Journal of Experimental Neuroscience最新文献

Movements cause changes in cortical rhythms emanating from the sensorimotor area. It is known that alpha and beta brainwaves take an important role of motor activity and motor imagery. Besides, theta rhythm is considered to carry substantial information about movement initiation and execution. In this study, effect of theta brainwave on movement detection was investigated in four-right handed participants who performed extensions with fingers of right hand using electroencephalography (EEG). Movement and rest epochs from continuous EEG record were extracted using muscle signals. Channels located over sensorimotor area were selected and referenced according to common average and Laplacian reference methods. Power spectral density function was used to display existence of theta band in frequency domain. To analyze theta, alpha and beta rhythms of the epochs individually and together, we filtered them to their interval range with Butterworth bandpass infinite filter before feature extraction and classification stages. Then, principal component analysis and Hjorth parameters were chosen to extract efficient features in the study aiming to investigate the effect of theta brainwaves on finger movement detection. According to classification accuracies using support vector machine classifier, alpha, beta, theta rhythms and also their different combinations were compared with each other. The performance of the epochs including alpha, beta and theta rhythms were the best and they were classified ~2% to 4% higher value in accuracy than the signals including only alpha and beta rhythms. According to this, it has proved that theta brainwave takes a role and makes contribution to motor activity.

Changes in chromatin and epigenetic modifications have been associated with aging and aging-associated neurodegenerative diseases, although the causal relationship between these changes and disease-related pathology has been unclear. Recent studies have now made direct connections between neurodegeneration-associated proteins and derepression of repetitive element transcription due to changes in heterochromatin. We suggest that this derepression leads to an increased accumulation of intracellular double-stranded RNA (dsRNA), with an attendant induction of innate immune responses that contribute to the neuroinflammation found in essentially all age-associated neurodegenerative diseases.

In the last decade or more, there have been reports suggesting a rise in the incidence of stroke in young adults. Presently, it appears that the risk factors associated with the cause of stroke in young adults remain relatively constant across different geographic regions of the world. Moreover, the endogenous rhythm of a neurohormone such as melatonin is known to play certain roles in the modulation of some of the risk factors that are associated with an increased risk of stroke in young people. Whereas animal studies have shown that melatonin plays diverse roles in stroke, only a limited number of human studies examined the roles of exogenous melatonin administration in the prevention of stroke, attenuation of neuronal damage, and improving outcome or well-being in stroke patients. In this review, first we summarize existing studies of stroke in the young adult and then provide insights on melatonin and stroke. Thereafter, we discuss the role of melatonin in models of stroke and how melatonin can be regulated to prevent stroke in young adults. Finally, we highlight the possible roles of melatonin in the management and outcome of stroke, especially in the young adult stroke population.

Traumatic brain injury is a major cause of death and disability in adults. This study investigated the effect of oral administration of amantadine on the neurological outcomes of patients with diffuse axonal injury (DAI) in the intensive care unit (ICU). This double-blind clinical trial was conducted in the ICU of Imam Hospital in Urmia. Patients with DAI were intubated and received mechanical ventilation in the ICU. They were divided into 2 groups: patients receiving amantadine (A) and placebo (P). The acquired data were analyzed using SPSS, P < .05 significant level. Findings showed no significant difference between the 2 groups in age and sex. There was no significant difference between the mean Glasgow Coma Scale (GCS) at the time of admission and discharge, and the mean Glasgow Outcome Scale (GOS) of the patients in 2 groups. No significant difference was observed in the duration of mechanical ventilation, hospitalization, and mortality in both groups (P > .05) in ICU. However, there was a significant difference between the mean GCS at the time of admission and discharge and death. Also, significant differences existed between the mean GOS in discharged and deceased patients (P = .001). This study showed no significant difference between the mean GCS at the time of admission and discharge and the mean GOS of the discharged patients and the mortality rate in the 2 groups. However, there were clear statistical differences between these variables in discharged and deceased patients. It is recommended that further studies are conducted with a larger sample size.

Multiple sclerosis, and its animal model-experimental autoimmune encephalomyelitis (EAE), is a demyelinating disease causing motor and sensory dysfunction, as well as behavioral comorbidities. In exploring possible functional changes underlying behavioral comorbidities in EAE, we observed increased excitatory drive onto the major cells of the basolateral amygdala. This was associated with increased numbers of dendritic spines. An unexpected finding was that microglial cells at this time were in a "deactivated" state, and further studies suggested that the microglial deactivation was responsible for the increased excitatory drive. This is the first report of microglial deactivation in an inflammatory disease and raises many questions as to the underlying mechanisms and functional relevance.

Background/main objectives: No effective strategy exists to treat the well-recognized, devastating impact of traumatic brain injury (TBI) and chronic traumatic encephalopathy (CTE), which is the brain degeneration likely caused by repeated head trauma. The goals of this project were (1) to study the effects of single and recurrent TBI (rTBI) on Drosophila melanogaster's (a) life span, (b) response to sedatives, and (c) behavioral responses to light and gravity and (2) to determine whether therapeutic hypothermia can mitigate the deleterious effects of TBI.

Methods: Five experimental groups were created: (1) control, (2) single TBI or concussion; (3) concussion + hypothermia, (4) rTBI, and (5) rTBI + hypothermia. A "high-impact trauma" (HIT) device was built, which used a spring-based mechanism to propel flies against the wall of a vial, causing mechanical damage to the brain. Hypothermia groups were cooled to 15°C for 3 minutes. Group differences were analyzed with chi-square tests for the categorical variables and with ANOVA tests for the continuous variables.

Results: Survival curve analysis showed that rTBI can decrease Drosophila lifespan and hypothermia diminished this impact. Average sedation time for control vs concussion vs concussion + hypothermia was 78 vs 52 vs 61 seconds (P < .0001). Similarly, rTBI vs rTBI/hypothermia groups took 43 vs 59 seconds (P < .0001). Concussed flies preferred dark environments compared with control flies (risk ratio 3.3, P < .01) while flies who were concussed and cooled had a risk ratio of 2.7 (P < .01). Flies with rTBI were almost 4 times likely to prefer the dark environment but only 3 times as likely if they were cooled, compared with controls. Geotaxis was significantly affected by rTBI only and yet less so if rTBI flies were cooled.

Conclusions: Hypothermia successfully mitigated many deleterious effects of single TBI and rTBI in Drosophila and may represent a promising breakthrough in the treatment of human TBI.

As in other excitable tissues, two classes of electrical signals are of fundamental importance to the functioning of smooth muscles: junction potentials, which arise from neurotransmission and represent the initiation of excitation (or in some instances inhibition) of the tissue, and spikes or action potentials, which represent the accomplishment of excitation and lead on to contractile activity. Unlike the case in skeletal muscle and in neurons, junction potentials and spikes in smooth muscle have been poorly understood in relation to the electrical properties of the tissue and in terms of their spatiotemporal spread within it. This owes principally to the experimental difficulties involved in making precise electrical recordings from smooth muscles and also to two inherent features of this class of muscle, ie, the syncytial organization of its cells and the distributed innervation they receive, which renders their biophysical analysis problematic. In this review, we outline the development of hypotheses and knowledge on junction potentials and spikes in syncytial smooth muscle, showing how our concepts have frequently undergone radical changes and how recent developments hold promise in unraveling some of the many puzzles that remain. We focus especially on computational models and signal analysis approaches. We take as illustrative examples the smooth muscles of two organs with distinct functional characteristics, the vas deferens and urinary bladder, while also touching on features of electrical functioning in the smooth muscles of other organs.

Objective: There is a plethora of theories about the pathophysiology behind a sport-related concussion. In this review of the literature, the authors evaluated studies on the pathophysiology of sport-related concussion and professional athlete return-to-play guidelines. The goal of this article is to summarize the most common hypotheses for sport-related concussion, evaluate if there are common underlying mechanisms, and determine if correlations are seen between published mechanisms and the most current return-to-play recommendations.

Methods: Two authors selected papers from the past 5 years for literature review involving discussion of sport-related concussion and pathophysiology, pathology, or physiology of concussion using mutually agreed-upon search criteria. After the articles were filtered based on search criteria, pathophysiological explanations for concussion were organized into tables. Following analysis of pathophysiology, concussion protocols and return-to-play guidelines were obtained via a Google search for the major professional sports leagues and synthesized into a summary table.

Results: Out of 1112 initially identified publications, 53 met our criteria for qualitative analysis. The 53 studies revealed 5 primary neuropathological explanations for sport-related concussion, regardless of the many theories talked about in the different papers. These 5 explanations, in order of predominance in the articles analyzed, were (1) tauopathy, (2) white matter changes, (3) neural connectivity alterations, (4) reduction in cerebral perfusion, and (5) gray matter atrophy. Pathology may be sport specific: white matter changes are seen in 47% of football reports, tauopathy is seen in 50% of hockey reports, and soccer reports 50% tauopathy as well as 50% neural connectivity alterations. Analysis of the return-to-play guidelines across professional sports indicated commonalities in concussion management despite individual policies.

Conclusions: Current evidence on pathophysiology for sport-related concussion does not yet support one unifying mechanism, but published hypotheses may potentially be simplified into 5 primary groups. The unification of the complex, likely multifactorial mechanisms for sport-related concussion to a few common explanations, combined with unique findings within individual sports presented in this report, may help filter and link concussion pathophysiology in sport. By doing so, the authors hope that this review will help guide future concussion research, treatment, and management.