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

par Xu, Hao;Perez, Sylvie;Cornil, Amandine ;Detraux, Bérangère ;Prokin, Ilya;Cui, Yihui;Degos, Bertrand;Berry, Hugues;de Kerchove d'Exaerde, Alban ;Venance, Laurent
Référence Nature communications, 9, 1, 4118
Publication Publié, 2018-12-01

Article révisé par les pairs

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Résumé :

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.