Martinboll1177

Motor Complexes (more than one motor pattern occurring in close proximity), High-Amplitude Propagating Pressure Waves followed by Simultaneous Pressure Waves (HAPW-SPWs) and HAPWs without SPWs are all associated with an increase in RSA and a decrease in SI. Hence RSA and SI may best reflect autonomic activity in the colon during these motor patterns as compared to RMSSD and PEP. SI and PEP do not measure identical sympathetic reactivity. The SPW, which is a very low amplitude pressure wave, did not significantly change the autonomic measures employed here. In conclusion, colonic motor patterns are associated with activity in the ANS which is reflected in autonomic measures of heart rate variability. These autonomic measures may serve as proxies for autonomic neural dysfunction in patients with colonic dysmotility. Copyright © 2020 Yuan, Ali, Mathewson, Sharma, Faiyaz, Tan, Parsons, Zhang, Milkova, Liu, Ratcliffe, Armstrong, Schmidt, Chen and Huizinga.Study Objectives Gentle rocking movements provided by a moving bed have been proposed as a promising non-pharmacological way to promote sleep. In rodents the sleep promoting effect of rocking movements depended on the peak acceleration (named "stimulation intensity") perceived by the vestibular system. We set out to verify previous reports on the sleep promoting effect of rocking movements and to investigate the importance of stimulation intensity in this process. Methods Side-to-side rocking movements along a pendulum trajectory with different peak accelerations (control 0 m/s2, low intensity 0.15 m/s2, medium intensity 0.25 m/s2, high intensity 0.35 m/s2) were provided for 45 min during an afternoon nap opportunity. Participants were assigned to a low intensity group (n = 10) experiencing control, low and medium intensity stimulation or a high intensity group (n = 12) experiencing control, medium and high intensity stimulation. Sleep and sleep-related memory performance were assessed using polysomnography aween the low and high intensity group no conclusion regarding the influence of stimulation intensity were possible. Thus, optimal stimulation settings in humans need further investigation. Copyright © 2020 van Sluijs, Rondei, Schluep, Jäger, Riener, Achermann and Wilhelm.Background Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with poor clinical outcome. Nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome serves a key role in inflammatory response, which may lead to endothelial cell injury and blood-brain barrier (BBB) disruption. Hydrogen (H2) is considered a neuroprotective antioxidant. This study was set out to explore whether hydrogen inhalation protects against SAH induced endothelial cell injury, BBB disruption, microthrombosis and vasospasm in rats. Methods One hundred eighty-two male SD rats were used for the study. SAH was induced by endovascular perforation. H2 at a concentration of 3.3% was inhaled beginning at 0.5 h after SAH for duration of 30, 60 or 120 min, followed by single administration or once daily administration for 3 days. The temporal expression of NLRP3 and ASC in the brain was determined, with the effect of hydrogen inhalation evaluated. In addition, brain water content, oxidative stress markers, inflammasome, apoptotic markers, microthrombosis, and vasospasm were evaluated at 24 or 72 h after SAH. Results The expression of NLRP3 and ASC were upregulated after SAH associated with elevated expression of MDA, 8-OHdG, 4-HNE, HO-1, TLR4/NF-κB, inflammatory and apoptotic makers. Hydrogen inhalation reduced the expression of these inflammatory and apoptotic makers in the vessels, brain edema, microthrombi formation, and vasospasm in rats with SAH relative to control. Hydrogen inhalation also improved short-term and long-term neurological recovery after SAH. Conclusion Hydrogen inhalation can ameliorate oxidative stress related endothelial cells injury in the brain and improve neurobehavioral outcomes in rats following SAH. Mechanistically, the above beneficial effects might be related to, at least in part, the inhibition of activation of ROS/NLRP3 axis. Copyright © 2020 Zhuang, Zuo, Sherchan, Wang, Yan and Liu.The cholinergic system enhances attention and gates plasticity, making it a major regulator of adult learning. With aging, however, progressive degeneration of the cholinergic system impairs both the acquisition of new skills and functional recovery following neurological injury. Although cognitive training and perceptual learning have been shown to enhance auditory cortical processing, their specific impact on the cholinergic system remains unknown. Here we used [18F]FEOBV, a positron emission tomography (PET) radioligand that selectively binds to the vesicular acetylcholine transporter (VAChT), as a proxy to assess whether training on a perceptual task results in increased cholinergic neurotransmission. We show for the first time that perceptual learning is associated with region-specific changes in cholinergic neurotransmission, as detected by [18F]FEOBV PET imaging and corroborated with immunohistochemistry. Copyright © 2020 Cisneros-Franco, Voss, Kang, Thomas, Côté, Ross, Gaudreau, Rudko, Rosa-Neto and de-Villers-Sidani.Blood brain barrier (BBB) conserves unique regulatory system to maintain barrier tightness while allowing adequate transport between neurovascular units. This mechanism possess a challenge for drug delivery, while abnormality may result in pathogenesis. Communication between vascular and neural system is mediated through paracellular and transcellular (transcytosis) pathway. Transcytosis itself showed dependency with various components, focusing on caveolae-mediated. Among several factors, intense communication between endothelial cells, pericytes, and astrocytes is the key for a normal development. Regulatory signaling pathway such as VEGF, Notch, S1P, PDGFβ, Ang/Tie, and TGF-β showed interaction with the transcytosis steps. Recent discoveries showed exploration of various factors which has been proven to interact with one of the process of transcytosis, either endocytosis, endosomal rearrangement, or exocytosis. As well as providing a hypothetical regulatory pathway between each factors, specifically miRNA, mechanical stress, various cytokines, physicochemical, basement membrane and junctions remodeling, and crosstalk between developmental regulatory pathways. Finally, various hypotheses and probable crosstalk between each factors will be expressed, to point out relevant research application (Drug therapy design and BBB-on-a-chip) and unexplored terrain. Copyright © 2020 Tjakra, Wang, Vania, Hou, Durkan, Wang and Wang.Up to 50% of traumatic brain injury (TBI) survivors demonstrate persisting and late-onset anxiety disorders indicative of limbic system dysregulation, yet the pathophysiology underlying the symptoms is unclear. We hypothesize that the development of TBI-induced anxiety-like behavior in an experimental model of TBI is mediated by changes in glutamate neurotransmission within the amygdala. Adult, male Sprague-Dawley rats underwent midline fluid percussion injury or sham surgery. Anxiety-like behavior was assessed at 7 and 28 days post-injury (DPI) followed by assessment of real-time glutamate neurotransmission in the basolateral amygdala (BLA) and central nucleus of the amygdala (CeA) using glutamate-selective microelectrode arrays. The expression of anxiety-like behavior at 28 DPI coincided with decreased evoked glutamate release and slower glutamate clearance in the CeA, not BLA. selleck inhibitor Numerous factors contribute to the changes in glutamate neurotransmission over time. In two additional animal cohorts, protein levels of glutamatergic transporters (Glt-1 and GLAST) and presynaptic modulators of glutamate release (mGluR2, TrkB, BDNF, and glucocorticoid receptors) were quantified using automated capillary western techniques at 28 DPI. Astrocytosis and microglial activation have been shown to drive maladaptive glutamate signaling and were histologically assessed over 28 DPI. Alterations in glutamate neurotransmission could not be explained by changes in protein levels for glutamate transporters, mGluR2 receptors, astrocytosis, and microglial activation. Presynaptic modulators, BDNF and TrkB, were significantly decreased at 28 DPI in the amygdala. Dysfunction in presynaptic regulation of glutamate neurotransmission may contribute to anxiety-related behavior and serve as a therapeutic target to improve circuit function. Copyright © 2020 Beitchman, Griffiths, Hur, Ogle, Bromberg, Morrison, Lifshitz, Adelson and Currier Thomas."Social mindfulness" refers to being thoughtful of others and considering their needs before making decisions, and can be characterized by low-cost and subtle gestures. The present study compared the behavioral and neural responses triggered by observing others' socially mindful/unmindful choices and how these responses were modulated by the social status of the agency. At the behavioral level, observing socially mindful choices made observers feel better, rate the actors as more likable, and behave more cooperatively than did observing socially unmindful choices. Analysis of event-related potentials in the brain revealed that compared with socially unmindful choices, mindful choices elicited more negative feedback-related negativity (FRN). Notably, while this effect of social mindfulness was only significant when the actor's social status was medium and high, it was undetectable when the actor's social status was low. These results demonstrate that the social mindfulness of others can be rapidly detected and processed, as reflected by FRN, even though it does not seem to receive further, more elaborate evaluation. These findings indicated that low-cost cooperative behaviors such as social mindfulness can also be detected and appreciated by our brain, which may result in better mood and more cooperative behaviors in the perceivers. Besides, the perception of social mindfulness is sensitive to important social information, such as social status. Copyright © 2020 Lu, Huang, Liao, Guan, Qi and Cui.The coordination of brain activity between disparate neural populations is highly dynamic. Investigations into intrinsic brain organization by evaluating dynamic resting-state functional connectivity (dRSFC) have attracted great attention in recent years. However, there are few dRSFC studies based on functional near-infrared spectroscopy (fNIRS) even though it has some advantages for studying the temporal evolution of brain function. In this research, we recruited 20 young adults and measured their resting-state brain fluctuations in several areas of the frontal, parietal, temporal, and occipital lobes using fNIRS-electroencephalography (EEG) simultaneous recording. Based on a sliding-window approach, we found that the variability of the dRSFC within any region of interest was significantly lower than the connections between region of interests but noticeably greater than the correlation between the channels with a short interoptode distance, which mainly consist of physiological fluctuations occurring in the superficial layers. Furthermore, based on a time-resolved k-means clustering analysis, the temporal evolution was extracted for three dominant functional networks. These networks were roughly consistent between different subject subgroups and in varying sliding time window lengths of 20, 30, and 60 s. Between these three functional networks, there were obvious time-varied and system-specific synchronous relationships. In addition, the oscillation of the frontal-parietal-temporal network showed significant correlation with the switching of one EEG microstate, a finding which is consistent with a previous functional MRI-EEG study. All this evidence implies the functional significance of fNIRS-dRSFC and demonstrates the feasibility of fNIRS for extracting the dominant functional networks based on RSFC dynamics. Copyright © 2020 Zhang and Zhu.