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1.
Pathol Biol (Paris) ; 62(5): 252-61, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25110283

RESUMO

Traumatic brain injury (TBI) is a major health concern in industrialised countries. Sleep and wake disturbances are among the most persistent and disabling sequelae after TBI. Yet, despite the widespread complaints of post-TBI sleep and wake disturbances, studies on their etiology, pathophysiology, and treatments remain inconclusive. This narrative review aims to summarise the current state of knowledge regarding the nature of sleep and wake disturbances following TBI, both subjective and objective, spanning all levels of severity and phases post-injury. A second goal is to outline the various causes of post-TBI sleep-wake disturbances. Globally, although sleep-wake complaints are reported in all studies and across all levels of severity, consensus regarding the objective nature of these disturbances is not unanimous and varies widely across studies. In order to optimise recovery in TBI survivors, further studies are required to shed light on the complexity and heterogeneity of post-TBI sleep and wake disturbances, and to fully grasp the best timing and approach for intervention.


Assuntos
Lesões Encefálicas/complicações , Transtornos Cronobiológicos/etiologia , Transtornos Intrínsecos do Sono/etiologia , Traumatismos por Explosões/complicações , Traumatismos por Explosões/fisiopatologia , Dano Encefálico Crônico/etiologia , Dano Encefálico Crônico/fisiopatologia , Lesões Encefálicas/fisiopatologia , Transtornos Cronobiológicos/fisiopatologia , Terapia Cognitivo-Comportamental , Distúrbios do Sono por Sonolência Excessiva/etiologia , Distúrbios do Sono por Sonolência Excessiva/fisiopatologia , Doenças do Sistema Endócrino/etiologia , Doenças do Sistema Endócrino/fisiopatologia , Hospitalização , Humanos , Hipnóticos e Sedativos/uso terapêutico , Pacientes Internados/psicologia , Melatonina/uso terapêutico , Militares , Transtornos Intrínsecos do Sono/fisiopatologia , Transtornos Intrínsecos do Sono/reabilitação , Transtornos Intrínsecos do Sono/terapia , Guerra , Ferimentos não Penetrantes/complicações , Ferimentos não Penetrantes/fisiopatologia
2.
Genes Brain Behav ; 17(1): 82-92, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28425198

RESUMO

Circadian (∼24 h) rhythms of cellular network plasticity in the central circadian clock, the suprachiasmatic nucleus (SCN), have been described. The neuronal network in the SCN regulates photic resetting of the circadian clock as well as stability of the circadian system during both entrained and constant conditions. EphA4, a cell adhesion molecule regulating synaptic plasticity by controlling connections of neurons and astrocytes, is expressed in the SCN. To address whether EphA4 plays a role in circadian photoreception and influences the neuronal network of the SCN, we have analyzed circadian wheel-running behavior of EphA4 knockout (EphA4-/- ) mice under different light conditions and upon photic resetting, as well as their light-induced protein response in the SCN. EphA4-/- mice exhibited reduced wheel-running activity, longer endogenous periods under constant darkness and shorter periods under constant light conditions, suggesting an effect of EphA4 on SCN function. Moreover, EphA4-/- mice exhibited suppressed phase delays of their wheel-running activity following a light pulse during the beginning of the subjective night (CT15). Accordingly, light-induced c-FOS (FBJ murine osteosarcoma viral oncogene homolog) expression was diminished. Our results suggest a circadian role for EphA4 in the SCN neuronal network, affecting the circadian system and contributing to the circadian response to light.


Assuntos
Relógios Circadianos/fisiologia , Receptor EphA4/fisiologia , Núcleo Supraquiasmático/fisiologia , Animais , Adesão Celular/fisiologia , Relógios Circadianos/genética , Ritmo Circadiano/fisiologia , Feminino , Masculino , Camundongos , Camundongos Knockout , Atividade Motora/fisiologia , Neurônios/metabolismo , Estimulação Luminosa , Condicionamento Físico Animal , Proteínas Proto-Oncogênicas c-fos/metabolismo , Receptor EphA4/genética , Receptor EphA4/metabolismo , Núcleo Supraquiasmático/metabolismo
3.
Neuroscience ; 289: 242-50, 2015 Mar 19.
Artigo em Inglês | MEDLINE | ID: mdl-25595979

RESUMO

Neuroligin 1 (NLGN1) is a postsynaptic adhesion molecule that determines N-methyl-d-aspartate receptor (NMDAR) function and cellular localization. Our recent work showed that Nlgn1 knockout (KO) mice cannot sustain neuronal activity occurring during wakefulness for a prolonged period of time. Since NMDAR-dependent neuronal activity drives an important vascular response, we used multispectral optical imaging to determine if the hemodynamic response to neuronal stimulation is modified in Nlgn1 KO mice. We observed that Nlgn1 KO mice show a 10% lower response rate to forepaw electrical stimulation compared to wild-type (WT) and heterozygote (HET) littermates on both the contra- and ipsilateral sides of the somatosensory cortex. Moreover, Nlgn1 mutant mice showed an earlier oxyhemoglobin peak response that tended to return to baseline faster than in WT mice. Analysis of the time course of the hemodynamic response also showed that HET mice express a faster dynamics of cerebrovascular response in comparison to WT. Taken together, these data are indicative of an altered immediate response of the brain to peripheral stimulation in Nlgn1 KO mice, and suggest a role for NLGN1 in the regulation of cerebrovascular responses.


