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Chronic partial sleep deprivation reduces brain sensitivity to glutamate N ‐methyl‐ d ‐aspartate receptor‐mediated neurotoxicity
Author(s) -
NOVATI ARIANNA,
HULSHOF HENRIËTTE J.,
GRANIC IVICA,
MEERLO PETER
Publication year - 2012
Publication title -
journal of sleep research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.297
H-Index - 117
eISSN - 1365-2869
pISSN - 0962-1105
DOI - 10.1111/j.1365-2869.2011.00932.x
Subject(s) - excitotoxicity , neurotoxicity , neuroscience , nmda receptor , glutamate receptor , cholinergic , sleep deprivation , neurodegeneration , endocrinology , medicine , sleep (system call) , nucleus basalis , cholinergic neuron , psychology , receptor , circadian rhythm , toxicity , disease , computer science , operating system
Summary It has been hypothesized that insufficient sleep may compromise neuronal function and contribute to neurodegenerative processes. While sleep loss by itself may not lead to cell death directly, it may affect the sensitivity to a subsequent neurodegenerative insult. Here we examined the effects of chronic sleep restriction (SR) on the vulnerability of the brain to N ‐methyl‐ d ‐aspartate (NMDA)‐induced excitotoxicity. Animals were kept awake 20 h per day and were only allowed to rest during the first 4 h of the light phase, i.e. their normal circadian resting phase. After 30 days of SR all rats received a unilateral injection with a neurotoxic dose of NMDA into the nucleus basalis magnocellularis (NBM). Brains were collected for assessment of damage. In the intact non‐injected hemisphere, the number of cholinergic cells in the NBM and the density of their projections in the cortex were not affected by SR. In the injected hemisphere, NMDA caused a significant loss of cholinergic NBM cells and cortical fibres in all animals. However, the loss of cholinergic cells was attenuated in the SR group as compared with the controls. These data suggest that, if anything, SR reduces the sensitivity to a subsequent excitotoxic insult. Chronic SR may constitute a mild threat to the brain that does not lead to neurodegeneration by itself but prepares the brain for subsequent neurotoxic challenges. These results do not support the hypothesis that sleep loss increases the sensitivity to neurodegenerative processes.