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

alpha-Synuclein (alpha-Syn) is a 14 kDa protein of unknown function that has been implicated in the pathophysiology of Parkinson's disease (PD). Here, we show that alpha-Syn-/- mice are viable and fertile, exhibit intact brain architecture, and possess a normal complement of dopaminergic cell bodies, fibers, and synapses. Nigrostriatal terminals of alpha-Syn-/- mice display a standard pattern of dopamine (DA) discharge and reuptake in response to simple electrical stimulation. However, they exhibit an increased release with paired stimuli that can be mimicked by elevated Ca2+. Concurrent with the altered DA release, alpha-Syn-/- mice display a reduction in striatal DA and an attenuation of DA-dependent locomotor response to amphetamine. These findings support the hypothesis that alpha-Syn is an essential presynaptic, activity-dependent negative regulator of DA neurotransmission.

Pubmed ID: 10707987


  • Abeliovich A
  • Schmitz Y
  • FariƱas I
  • Choi-Lundberg D
  • Ho WH
  • Castillo PE
  • Shinsky N
  • Verdugo JM
  • Armanini M
  • Ryan A
  • Hynes M
  • Phillips H
  • Sulzer D
  • Rosenthal A



Publication Data

January 23, 2000

Associated Grants


Mesh Terms

  • Amphetamine
  • Animals
  • Autoreceptors
  • Calbindins
  • Calcium
  • Corpus Striatum
  • Dopamine
  • Dopamine Agents
  • Female
  • Gene Expression
  • Glutamic Acid
  • Hippocampus
  • Locomotion
  • Long-Term Potentiation
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Motor Activity
  • Nerve Tissue Proteins
  • Neurons
  • Presynaptic Terminals
  • S100 Calcium Binding Protein G
  • Substantia Nigra
  • Synaptic Transmission
  • Synucleins
  • alpha-Synuclein
  • rab3A GTP-Binding Protein