Rapid eye movement sleep deprivation impairs neuronal plasticity and reduces hippocampal neuronal arborization in male albino rats: Noradrenaline is involved in the process

Abstract

Rapid eye movement sleep (REMS) favors brain development and memory, while it is decreased in neurodegenerative diseases. REMS deprivation (REMSD) affects several physiological processes including memory consolidation; however, its detailed mechanism(s) of action was unknown. REMS reduces, while REMSD elevates noradrenaline (NA) level in the brain; the latter induces several deficiencies and disorders, including changes in neuronal cytomorphology and apoptosis. Therefore, we proposed that REMS‐ and REMSD‐associated modulation of NA level might affect neuronal plasticity and affect brain functions. Male albino rats were REMS deprived by flower‐pot method for 6 days, and its effects were compared with home cage and large platform controls as well as post‐REMSD recovered and REMS‐deprived prazosin (α1‐adrenoceptor antagonist)‐treated rats. We observed that REMSD reduced CA1 and CA3 neuronal dendritic length, branching, arborization, and spine density, while length of active zone and expressions of pre‐ as well as post‐synaptic proteins were increased as compared to controls; interestingly, prazosin prevented most of the effects in vivo. Studies on primary culture of neurons from chick embryo brain confirmed that NA at lower concentration(s) induced neuronal branching and arborization, while higher doses were destructive. The findings support our contention that REMSD adversely affects neuronal plasticity, branching, and synaptic scaffold, which explain the underlying cytoarchitectural basis of REMSD‐associated patho‐physio‐behavioral changes. Consolidation of findings of this study along with that of our previous reports suggest that the neuronal disintegration could be due to either withdrawal of direct protective and proliferative role of low dose of NA or indirect effect of high dose of NA or both.

CX3C-chemokine receptor 1 modulates cognitive dysfunction induced by sleep deprivation

“…Our data showed that CX3CR1 −/− SD mice had more synapses and better cognitive function. Giri et al [ 47 ] proved that SD reduced neuronal dendritic length, branching, arborization, and spine density in hippocampus, which is in line with our results. It was also found that compared with the waking state, the sleeping state is more conducive to the correct implementation of synaptic pruning.…”

Alzheimer’s Disease, Sleep Disordered Breathing, and Microglia: Puzzling out a Common Link

“…Given that sleep disturbances are common in AD, and that SDB is associated with exacerbated AD related pathological changes, we suggest that SDB enhances and/or accelerates AD pathology. Patients with severe SDB exhibit hippocampal atrophy, as is observed in AD [ 30 , 147 , 148 , 149 ], and rats with reduced REM sleep showed reduced neuronal arborization in the hippocampus [ 150 ] and increased neuronal apoptosis in the locus coeruleus, laterodorsal tegmentum, pedunculopontine tegmentum, and medial preoptic area [ 140 , 151 ]. Rodents exposed to chronic sleep deprivation have decreased volume in brainstem respiratory nuclei (NTS and parabrachial nucleus) [ 152 ], in the medial prefrontal cortex [ 153 ], in the dorsal and CA2/CA3 hippocampal regions [ 154 ], and in the CA1 and dentate gyrus hippocampal regions [ 155 ], indicating a detrimental effect on key brain regions involved in cognition and autonomic nervous system function.…”

Electroacupuncture Enhances Cognitive Deficits in a Rat Model of Rapid Eye Movement Sleep Deprivation via Targeting MiR-132

“…e hippocampus becomes an essential part of the nervous system related to learning and memory [7][8][9]. e impact of REMSD on learning and memory often re ects changes in the synaptic plasticity of hippocampal neurons [10][11][12][13][14]. Additionally, long-term SD increases the risk of insomnia and dementia.…”