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

Our data provide evidence that overexpression of mutated human A30P α-synuclein in mice leads to a reduced size of the dopamine storage pool. This is in agreement with the previously postulated involvement of α-synuclein in the turnover of transmitter vesicles and may explain the observed motor deficits in A30P mice.