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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 A 2A  receptors (A 2A Rs), which are essential for adenosine-induced sleep. Here we showed that chemogenetic activation of A 2A R 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 A 2A R 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 A 2A R neurons. In addition, chemogenetic inhibition of striatal A 2A R 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 A 2A R neuron/GPe PV neuron circuit in sleep control.

Striatal adenosine A 2A receptor neurons control active-period sleep via parvalbumin neurons in external globus pallidus