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- W2894991744 abstract "Abstract Dopamine modulates striatal synaptic plasticity, a key substrate for action selection and procedural learning. Thus, characterizing the repertoire of activity-dependent plasticity in striatum and its dependence on dopamine is of crucial importance. We recently unraveled a striatal spike-timing-dependent long-term potentiation (tLTP) mediated by endocannabinoids (eCBs) and induced with few spikes (~5–15). Whether this eCB-tLTP interacts with the dopaminergic system remains to be investigated. Here, we report that eCB-tLTP is impaired in a rodent model of Parkinson’s disease and rescued by L-DOPA. Dopamine controls eCB-tLTP via dopamine type-2 receptors (D 2 R) located presynaptically in cortical terminals. Dopamine–endocannabinoid interactions via D 2 R are required for the emergence of tLTP in response to few coincident pre- and post-synaptic spikes and control eCB-plasticity by modulating the long-term potentiation (LTP)/depression (LTD) thresholds. While usually considered as a depressing synaptic function, our results show that eCBs in the presence of dopamine constitute a versatile system underlying bidirectional plasticity implicated in basal ganglia pathophysiology." @default.
- W2894991744 created "2018-10-12" @default.
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- W2894991744 date "2018-10-08" @default.
- W2894991744 modified "2023-09-26" @default.
- W2894991744 title "Dopamine–endocannabinoid interactions mediate spike-timing-dependent potentiation in the striatum" @default.
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- W2894991744 doi "https://doi.org/10.1038/s41467-018-06409-5" @default.
- W2894991744 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6175920" @default.
- W2894991744 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30297767" @default.
- W2894991744 hasPublicationYear "2018" @default.
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