Dopamine–endocannabinoid interactions mediate spike-timing-dependent potentiation in the striatum

Hao Xu, Sylvie Perez, Amandine Cornil, Bérangère Detraux, Ilya Prokin, Yihui Cui, Bertrand Degos, Hugues Berry, Alban Kerchove d’Exaerde and Laurent Venance ()
Additional contact information
Hao Xu: Labex Memolife
Sylvie Perez: Labex Memolife
Amandine Cornil: ULB Neuroscience Institute
Bérangère Detraux: ULB Neuroscience Institute
Ilya Prokin: INRIA
Yihui Cui: Labex Memolife
Bertrand Degos: Labex Memolife
Hugues Berry: INRIA
Alban Kerchove d’Exaerde: ULB Neuroscience Institute
Laurent Venance: Labex Memolife

Nature Communications, 2018, vol. 9, issue 1, 1-18

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 (D2R) located presynaptically in cortical terminals. Dopamine–endocannabinoid interactions via D2R 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.

Date: 2018
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DOI: 10.1038/s41467-018-06409-5

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