[HTML][HTML] Role of REM sleep, melanin concentrating hormone and orexin/hypocretin systems in the sleep deprivation pre-ischemia
PloS one, 2017•journals.plos.org
Study Objectives Sleep reduction after stroke is linked to poor recovery in patients.
Conversely, a neuroprotective effect is observed in animals subjected to acute sleep
deprivation (SD) before ischemia. This neuroprotection is associated with an increase of the
sleep, melanin concentrating hormone (MCH) and orexin/hypocretin (OX) systems. This
study aims to 1) assess the relationship between sleep and recovery; 2) test the association
between MCH and OX systems with the pathological mechanisms of stroke. Methods …
Conversely, a neuroprotective effect is observed in animals subjected to acute sleep
deprivation (SD) before ischemia. This neuroprotection is associated with an increase of the
sleep, melanin concentrating hormone (MCH) and orexin/hypocretin (OX) systems. This
study aims to 1) assess the relationship between sleep and recovery; 2) test the association
between MCH and OX systems with the pathological mechanisms of stroke. Methods …
Study Objectives
Sleep reduction after stroke is linked to poor recovery in patients. Conversely, a neuroprotective effect is observed in animals subjected to acute sleep deprivation (SD) before ischemia. This neuroprotection is associated with an increase of the sleep, melanin concentrating hormone (MCH) and orexin/hypocretin (OX) systems. This study aims to 1) assess the relationship between sleep and recovery; 2) test the association between MCH and OX systems with the pathological mechanisms of stroke.
Methods
Sprague-Dawley rats were assigned to four experimental groups: (i) SD_IS: SD performed before ischemia; (ii) IS: ischemia; (iii) SD_Sham: SD performed before sham surgery; (iv) Sham: sham surgery. EEG and EMG were recorded. The time-course of the MCH and OX gene expression was measured at 4, 12, 24 hours and 3, 4, 7 days following ischemic surgery by qRT-PCR.
Results
A reduction of infarct volume was observed in the SD_IS group, which correlated with an increase of REM sleep observed during the acute phase of stroke. Conversely, the IS group showed a reduction of REM sleep. Furthermore, ischemia induces an increase of MCH and OX systems during the acute phase of stroke, although, both systems were still increased for a long period of time only in the SD_IS group.
Conclusions
Our data indicates that REM sleep may be involved in the neuroprotective effect of SD pre-ischemia, and that both MCH and OX systems were increased during the acute phase of stroke. Future studies should assess the role of REM sleep as a prognostic marker, and test MCH and OXA agonists as new treatment options in the acute phase of stroke.
PLOS