Rapid eye movement sleep disorder, narcolepsy, and cataplexy can be treated by suppressing glycinergic neurons in the ventral medial medulla.

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Rapid eye movement sleep disorder, narcolepsy, and cataplexy can be treated by suppressing glycinergic neurons in the ventral medial medulla thereby blocking the SLD-to-ventral medial medulla and reducing cataplexy episodes.
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The team identified a specific group of neurons as likely candidates in mice. The cells located in the ventral medial medulla receive input from an area called the sublaterodorsal tegmental nucleus, or SLD.
Sakurai said, “The anatomy of the neurons we found matched what we know. They were connected to neurons that control voluntary movements, but not those that control muscles in the eyes or internal organs. Importantly, they were inhibitory, meaning that they can prevent muscle movement when active.”
On blocking the input to these neurons, the mice began to move during their sleep similar to someone with REM sleep behavior disorder.
Narcolepsy is characterized by suddenly falling asleep at any time during the day, even in mid-sentence. Cataplexy is characterized by sudden loss of muscle tone and collapse; even if they are awake their muscles act as if they are in REM sleep. It was found that the special neurons were related to these two disorders.
Sakurai said, “We found that silencing the SLD-to-ventral medial medulla reduced the number of cataplexic bouts. The glycinergic neurons we have identified in the ventral medial medulla could be a good target for drug therapies for people with narcolepsy, cataplexy, or REM sleep behavior disorder. Future studies will have to examine how emotions, which are known to trigger cataplexy, can affect these neurons.”
Source-Medindia
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