par Yuan, Xiang-Shan;Wang, Lucun;Dong, Hui;Qu, Wei-Min;Yang, Su-Rong;Cherasse, Yoan;Lazarus, Michael;Schiffmann, Serge N.
;de Kerchove d'Exaerde, Alban
;Li, Rui-Xi;Huang, Zhi-Li
Référence eLife, 6, e29055
Publication Publié, 2017-10


Référence eLife, 6, e29055
Publication Publié, 2017-10
Article révisé par les pairs
Résumé : | Dysfunction of the striatum is frequently associated with sleep disturbances. However, its role in sleep-wake regulation has been paid little attention even though the striatum densely expresses adenosine A2A receptors (A2ARs), which are essential for adenosine-induced sleep. Here we showed that chemogenetic activation of A2AR neurons in specific subregions of the striatum induced a remarkable increase in non-rapid eye movement (NREM) sleep. Anatomical mapping and immunoelectron microscopy revealed that striatal A2AR neurons innervated the external globus pallidus (GPe) in a topographically organized manner and preferentially formed inhibitory synapses with GPe parvalbumin (PV) neurons. Moreover, lesions of GPe PV neurons abolished the sleep-promoting effect of striatal A2AR neurons. In addition, chemogenetic inhibition of striatal A2AR neurons led to a significant decrease of NREM sleep at active period, but not inactive period of mice. These findings reveal a prominent contribution of striatal A2AR neuron/GPe PV neuron circuit in sleep control. |