alzheimer's disease model Tg2576 by intraventricular antiamyloid β antibody

Chauhan

Siegel

2002

J of Neuroscience Research

View full text Add to dashboard Cite

show abstract

“…It acts in concert with vesicleassociated membrane protein (VAMP)/synaptobrevin and syntaxin 1a/1b to effect neurotransmitter release at synapses. 42 The coloboma (Cm/ þ ) mutant mouse has SNAP-25 and several other genes deleted, and exhibits spontaneous locomotor activity, similar to the hyperactivity seen with the VH-lesioned F344 rats. The Cm/ þ mouse hyperactivity was corrected when a SNAP-25 transgene was bred into the strain, showing that the hyperactivity was a result of the SNAP-25 deletion.…”

Section: Discussionmentioning

confidence: 99%

Identification of candidate genes for psychosis in rat models, and possible association between schizophrenia and the 14-3-3η gene

et al. 2003

View full text Add to dashboard Cite

Although the genetic contribution to schizophrenia is substantial, positive findings in wholegenome linkage scans have not been consistently replicated. We analyzed gene expression in various rat conditions to identify novel candidate genes for schizophrenia. Suppression subtraction hybridization (SSH), with polyA mRNA from temporal and frontal cortex of rats, was used to identify differentially expressed genes. Expression of mRNA was compared between adult Lewis and Fischer 344 (F344) rats, adult and postnatal day 6 (d6) F344, and adult F344 treated with haloperidol or control vehicle. These groups were chosen because each highlights a particular aspect of schizophrenia: differences in strain vulnerability to behavioral analogs of psychosis; factors that may relate to disease onset in relation to CNS development; and improvement of symptoms by haloperidol. The 14-3-3 gene family, as represented by 14-3-3c and 14-3-3f isoforms in the SSH study, and SNAP-25 were among the candidate genes. Genetic association between schizophrenia and the 14-3-3g gene, positioned close to a genomic locus implicated in schizophrenia, and SNAP-25 genes was analyzed in 168 schizophrenia probands and their families. These findings address three different genes in the 14-3-3 family. We find a significant association with schizophrenia for two polymorphisms in the 14-3-3g gene: a 7 bp variable number of tandem repeats in the 5 0 noncoding region (P ¼ 0.036, 1 df), and a 3 0 untranslated region SNP (753G/A) that is an RFLP visualized with Ava II (P ¼ 0.028). There was no significant genetic association with SNAP-25. The candidate genes identified may be of functional importance in the etiology, pathophysiology or treatment response of schizophrenia or psychotic symptoms. This is to our knowledge the first report of a significant association between the 14-3-3g-chain gene and schizophrenia in a family-based sample, strengthening prior association reports in case-control studies and microarray gene expression studies.

show abstract

“…The latter variant may influence synaptic plasticity. 63 Finally, the v-SNARE protein synaptobrevin (VAMP) has two neuronal isoforms 64 and is anchored to the vesicle by a C-terminal TM domain, interacting with t-SNARES by a short motif. It interacts with syntaxin 1A and SNAP-25 but does not bind the II-III linker in any of N-, P/Q-or R-type (Fig.…”

Section: Functional Interactions Between Presynaptic Calcium Channelsmentioning

confidence: 99%

Old proteins, developing roles: The regulation of calcium channels by synaptic proteins

Davies

Zamponi²

2008

Channels

View full text Add to dashboard Cite

SNAP-25, enSNAREd in neurotransmission and regulation of behaviour

Cited by 14 publications

References 20 publications

Reversal of amyloid β toxicity in Alzheimer's disease model Tg2576 by intraventricular antiamyloid β antibody

Reversal of amyloid β toxicity in Alzheimer's disease model Tg2576 by intraventricular antiamyloid β antibody

Identification of candidate genes for psychosis in rat models, and possible association between schizophrenia and the 14-3-3η gene

Old proteins, developing roles: The regulation of calcium channels by synaptic proteins

Contact Info

Product

Resources

About