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Parkinson's disease causes the most profound loss of the aldehyde dehydrogenase 1A1-positive (ALDH1A1+) nigrostriatal dopaminergic neuron (nDAN) subpopulation. The connectivity and functionality of ALDH1A1+ nDANs, however, remain poorly understood. Here, we show in rodent brains that ALDH1A1+ nDANs project predominantly to the rostral dorsal striatum, from which they also receive most monosynaptic inputs, indicating extensive reciprocal innervations with the striatal spiny projection neurons (SPNs). Functionally, genetic ablation of ALDH1A1+ nDANs causes severe impairments in motor skill learning, along with a reduction in high-speed walking. While dopamine replacement therapy accelerated walking speed, it failed to improve motor skill learning in ALDH1A1+ nDAN-ablated mice. Altogether, our study provides a comprehensive whole-brain connectivity map and reveals a key physiological function of ALDH1A1+ nDANs in motor skill acquisition, suggesting the motor learning processes require ALDH1A1+ nDANs to integrate diverse presynaptic inputs and supply dopamine with dynamic precision.
Pubmed ID: 31365862
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This unknown targets
View all literature mentionsThis polyclonal targets Green Fluorescent Protein (GFP)
View all literature mentionsThis polyclonal targets Human Aldehyde Dehydrogenase 1-A1 / ALDH1A1
View all literature mentionsThis polyclonal targets Tyrosine Hydroxylase (TH)
View all literature mentionsThis monoclonal targets Calbindin
View all literature mentionsThis polyclonal targets Oligodendrocute transcription factor 2
View all literature mentionsThis unknown targets Human ALDH1A1
View all literature mentionsThis polyclonal targets Mouse GFAP
View all literature mentionsThis polyclonal targets Synthetic rat MOR1 (384-398)
View all literature mentionsThis polyclonal targets RFP
View all literature mentionsThis monoclonal targets Dopamine Transporter N-terminus clone DAT-Nt
View all literature mentionsThis monoclonal targets Tyrosine Hydroxylase
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