Mice lacking alpha-synuclein display functional deficits in the nigrostriatal dopamine system.

By A. Abeliovich, Y. Schmitz, I. Fariñas, D. Choi-Lundberg, W. Ho, P. Castillo, N. Shinsky, J. M. Verdugo, M. Armanini, A. Ryan and 4 more. Neuron, 2000

871 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/ec776ba085782169aa163d73e29c2ec76dd6e730

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Citations in the corpus

• Intravesicular Localization and Exocytosis of α-Synuclein and its Aggregates (2005, background): “-Syn localizes to nerve terminals (Iwai et al., 1995) and has been implicated in synaptic transmission (Abeliovich et al., 2000; Cabin et al., 2002; Liu et al., 2004; Yavich et al., 2004).”
• α-Synuclein in Parkinson's disease. (2012, unknown): “…of cellular systems in which WT a-synuclein is overexpressed have been instrumental in this regard, as they reveal alterations in neurotransmitter release, which are not always consistent across neuronal systems (Abeliovich et al. 2000; Murphy et al. 2000; Cabin et al., 2002; Larsen et al. 2006).”
• α‐Synuclein implicated in Parkinson's disease is present in extracellular biological fluids, including human plasma (2003, unknown): “The function of α-syn remains to be established; however, it has been implicated in the regulation of synaptic plasticity (12) and neuronal differentiation (13, 14), as well as in regulation of dopamine synthesis (15, 16 ), and it also has chaperone-like activity (17).”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, unknown): “Mice lacking a -synuclein were reported to show increased dopamine release upon stimulation, pointing to a role of a - synuclein in negatively regulating dopamine neurotransmission (Abeliovich et al , 2000; Yavich et al , 2004).”
• Dopamine release in the basal ganglia (2011, background): “…has little effect on single-pulse or brief pulse-train evoked [DA] o , there is evidence for modified regulation of DA re-release with repetitive stimulation in some studies but not others (Abeliovich et al., 2000; Yavich et al., 2004; Yavich et al., 2005; Senior et al., 2008; Anwar et al., 2011).”
• Intracerebral inoculation of pathological α-synuclein initiates a rapidly progressive neurodegenerative α-synucleinopathy in mice (2012, methodology): “M83 mice overexpressing human A53T Syn under the control of the mouse prion protein promoter (Giasson et al., 2002) were maintained on a C57BL/C3H background and Syn/ mice (Abeliovich et al., 2000) were maintained on a C57BL/6 background.”
• DJ-1 Is a Redox-Dependent Molecular Chaperone That Inhibits α-Synuclein Aggregate Formation (2004, unknown): “Undifferentiated ES cells, CAD neuroblastoma cells, and HeLa cells were cultured using standard techniques (Abeliovich et al. 2000; Staropoli et al. 2003).”
• A Role for α-Synuclein in the Regulation of Dopamine Biosynthesis (2002, background): “-Synuclein knock-out mice have normal numbers of DA neurons at 3–6 weeks (Abeliovich et al., 2000).”
• Alpha-synuclein in Parkinson’s disease and other synucleinopathies: from overt neurodegeneration back to early synaptic dysfunction (2023, background): “Mutant mice lacking α-syn show a reduced DA striatal content and inhibition of DA-dependent motor response to amphetamine, which enhances motor activity through the DA active transporter (DAT)-dependent mechanism [34, 35].”
• Parkin ubiquitinates the α-synuclein–interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease (2001, unknown): “Targeted disruption of α-synuclein in mice does not yield a parkinsonian phenotype, but instead leads to abnormalities in striatal dopaminergic neurotransmission indicating that α-synuclein has important physiological roles in regulating dopamine activit”
• Oxidative stress and nitration in neurodegeneration: cause, effect, or association? (2003, unknown): “function related to dopamine metabolism (66).”