Chiao-Chi Chen1, Yi-Hua Hsu1, Nai-Wei Yao1, and Chen Chang1
The dopaminergic system
possesses striking plasticity compensating for motor aberrations from neuronal
loss. Little is known regarding the compensation mechanism during dopaminergic
loss, preventing the aberration from being arrested and treated early. Here we
present in vivo imaging evidence from
functional magnetic resonance imaging showing that, after dopaminergic
depletion, the dorsolateral striatum (DOLS) exhibited an early and transient
vasodilation cluster in response to specific forepaw stimulation. Activation of
DOLS NMDA receptors causes this vasodilation, protects dopaminergic fibers from
denervation, and counteracts motor deficits. The findings have clinical
implications for early detection and intervention in brain disorders such as
Parkinson’s disease.
