Leptin response to short-term fasting in sympathectomized men: role of the SNS

2003 ◽  
Vol 284 (3) ◽  
pp. E634-E640 ◽  
Author(s):  
Justin Y. Jeon ◽  
Vicki J. Harber ◽  
Robert D. Steadward
Keyword(s):  
Body Mass Index ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Short Term ◽  
Cord Injury ◽  
Before And After ◽  
Sympathetic Nervous ◽  
Plasma Leptin

We studied plasma leptin levels in six people with high-lesion spinal cord injury [SCI; body mass index (BMI) 25.9 ± 1.5 kg/m2, age 37 ± 3.0 yr] and six able-bodied (AB) controls (BMI 29.1 ± 1.9 kg/m2, age 35 ± 3.5 yr) before and after 12, 24, and 36 h of fasting. The plasma leptin levels significantly decreased during 36 h fasting by 48.8 ± 4.5% (pre: 11.3 ± 2.3, post: 6.2 ± 1.5 ng/ml) and 38.6 ± 7.9% (pre: 7.6 ± 5.0, post: 4.2 ± 1.0 ng/ml) in SCI and AB, respectively. Plasma leptin started to decrease at 24 h of fasting in the SCI group, whereas plasma leptin started to decrease at 12 h of fasting in the AB group. The current study demonstrated that plasma leptin decreased with fasting in both SCI and AB groups, with the leptin decrease being delayed in the SCI group. The delayed leptin response to fasting in the SCI group may be because of increased fat mass (%body fat, SCI: 33.8 ± 3.0, AB: 24.1 ± 2.9) and sympathetic nervous system dysfunction.

scholarly journals Effects of 16-Form Wheelchair Tai Chi on the Autonomic Nervous System among Patients with Spinal Cord Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Yan Qi ◽  
Haixia Xie ◽  
Yunlin Shang ◽  
Lejun Wang ◽  
Ce Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Tai Chi ◽  
Low Frequency ◽  
Rr Intervals ◽  
Cord Injury ◽  
Before And After ◽  
Frequency Area

Objective. This study aims to investigate the effects of 16-form Wheelchair Tai Chi (WCTC16) on the autonomic nervous system among patients with spinal cord injury (SCI). Methods. Twenty patients with chronic complete thoracic SCI were recruited. Equivital life monitoring system was used to record and analyze heart rate variability (HRV) of patients for five minutes before and after five consecutive sets of WCTC16, respectively. The analysis of HRV in the time domain included RR intervals, the standard deviation of all normal RR intervals (SDNN), and the root mean square of the differences between adjacent NN intervals (RMSSD). The analysis of HRV in the frequency domain included total power (TP), which could be divided into very-low-frequency area (VLFP), low-frequency area (LFP), and high-frequency area (HFP). The LF/HF ratio as well as the normalized units of LFP (LFPnu) and HFP (HFPnu) reflected the sympathovagal balance. Results. There was no significant difference in RR interval, SDNN, RMSSD, TP, HEP, VLFP, and LFP of SCI patients before and after WCTC16 exercise ( P > 0.05 ). LFPnu and HF peak decreased, while HFPnu and LF/HF increased in SCI patients after WCTC16 exercise. The differences were statistically significant ( P < 0.001 ). Conclusion. WCTC16 can enhance vagal activity and decrease sympathetic activity so that patients with chronic complete thoracic SCI can achieve the balanced sympathovagal tone.

scholarly journals The role of connexin43 in neuropathic pain induced by spinal cord injury

2019 ◽  
Vol 51 (6) ◽  
pp. 555-561 ◽  
Author(s):  
Anhui Wang ◽  
Changshui Xu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Cell Metabolism ◽  
Pain Models ◽  
Cord Injury ◽  
The Central Nervous System ◽  
And Function

