Microglial Regulation of Sleep and Wakefulness.

Sleep serves a multitude of roles in brain maturation and function. Although the neural networks involved in sleep regulation have been extensively characterized, it is increasingly recognized that neurons are not the sole conductor orchestrating the rhythmic cycle of sleep and wakefulness. In the central nervous system, microglia have emerged as an important player in sleep regulation.

Microglia modulate sleep/wakefulness under baseline conditions and under acute social defeat stress in adult mice.

Although sleep is tightly regulated by multiple neuronal circuits in the brain, nonneuronal cells such as glial cells have been increasingly recognized as crucial sleep regulators. Recent studies have shown that microglia may act to maintain wakefulness. Here, we investigated the possible involvement of microglia in the regulation of sleep quantity and quality under baseline and stress conditions through electroencephalography (EEG)/electromyography (EMG) recordings, and by employing pharmacological methods to eliminate microglial cells in the adult mouse brain.

Microglia and the Aging Brain: Are Geriatric Microglia Linked to Poor Sleep Quality?

Poor sleep quality and disrupted circadian behavior are a normal part of aging and include excessive daytime sleepiness, increased sleep fragmentation, and decreased total sleep time and sleep quality. Although the neuronal decline underlying the cellular mechanism of poor sleep has been extensively investigated, brain function is not fully dependent on neurons. A recent antemortem autographic study and postmortem RNA sequencing and immunohistochemical studies on aged human brain have investigated the relationship between sleep fragmentation and activation of the innate immune cells of the brain, microglia.

Synaptic elimination by microglia and disturbed higher brain functions.

Microglial cells in normal mature brains have long been considered to be cells that are resting until pathological events take place, activating the microglial cells. However, it is currently well known that the microglia that have resting ramified morphology in normal mature brains move actively in the brain parenchyma and phagocytose synapses, thus forming and maintaining neural circuits. This review summarizes recent findings on the roles of microglia in mature brains, with special reference to phagocytosis of synapses and higher brain functions.

Lister hooded rats as a novel animal model of attention-deficit/hyperactivity disorder.

Appropriate animal models are necessary to determine the molecular and cellular mechanisms underlying attention-deficit/hyperactivity disorder (ADHD). This study used a battery of behavioral tests to compare Lister hooded rats (LHRs), an old outbred strain frequently used for autistic epilepsy research, with Wistar rats and spontaneously hypertensive rats (SHRs), a commonly used ADHD model. The open field, elevated plus maze, light/dark box, and drop tests demonstrated that LHRs were the most hyperactive animals and displayed the most inattentive- and impulsive-like behaviors, which are characteristics of ADHD.

Aggravating effects of treadmill exercises during the early-onset period in a rat traumatic brain injury model: When should rehabilitation exercises be initiated?

Physical exercise is one of the best interventions for improving traumatic brain injury (TBI) outcomes. However, an argument has been raised regarding the timing at which physical exercise should be initiated. In this study, male Wistar rats were subjected to stab wounding of the right hemisphere to develop a TBI model and were forced to walk once on a treadmill at a 5-m/min pace at 24 h or 48 h after TBI for 10 min.

Phagocytic elimination of synapses by microglia during sleep.

Synaptic strength reduces during sleep, but the underlying mechanisms of this process are unclear. This study showed reduction of synaptic proteins in rat prefrontal cortex (PFC) at AM7 or Zeitgeber Time (ZT0), when the light phase or sleeping period for rats started. At this time point, microglia were weakly activated, displaying larger and more granular somata with increased CD11b expression compared with those at ZT12, as revealed by flow cytometry.

Behavioral tests predicting striatal dopamine level in a rat hemi-Parkinson's disease model.

Parkinson's disease (PD) is a frequent neurodegenerative disease causing bradykinesia, tremor, muscle rigidity and postural instability. Although its main pathology is progressive dopaminergic (DArgic) neuron loss in the substantia nigra, motor deficits are thought not to become apparent until most DArgic neurons are lost, probably due to compensatory mechanisms that overcome the decline of DA level in the striatum. Even in animal PD models, it is difficult to detect motor deficits when most DArgic neurons are functional.

Microglia may compensate for dopaminergic neuron loss in experimental Parkinsonism through selective elimination of glutamatergic synapses from the subthalamic nucleus.

Parkinson's disease (PD) symptoms do not become apparent until most dopaminergic neurons in the substantia nigra pars compacta (SNc) degenerate, suggesting that compensatory mechanisms play a role. Here, we investigated the compensatory involvement of activated microglia in the SN pars reticulata (SNr) and the globus pallidus (GP) in a 6-hydroxydopamine-induced rat hemiparkinsonism model. Activated microglia accumulated more markedly in the SNr than in the SNc in the model.

Hyperphosphatasemia in leiomyosarcoma of the uterus: Two case reports and a literature review.

Some tumors are known to produce alkaline phosphatase (ALP). Seven cases of uterine leiomyosarcoma were identified from the clinical records of Sakai City Medical Center from January 2006 to December 2014. Patients' ages ranged from 47 to 75 years (median: 58).

The hypnotic bromovalerylurea ameliorates 6-hydroxydopamine-induced dopaminergic neuron loss while suppressing expression of interferon regulatory factors by microglia.

The low molecular weight organic compound bromovalerylurea (BU) has long been used as a hypnotic/sedative. In the present study, we found that BU suppressed mRNA expression of proinflammatory factors and nitric oxide release in lipopolysaccharide (LPS)-treated rat primary microglial cell cultures. BU prevented neuronal degeneration in LPS-treated neuron-microglia cocultures.

Treadmill exercise ameliorates ischemia-induced brain edema while suppressing Na⁺/H⁺ exchanger 1 expression.

Exercise may be one of the most effective and sound therapies for stroke; however, the mechanisms underlying the curative effects remain unclear. In this study, the effects of forced treadmill exercise with electric shock on ischemic brain edema were investigated. Wistar rats were subjected to transient (90 min) middle cerebral artery occlusion (tMCAO).

[A case of gastric cancer with bilateral ovarian metastasis after gastrectomy performed ovarian resection].

The patient was a 51-year-old female, who underwent radical surgery for cancer of remnant stomach in May 2006 (f-T4N0M0P0H0CY0, por 2, Stage IIIA, Cur B). Bilateral ovarian resection was performed in March 2009 for bilateral ovarian metastasis, so called "Krukenberg tumor" with peritoneal dissemination detected with CT scan after one-year adjuvant chemotherapy with S-1 (80 mg/m2, 4 weeks on and 2 weeks off). As of June 2010, she is alive and maintain her status quo after 6 courses of S-1 plus CDDP combination therapy (S-1 80 mg/m2, 3 weeks on, CDDP 60 mg/m2, started at day 8, ended 35 days later) followed by S-1 for residual peritoneal dissemination detected at operation.