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Article Abstract
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 receptors (ARs), which are essential for adenosine-induced sleep. Here we showed that chemogenetic activation of AR 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 AR 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 AR neurons. In addition, chemogenetic inhibition of striatal AR 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 AR neuron/GPe PV neuron circuit in sleep control.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5655138 | PMC |
| http://dx.doi.org/10.7554/eLife.29055 | DOI Listing |
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