Abstract Neuropathic pain is caused by the damage or dysfunction of the nervous system. In many neuropathic pain models, there is an increase in the number of gap junction (GJ) channels, especially the upregulation of the expression of connexin43 (Cx43), leading to the secretion of various types of cytokines and involvement in the formation of neuropathic pain. GJs are widely distributed in mammalian organs and tissues, and Cx43 is the most abundant connexin (Cx) in mammals. Astrocytes are the most abundant glial cell type in the central nervous system (CNS), which mainly express Cx43. More importantly, GJs play an important role in regulating cell metabolism, signaling, and function. Many existing literatures showed that Cx43 plays an important role in the nervous system, especially in the CNS under normal and pathological conditions. However, many internal mechanisms have not yet been thoroughly explored. In this review, we summarized the current understanding of the role and association of Cx and pannexin channels in neuropathic pain, especially after spinal cord injury, as well as some of our own insights and thoughts which suggest that Cx43 may become an emerging therapeutic target for future neuropathic pain, bringing new hope to patients.

scholarly journals Rho activation patterns after spinal cord injury and the role of activated Rho in apoptosis in the central nervous system

2003 ◽  
Vol 162 (2) ◽  
pp. 233-243 ◽  
Author(s):  
Catherine I. Dubreuil ◽  
Matthew J. Winton ◽  
Lisa McKerracher
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Axon Growth ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Cord Injury ◽  
The Central Nervous System

Growth inhibitory proteins in the central nervous system (CNS) block axon growth and regeneration by signaling to Rho, an intracellular GTPase. It is not known how CNS trauma affects the expression and activation of RhoA. Here we detect GTP-bound RhoA in spinal cord homogenates and report that spinal cord injury (SCI) in both rats and mice activates RhoA over 10-fold in the absence of changes in RhoA expression. In situ Rho-GTP detection revealed that both neurons and glial cells showed Rho activation at SCI lesion sites. Application of a Rho antagonist (C3–05) reversed Rho activation and reduced the number of TUNEL-labeled cells by ∼50% in both injured mouse and rat, showing a role for activated Rho in cell death after CNS injury. Next, we examined the role of the p75 neurotrophin receptor (p75NTR) in Rho signaling. After SCI, an up-regulation of p75NTR was detected by Western blot and observed in both neurons and glia. Treatment with C3–05 blocked the increase in p75NTR expression. Experiments with p75NTR-null mutant mice showed that immediate Rho activation after SCI is p75NTR dependent. Our results indicate that blocking overactivation of Rho after SCI protects cells from p75NTR-dependent apoptosis.

scholarly journals Role of NETosis in Central Nervous System Injury

2022 ◽  
Vol 2022 ◽  
pp. 1-15
Author(s):  
Yituo Chen ◽  
Haojie Zhang ◽  
Xinli Hu ◽  
Wanta Cai ◽  
Wenfei Ni ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Nervous System ◽  
Brain Injury ◽  
Cns Injury ◽  
Cell Death Pathways ◽  
Cord Injury

Central nervous system (CNS) injury is divided into brain injury and spinal cord injury and remains the most common cause of morbidity and mortality worldwide. Previous reviews have defined numerous inflammatory cells involved in this process. In the human body, neutrophils comprise the largest numbers of myeloid leukocytes. Activated neutrophils release extracellular web-like DNA amended with antimicrobial proteins called neutrophil extracellular traps (NETs). The formation of NETs was demonstrated as a new method of cell death called NETosis. As the first line of defence against injury, neutrophils mediate a variety of adverse reactions in the early stage, and we consider that NETs may be the prominent mediators of CNS injury. Therefore, exploring the specific role of NETs in CNS injury may help us shed some light on early changes in the disease. Simultaneously, we discovered that there is a link between NETosis and other cell death pathways by browsing other research, which is helpful for us to establish crossroads between known cell death pathways. Currently, there is a large amount of research concerning NETosis in various diseases, but the role of NETosis in CNS injury remains unknown. Therefore, this review will introduce the role of NETosis in CNS injury, including traumatic brain injury, cerebral ischaemia, CNS infection, Alzheimer’s disease, and spinal cord injury, by describing the mechanism of NETosis, the evidence of NETosis in CNS injury, and the link between NETosis and other cell death pathways. Furthermore, we also discuss some agents that inhibit NETosis as therapies to alleviate the severity of CNS injury. NETosis may be a potential target for the treatment of CNS injury, so exploring NETosis provides a feasible therapeutic option for CNS injury in the future.

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