Neurobiology of Sleep and Circadian Rhythms最新文献

The response to a zeitgeber, particularly the light/dark cycle, may vary phenotypically. Phenotypic plasticity can be defined as the ability of one genome to express different phenotypes in response to environmental variation. In this opinion paper, we present some evidence that one of the most prominent effects of the introduction of electric light to the everyday life of humans is a significant increase in phenotypic plasticity and differences in interindividual phases of entrainment. We propose that the healthy limits of phenotypic plasticity have been surpassed in contemporary society.

Circadian rhythms evolved within single cell organisms and serve to regulate rest-activity cycles in most single-cell and multiple-cell organisms. In contrast, sleep is a network emergent property found in animals with a nervous system. Rhythms and sleep are much entangled involving shared regulatory molecules such as adenosine, ATP, cytokines, neurotrophins, and nitric oxide. These molecules are activity-dependent and act locally to initiate regulatory events involved in rhythms, sleep, and plasticity.

Traumatic brain injury (TBI) is a complex and costly worldwide phenomenon that can lead to many negative health outcomes including disrupted circadian function. There is a bidirectional relationship between the immune system and the circadian system, with mammalian coordination of physiological activities being controlled by the primary circadian pacemaker in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN receives light information from the external environment and in turn synchronizes rhythms throughout the brain and body. The SCN is capable of endogenous self-sustained oscillatory activity through an intricate clock gene negative feedback loop. Following TBI, the response of the immune system can become prolonged and pathophysiological. This detrimental response not only occurs in the brain, but also within the periphery, where a leaky blood brain barrier can permit further infiltration of immune and inflammatory factors. The prolonged and pathological immune response that follows TBI can have deleterious effects on clock gene cycling and circadian function not only in the SCN, but also in other rhythmic areas throughout the body. This could bring about a state of circadian desynchrony where different rhythmic structures are no longer working together to promote optimal physiological function. There are many parallels between the negative symptomology associated with circadian desynchrony and TBI. This review discusses the significant contributions of an immune-disrupted circadian system on the negative symptomology following TBI. The implications of TBI symptomology as a disorder of circadian desynchrony are discussed.

The Ts65Dn mouse is a well-studied model of trisomy 21, Down syndrome. This mouse strain has severe learning disability as measured by several rodent learning tests that depend on hippocampal spatial memory function. Hippocampal long-term potentiation (LTP) is deficient in these mice. Short-term daily treatment with low-dose GABA receptor antagonists rescue spatial learning and LTP in Ts65Dn mice leading to the hypothesis that the learning disability is due to GABAergic over-inhibition of hippocampal circuits. The fact that the GABA receptor antagonists were only effective if delivered during the daily light phase suggested that the source of the excess GABA was controlled directly or indirectly by the circadian system. The central circadian pacemaker of mammals is the suprachiasmatic nucleus (SCN), which is largely a GABAergic nucleus. In this study we investigated whether elimination of the SCN in Ts65Dn mice would restore their ability to form recognition memories as tested by the novel object recognition (NOR) task. Full, but not partial lesions of the SCN of Ts65Dn mice normalized their ability to perform on the NOR test. These results suggest that the circadian system modulates neuroplasticity over the time frame involved in the process of consolidation of recognition memories.

Background

Multiple sclerosis (MS) is an autoimmune disease of the nervous system which appears with de-myelination of the central nervous system. Sleep disorder and fatigue are very common in MS patients and are part of the main debilitating factors in patients. The present study was conducted to survey sleep quality and fatigue in MS patients.

Methods

A descriptive-analytical study was conducted on 87 MS patients, who were referred to the Kermanshah MS Center in 2017. Data collection tools include a demographics form, fatigue severity scale, and Pittsburg sleep quality inventory. The questionnaires were self-reporting. The collected data was analyzed in SPSS23.

Results

The mean age of the participants was 35.50±9.25 years and the majority of the participants were married (54; 62.1%). Quality of sleep was related to family history of MS and history of using medications (antidepressants like tricyclics, MAOIs, SSRIs, and SNRIs and anxiety drugs such as diazepam, oxazepam, and alprazolam (p < 0.05). Moreover, there was a significant relationship between length of sleep and history of using medicines (p < 0.05). Finally, the results showed that there was a strong statistical relationship between performance during the day and fatigue (p < 0.05).

Conclusions

The results recommend holding relaxation and exercise courses by nurses to ease fatigue in MS patients. Clinics can also play a more effective role by being more supportive and holding more efficient training programs. The program is taught by the researchers.

Trial registration

This study was carried out following the permission from Ethics Committee, Department of Research and Technology, Kermanshah University of Medical Sciences (approval number: KUMS.REC.1395.680).