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Locomotor activity and evoked dopamine release are reduced in mice overexpressing A30P-mutated human alpha-synuclein

Leonid Yavich1, Mari Oksman, Heikki Tanila

  • 1Department of Pharmacology and Toxicology, University of Kuopio, FIN-70211 Kuopio, Finland. leonid.yavich@uku.fi

Neurobiology of Disease
|October 26, 2005
PubMed

Insights

Transgenic mice overexpressing mutated alpha-synuclein (A30P) showed motor deficits due to a reduced dopamine storage pool, not cell loss.

Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Alpha-synuclein aggregation is implicated in neurodegenerative diseases.
  • Mutations in alpha-synuclein can alter its function and contribute to pathology.

Purpose of the Study:

  • To investigate the in vivo effects of overexpressing mutated human A30P alpha-synuclein.
  • To determine the impact on motor function and dopamine neurotransmission.

Main Methods:

  • Generation of a transgenic mouse model overexpressing A30P alpha-synuclein.
  • Immunohistochemistry to detect protein expression.
  • Behavioral tests for motor function.
  • In vivo voltammetry to measure dopamine release and kinetics.

Main Results:

  • A30P alpha-synuclein was detected in various brain regions without gross morphological changes or dopaminergic cell loss.
  • Transgenic mice exhibited decreased locomotion and impaired motor coordination.
  • Reduced dopamine release and slower dopamine decline were observed in the striatum of A30P mice.
  • Dopamine re-uptake and transporter levels remained unchanged.

Conclusions:

  • Overexpression of mutated A30P alpha-synuclein leads to a reduced dopamine storage pool size.
  • This finding supports the role of alpha-synuclein in dopamine vesicle turnover.
  • The reduced dopamine storage pool likely explains the observed motor deficits in A30P mice.

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