Regular ArticleAbnormal Phosphorylation of Synapsin I Predicts a Neuronal Transmission Impairment in the R6/2 Huntington's Disease Transgenic Mice
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An updated reappraisal of synapsins: structure, function and role in neurological and psychiatric disorders
2021, Neuroscience and Biobehavioral ReviewsIntegrative Characterization of the R6/2 Mouse Model of Huntington's Disease Reveals Dysfunctional Astrocyte Metabolism
2018, Cell ReportsCitation Excerpt :We and others have observed elevated glutamine levels in R6/2 brains (Table S5; Behrens et al., 2002; Tsang et al., 2006; Tkac et al., 2007; Zacharoff et al., 2012), which could either indicate that astrocytic glutamine synthesis is increased or that glutamine release is impaired. The latter is in line with reduced expression of SNAT3 (Figure 3; Figure S5), whereas the former appears less likely since we and others have observed decreased expression of GS in R6/2 brains (Liévens et al., 2002; Boussicault et al., 2014; Tong et al., 2014). Furthermore, we did not observe reductions in glutamine labeling or levels after incubation with either [U-13C]glutamate or [U-13C]glutamine, indicating normal GS activity and glutamine uptake, respectively.
N-type Ca<sup>2+</sup> channels are affected by full-length mutant huntingtin expression in a mouse model of Huntington's disease
2017, Neurobiology of AgingCitation Excerpt :Thus, it is possible that earlier pathological events causing dysfunction of neurotransmission may contribute to phase I HD symptoms. The htt can directly interact with synaptic vesicle proteins and alter vesicle trafficking and exocytosis (DiFiglia et al., 1995; Lievens et al., 2002; Morton et al., 2001). Moreover, an increase in glutamate release has been observed in synaptosomes from 6-month old Hdh140Q/140Q knock-in HD mice (Valencia et al., 2013).
Synaptopathic mechanisms of neurodegeneration and dementia: Insights from Huntington's disease
2017, Progress in NeurobiologyDevelopment of a high-throughput alphascreen assay for modulators of synapsin i phosphorylation in primary neurons
2014, Journal of Biomolecular ScreeningCitation Excerpt :Alterations in the phosphorylation of synapsin I may play a role in diseases associated with aberrant synaptic transmission. Indeed, reduced phosphorylation at site 1 has been observed in Alzheimer disease postmortem tissues,16 and hyper- and hypophosphorylation at sites 3 to 5 and 6, respectively, have been observed in a Huntington disease mouse model.17 The important role of synapsin I in synaptic transmission and its significance in CNS disease biology make it an attractive target for the identification of small molecular modulators of synaptic function.
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To whom correspondence should be addressed at Division of Medical and Molecular Genetics, GKT School of Medicine, 8th Floor Guy's Tower, Guy's Hospital, London SE1 9RT, UK. Fax: 020 7955 4444. E-mail: [email protected].