Abstract
Neuroglobin (Ngb) is a protein member of the globin family, expressed mainly in the central and peripheral nervous system. It is involved in the transport of oxygen in response to hypoxic/ischemic and oxidative stress-related insults. We recently showed that sleep deprivation reduces the number of Ngb-positive cells in brain areas related to sleep. However, it is poorly understood whether Ngb expression correlates with sleep occurrence. Here, we aimed to study if sleep recovery produced by 24 h of sleep deprivation restores the number of Ngb-positive cells in the pedunculopontine tegmentum (PPTg) and laterodorsal tegmentum (LDTg), brain areas related to sleep-wake regulation. Male Wistar rats were sleep-deprived for 24 h using the gentle handling method. After sleep deprivation, rats were allowed a sleep recovery for three or six hours. After sleep recovery, rats were euthanized, and their brains processed for Ngb immunohistochemistry. We found that a 3 h sleep recovery is enough to restore the number of Ngb-positive cells in all the analyzed areas. A similar result was observed after a 6 h sleep recovery. These results suggest that Ngb expression is sleep dependent. We suggest that Ngb expression is involved in preventing cell damage due to prolonged wakefulness.
Highlights
Neuroglobin (Ngb) is a monomeric globin with a high affinity for oxygen and located mainly in the neurons [1]
We have previously described that 24 h sleep deprivation in rats reduces the number of Ngb-positive cells in pedunculopontine tegmentum (PPTg) and LTDg, suggesting that sleep is necessary to Ngb expression in these nuclei
Our results show that the number of Ngb-positive cells into the PPTg and laterodorsal tegmentum (LDTg) is restored after sleep recovery produced by sleep deprivation
Summary
Neuroglobin (Ngb) is a monomeric globin with a high affinity for oxygen and located mainly in the neurons [1]. Ngb acts as an oxygen reservoir and is a scavenger of reactive oxygen species and nitric oxide [2]. It is reported that Ngb expression increases after neuronal hypoxia in vitro and after focal cerebral ischemia in vivo [3, 4]. The size of cerebral infarction after middle cerebral artery occlusion is reduced by 30% in transgenic mice overexpressing Ngb [5]. Ngb overexpression is protective against Alzheimer’s disease [6]. All these pieces of evidence suggest that Ngb has a protective role when low oxygen levels are present
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