Assuntos
Moléculas de Adesão Celular Neuronais/deficiência , Circulação Cerebrovascular/fisiologia , Hemodinâmica/fisiologia , Córtex Somatossensorial/fisiopatologia , Animais , Moléculas de Adesão Celular Neuronais/genética , Estimulação Elétrica , Membro Anterior/fisiologia , Masculino , Camundongos Knockout , Músculo Esquelético/fisiologia , Imagem Óptica , Oxiemoglobinas/metabolismo , Propriocepção , Córtex Somatossensorial/irrigação sanguínea , Fatores de Tempo
4.
Transl Psychiatry ; 4: e347, 2014 Jan 21.
Artigo em Inglês | MEDLINE | ID: mdl-24448209

RESUMO

Sleep is critical for normal brain function and mental health. However, the molecular mechanisms mediating the impact of sleep loss on both cognition and the sleep electroencephalogram remain mostly unknown. Acute sleep loss impacts brain gene expression broadly. These data contributed to current hypotheses regarding the role for sleep in metabolism, synaptic plasticity and neuroprotection. These changes in gene expression likely underlie increased sleep intensity following sleep deprivation (SD). Here we tested the hypothesis that epigenetic mechanisms coordinate the gene expression response driven by SD. We found that SD altered the cortical genome-wide distribution of two major epigenetic marks: DNA methylation and hydroxymethylation. DNA methylation differences were enriched in gene pathways involved in neuritogenesis and synaptic plasticity, whereas large changes (>4000 sites) in hydroxymethylation where observed in genes linked to cytoskeleton, signaling and neurotransmission, which closely matches SD-dependent changes in the transcriptome. Moreover, this epigenetic remodeling applied to elements previously linked to sleep need (for example, Arc and Egr1) and synaptic partners of Neuroligin-1 (Nlgn1; for example, Dlg4, Nrxn1 and Nlgn3), which we recently identified as a regulator of sleep intensity following SD. We show here that Nlgn1 mutant mice display an enhanced slow-wave slope during non-rapid eye movement sleep following SD but this mutation does not affect SD-dependent changes in gene expression, suggesting that the Nlgn pathway acts downstream to mechanisms triggering gene expression changes in SD. These data reveal that acute SD reprograms the epigenetic landscape, providing a unique molecular route by which sleep can impact brain function and health.


Assuntos
Córtex Cerebral/metabolismo , Metilação de DNA/fisiologia , Genoma/genética , Plasticidade Neuronal/genética , Privação do Sono/metabolismo , Transcriptoma/genética , Animais , Moléculas de Adesão Celular Neuronais/genética , Córtex Cerebral/fisiopatologia , Metilação de DNA/genética , Eletroencefalografia , Epigênese Genética/genética , Epigênese Genética/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Privação do Sono/fisiopatologia , Fases do Sono/genética , Fases do Sono/fisiologia
5.
J Sleep Res ; 15(2): 162-6, 2006 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-16704571

RESUMO

Morningness-eveningness has been associated with the entrained circadian phase. However, we recently identified morning and evening types having similar circadian phases. In this paper, we compared parameters of slow-wave activity (SWA) decay in non-rapid-eye-movement (NREM) sleep between these two subgroups to test the hypothesis that differences in the dynamics of nocturnal homeostatic sleep pressure could explain differences in sleep timing preference. Twelve morning-type subjects and 12 evening-type subjects with evening types (aged 19-34 years) selected using the Morningness-Eveningness Questionnaire were further classified according to the phase of their dim light melatonin onset (DLMO). The six morning types with the earliest DLMO were compared to the six evening types with the latest DLMO ('extreme' phases), and the six morning types with the latest DLMO were compared to the six evening types with the earliest DLMO ('intermediate' phases). Subjects slept according to their preferred sleep schedule. Spectral activity in four midline derivations (Fz, Cz, Pz, Oz) was calculated in NREM sleep and an exponential decay function was applied on SWA data averaged per sleep cycle. In the subjects with intermediate circadian phases, both initial level and decay rate of SWA in Fz were significantly higher in morning than in evening types. No difference appeared between chronotypes of extreme circadian phases. There was no correlation between individual estimates of SWA decay and DLMO. These results support the hypothesis that chronotype can originate from differences in the dissipation of sleep pressure and that homeostatic and circadian processes influence the sleep schedule preference independently.


Assuntos
Ritmo Circadiano/fisiologia , Homeostase/fisiologia , Sono/fisiologia , Adulto , Idoso , Envelhecimento/fisiologia , Feminino , Hábitos , Humanos , Masculino , Melatonina/sangue , Pessoa de Meia-Idade , Fases do Sono/fisiologia , Inquéritos e Questionários
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