Synaptotagmin-1-dependent phasic axonal dopamine release is dispensable for basic motor behaviors in mice.

ABSTRACT: In Parkinson's disease (PD), motor dysfunctions only become apparent after extensive loss of DA innervation. This resilience has been hypothesized to be due to the ability of many motor behaviors to be sustained through a diffuse basal tone of DA; but experimental evidence for this is limited. Here we show that conditional deletion of the calcium sensor synaptotagmin-1 (Syt1) in DA neurons (Syt1 cKO^DA mice) abrogates most activity-dependent axonal DA release in the striatum and mesencephalon, leaving somatodendritic (STD) DA release intact. Strikingly, Syt1 cKO^DA mice showed intact performance in multiple unconditioned DA-dependent motor tasks and even in a task evaluating conditioned motivation for food. Considering that basal extracellular DA levels in the striatum

SUBMITTER: Delignat-Lavaud B 

PROVIDER: S-EPMC10336101 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature