Chronic Electrophysiological and Behavioral Response in Rats due to Cerebral Ischemic Stroke in the Motor Cortex

2009 ◽  
Vol 2 (1) ◽  
Author(s):  
M. A. Midgett ◽  
P. J. Rousche
Keyword(s):  
Motor Cortex ◽  
Firing Rate ◽  
Behavioral Response ◽  
Neural Firing ◽  
Dynamic Changes ◽  
Post Stroke ◽  
Cylinder Test ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Time Required

This work is the beginning of a study investigating dynamic changes of electrophysiological and correlative behavioral response in rats before, during and after stroke in the motor cortex. The animals need training sessions to regularly perform the behavioral tests. The standard deviation of total paw touches in the cylinder test (n=4) and the time required to eat a single strand of pasta (n=3) decreased by a factor of 1.7 and 3.6 respectively after 5 days of training. Behaviorally, post-stroke, average cylinder touches decreased by a factor of 5.6, and pasta adjustments increased by a factor of 3.6 suggesting impairments due to stroke. The pre-stroke mean neural firing rate was 94 spikes per second (spk/s), this increased to 146 spk/s during the 20 minute stroke induction, and was only 4 spk/s 20 min post-stroke. The firing rate has increased to near pre-stroke levels in the 2nd and 3rd days following stroke.

scholarly journals COMPARISON OF THE DYNAMIC CHANGES OF AMINO ACID BLOOD PLASMA SPECTRUM IN PATIENTS WITH THE PRIMARY CEREBRAL ISCHEMIC STROKE DEPENDING ON THE POSTAPOPLECTIC SPASTICITY DEVELOPMENT IN THE RECOVERY PERIOD

2016 ◽  
Vol 3 ◽  
pp. 17-23
Author(s):  
Anzhelika Payenok ◽  
Maria Bilobryn ◽  
Iryna Mitelman
Keyword(s):  
Ischemic Stroke ◽  
Blood Plasma ◽  
Recovery Period ◽  
Control Group ◽  
Cerebral Stroke ◽  
Early Recovery ◽  
Dynamic Changes ◽  
Acute Period ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

The aim of research was to reveal the dynamic changes of the level of excitatory and inhibitory neuroamino acids in patients with the primary cerebral ischemic stroke depending on postapoplectic spasticity presence at the end of the early recovery period. For this aim was studied the concentration of excitatory and inhibitory neuroamino acids in the blood plasma in first 72 hours in 97 patients with the primary ischemic cerebral stroke depending on postapoplectic spasticity on the sixth month after ischemic event. The control group included 15 patients with diagnosed chronic cerebral ischemia. In the result of research we revealed that the common sign for the two groups (with spasticity on the sixth month and without it) was the reliable rise of the level of excitatory amino acids comparing with the control. In patients without spasticity the heightened level of excitatory neurotransmitters in the most acute period of ischemic cerebral stroke was attended with the heightened level of inhibitory neuroamino acids. The distinctive feature of patients with postapoplectic spasticity was the decreased or stable level of transmitters of inhibitory action. During 6th moth after ischemic stroke was detected the rise of all studied neuroamino acids in patients with spasticity unlike to the ones without spasticity who were characterized only with the rise of taurine level and decrease of glycine and aspartate levels. So, the received results allow assume the insufficient activation of the inhibitory neuroamino acids system in the most acute period of the ischemic stroke in certain category of patients that in future are inclined to the spasticity development after stroke.

Abstract P806: Sirtuin1 Plays a Critical Role in Reversing Skeletal Muscle Atrophy in Cerebral Ischemic Stroke

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Junaith S Mohamed ◽  
Peter J Ferrandi ◽  
Paez G Hector ◽  
Christopher R Pitzer ◽  
Stephen E Alway
Keyword(s):  
Skeletal Muscle ◽  
Ischemic Stroke ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Rna Seq ◽  
Stroke Patients ◽  
Post Stroke ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

Stroke is a leading cause of mortality and long-term disability in patients worldwide. Skeletal muscle is the primary systemic target organ of stroke that severely induces muscle wasting and weakness, which contributes more to the long-term functional disability in stroke patients than any other disease. Currently, no approved pharmacological drug is available to treat stroke-induced muscle loss. Rehabilitative therapy is the only available option to improve muscle function in stroke patients. However, higher muscle fatigability and lower muscle strength from extensive muscle wasting in post-stroke patients provide poor rehabilitative outcomes. As a result, about two-thirds of stroke survivors persist in a state of insufficient recovery and experience physical disability that drastically reduces their health and quality of life. The major challenge in the drug discovery effort for treating post-stroke muscle wasting is the lack of our understanding of the molecular and/or cellular mechanisms that underlie the muscle wasting in stroke. To understand the molecular origin of stroke-induced muscle atrophy, gene expression profiling and associated biological pathway enrichment studies were performed in a mouse model of cerebral ischemic stroke using high-throughput RNA sequencing and extensive bioinformatic analyses. RNA-seq data revealed that the elevated atrophy in skeletal muscle observed in response to stroke was primairly associated with the altered expression of genes involved in the muscle protein degradation pathway. Further analysis of RNA-seq data identified Sirtuin1 (SirT1) as a critical protein that plays a significant role in regulating post-stroke muscle mass. SirT1 gain-of-function in skeletal muscle significantly reversed stroke-induced muscle atrophy via inhibiting the activation of the ubiquitin proteasomal pathway and restoring autophagy function. Collectively, this study identified suppression of SirT1as a novel mechanism by which stroke induces muscle atrophy.

scholarly journals Transcriptome Analysis of Skeletal Muscle Reveals Altered Proteolytic and Neuromuscular Junction Associated Gene Expressions in a Mouse Model of Cerebral Ischemic Stroke

Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 726
Author(s):  
Peter J. Ferrandi ◽  
Mohammad Moshahid Khan ◽  
Hector G. Paez ◽  
Christopher R. Pitzer ◽  
Stephen E. Alway ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ischemic Stroke ◽  
Neuromuscular Junction ◽  
Mouse Model ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Altered Expression ◽  
Post Stroke ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

Stroke is a leading cause of mortality and long-term disability in patients worldwide. Skeletal muscle is the primary systemic target organ of stroke that induces muscle wasting and weakness, which predominantly contribute to functional disability in stroke patients. Currently, no pharmacological drug is available to treat post-stroke muscle morbidities as the mechanisms underlying post-stroke muscle wasting remain poorly understood. To understand the stroke-mediated molecular changes occurring at the transcriptional level in skeletal muscle, the gene expression profiles and enrichment pathways were explored in a mouse model of cerebral ischemic stroke via high-throughput RNA sequencing and extensive bioinformatic analyses. RNA-seq revealed that the elevated muscle atrophy observed in response to stroke was associated with the altered expression of genes involved in proteolysis, cell cycle, extracellular matrix remodeling, and the neuromuscular junction (NMJ). These data suggest that stroke primarily targets muscle protein degradation and NMJ pathway proteins to induce muscle atrophy. Collectively, we for the first time have found a novel genome-wide transcriptome signature of post-stroke skeletal muscle in mice. Our study will provide critical information to further elucidate specific gene(s) and pathway(s) that can be targeted to mitigate accountable for post-stroke muscle atrophy and related weakness.

Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 329-336
Author(s):  
Wang Jinli ◽  
Xu Fenfen ◽  
Zheng Yuan ◽  
Cheng Xu ◽  
Zhang Piaopiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Major Complication ◽  
Lactic Dehydrogenase ◽  
Dependent Manner ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Myd88 Signaling ◽  
Hypoxia Reoxygenation

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

scholarly journals Activation of the p11/SMARCA3/Neurensin-2 pathway in parvalbumin interneurons mediates the response to chronic antidepressants

2021 ◽  
Author(s):  
Gali Umschweif ◽  
Lucian Medrihan ◽  
Kathryn A. McCabe ◽  
Yotam Sagi ◽  
Paul Greengard
Keyword(s):  
Chromatin Remodeling ◽  
Behavioral Response ◽  
Hippocampal Neurons ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Chronic Treatment ◽  
Target Genes ◽  
Delayed Response ◽  
Dynamic Changes ◽  
Parvalbumin Interneurons ◽  
Transcriptional Changes

AbstractThe delayed behavioral response to chronic antidepressants depends on dynamic changes in the hippocampus. It was suggested that the antidepressant protein p11 and the chromatin remodeling factor SMARCA3 mediate this delayed response by inducing transcriptional changes in hippocampal neurons. However, what target genes are regulated by the p11/SMARCA3 complex to mediate the behavioral response to antidepressants, and what cell type mediates these molecular changes remain unknown. Here we report that the p11/SMARCA3 complex represses Neurensin-2 transcription in hippocampal parvalbumin-expressing interneurons after chronic treatment with Selective Serotonin Reuptake Inhibitors (SSRI). The behavioral response to antidepressants requires upregulation of p11, accumulation of SMARCA3 in the cell nucleus, and a consequent repression of Neurensin-2 transcription in these interneurons. We elucidate a functional role for p11/SMARCA3/Neurensin-2 pathway in regulating AMPA-receptor signaling in parvalbumin-expressing interneurons, a function that is enhanced by chronic treatment with SSRIs. These results link SSRIs to dynamic glutamatergic changes and implicate p11/SMARCA3/Neurensin-2 pathway in the development of more specific and efficient therapeutic strategies for neuropsychiatric disorders.

scholarly journals Effect of opposing needling on motor cortex excitability in healthy participants and in patients with post-stroke hemiplegia: study protocol for a single-blind, randomised controlled trial

Trials ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Mindong Xu ◽  
Yinyu Zi ◽  
Jianlu Wu ◽  
Nenggui Xu ◽  
Liming Lu ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Motor Evoked Potentials ◽  
Controlled Trial ◽  
Secondary Outcome ◽  
Post Stroke ◽  
Motor Cortex Excitability ◽  
Opposing Needling ◽  
Single Blind ◽  
Healthy Participants

Abstract Background Opposing needling has an obvious curative effect in the treatment of post-stroke hemiplegia; however, the mechanism of the opposing needling in the treatment of post-stroke hemiplegia is still not clear. The purpose of this study is to investigate the effect of opposing needling on the excitability of primary motor cortex (M1) of healthy participants and patients with post-stroke hemiplegia, which may provide insight into the mechanisms of opposing needling in treating post-stroke hemiplegia. Methods This will be a single-blind, randomised, sham-controlled trial in which 80 healthy participants and 40 patients with post-stroke hemiplegia will be recruited. Healthy participants will be randomised 1:1:1:1 to the 2-Hz, 50-Hz, 100-Hz, and sham electroacupuncture groups. Patients with post-stroke hemiplegia will be randomised 1:1 to the opposing needling or conventional treatment groups. The M1 will be located in all groups by using neuroimaging-based navigation. The stimulator coil of transcranial magnetic stimulation (TMS) will be moved over the left and right M1 in order to identify the TMS hotspot, followed by a recording of resting motor thresholds (RMTs) and motor-evoked potentials (MEPs) of the thenar muscles induced by TMS before and after the intervention. The primary outcome measure will be the percent change in the RMTs of the thenar muscles at baseline and after the intervention. The secondary outcome measures will be the amplitude (μV) and latency (ms) of the MEPs of the thenar muscles at baseline and after the intervention. Discussion The aim of this trial is to explore the effect of opposing needling on the excitability of M1 of healthy participants and patients with post-stroke hemiplegia. Trial registration Chinese Clinical Trial Registry ChiCTR1900028138. Registered on 13 December 2019.

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