Response to commentary on “Therapeutic hypothermia attenuates paraplegia and neuronal damage in the lumbar spinal cord in a rat model of asphyxial cardiac arrest” by Lee et al.,. J Therm Biol 83 (2019) 1–7."

2020 ◽  
Vol 87 ◽  
pp. 102455
Author(s):  
Jae-Chul Lee ◽  
Moo-Ho Won
Keyword(s):  
Spinal Cord ◽  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Rat Model ◽  
Neuronal Damage ◽  
Lumbar Spinal Cord ◽  
Lumbar Spinal ◽  
Asphyxial Cardiac Arrest

scholarly journals Therapeutic Hypothermia Improves Hind Limb Motor Outcome and Attenuates Oxidative Stress and Neuronal Damage in the Lumbar Spinal Cord Following Cardiac Arrest

Antioxidants ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 38
Author(s):  
Ji Hyeon Ahn ◽  
Tae-Kyeong Lee ◽  
Bora Kim ◽  
Jae-Chul Lee ◽  
Hyun-Jin Tae ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Therapeutic Hypothermia ◽  
Hind Limb ◽  
Neuronal Damage ◽  
Ventral Horn ◽  
Lumbar Spinal Cord ◽  
Neuronal Protection ◽  
Endogenous Antioxidants ◽  
Lumbar Spinal

Hypothermia enhances outcomes of patients after resuscitation after cardiac arrest (CA). However, the underlying mechanism is not fully understood. In this study, we investigated effects of hypothermic therapy on neuronal damage/death, microglial activation, and changes of endogenous antioxidants in the anterior horn in the lumbar spinal cord in a rat model of asphyxial CA (ACA). A total of 77 adult male Sprague–Dawley rats were randomized into five groups: normal, sham ACA plus (+) normothermia, ACA + normothermia, sham ACA + hypothermia, and ACA + hypothermia. ACA was induced for 5 min by injecting vecuronium bromide. Therapeutic hypothermia was applied after return of spontaneous circulation (ROSC) via rapid cooling with isopropyl alcohol wipes, which was maintained at 33 ± 0.5 °C for 4 h. Normothermia groups were maintained at 37 ± 0.2 °C for 4 h. Neuronal protection, microgliosis, oxidative stress, and changes of endogenous antioxidants were evaluated at 12 h, 1 day, and 2 days after ROSC following ACA. ACA resulted in neuronal damage from 12 h after ROSC and evoked obvious degeneration/loss of spinal neurons in the ventral horn at 1 day after ACA, showing motor deficit of the hind limb. In addition, ACA resulted in a gradual increase in microgliosis with time after ACA. Therapeutic hypothermia significantly reduced neuronal loss and attenuated hind limb dysfunction, showing that hypothermia significantly attenuated microgliosis. Furthermore, hypothermia significantly suppressed ACA-induced increases of superoxide anion production and 8-hydroxyguanine expression, and significantly increased superoxide dismutase 1 (SOD1), SOD2, catalase, and glutathione peroxidase. Taken together, hypothermic therapy was found to have a substantial impact on changes in ACA-induced microglia activation, oxidative stress factors, and antioxidant enzymes in the ventral horn of the lumbar spinal cord, which closely correlate with neuronal protection and neurological performance after ACA.

scholarly journals Multi-pronged neuromodulation intervention engages the residual motor circuitry to facilitate walking in a rat model of spinal cord injury

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Marco Bonizzato ◽  
Nicholas D. James ◽  
Galyna Pidpruzhnykova ◽  
Natalia Pavlova ◽  
Polina Shkorbatova ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Rat Model ◽  
Stress Responses ◽  
Learning Algorithm ◽  
Lumbar Spinal Cord ◽  
Cord Injury ◽  
Potential Synergy ◽  
Lumbar Spinal ◽  
Deep Brain

AbstractA spinal cord injury usually spares some components of the locomotor circuitry. Deep brain stimulation (DBS) of the midbrain locomotor region and epidural electrical stimulation of the lumbar spinal cord (EES) are being used to tap into this spared circuitry to enable locomotion in humans with spinal cord injury. While appealing, the potential synergy between DBS and EES remains unknown. Here, we report the synergistic facilitation of locomotion when DBS is combined with EES in a rat model of severe contusion spinal cord injury leading to leg paralysis. However, this synergy requires high amplitudes of DBS, which triggers forced locomotion associated with stress responses. To suppress these undesired responses, we link DBS to the intention to walk, decoded from cortical activity using a robust, rapidly calibrated unsupervised learning algorithm. This contingency amplifies the supraspinal descending command while empowering the rats into volitional walking. However, the resulting improvements may not outweigh the complex technological framework necessary to establish viable therapeutic conditions.

scholarly journals Effect of Graphene Nanoribbons (TexasPEG) on locomotor function recovery in a rat model of lumbar spinal cord transection

2018 ◽  
Vol 13 (8) ◽  
pp. 1440 ◽  
Author(s):  
C-Yoon Kim ◽  
Sergio Canavero ◽  
WilliamK.A. Sikkema ◽  
Jin Kim ◽  
JeongAh Kim ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Rat Model ◽  
Graphene Nanoribbons ◽  
Spinal Cord Transection ◽  
Lumbar Spinal Cord ◽  
Locomotor Function ◽  
Function Recovery ◽  
Lumbar Spinal

scholarly journals Cholinergic imbalance in lumbar spinal cord of a rat model of multiple sclerosis

2018 ◽  
Vol 318 ◽  
pp. 29-35
Author(s):  
Chunling Liu ◽  
Hui Liu ◽  
Hongjun Jin ◽  
Xuyi Yue ◽  
Zonghua Luo ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Rat Model ◽  
Lumbar Spinal Cord ◽  
Lumbar Spinal

Protective effects of therapeutic hypothermia on renal injury in an asphyxial cardiac arrest rat model

2020 ◽  
Vol 94 ◽  
pp. 102761
Author(s):  
Anowarul Islam ◽  
So Eun Kim ◽  
Jae Chol Yoon ◽  
Ali Jawad ◽  
Weishun Tian ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Rat Model ◽  
Renal Injury ◽  
Protective Effects ◽  
Asphyxial Cardiac Arrest

scholarly journals Retrograde Transport of Transmissible Mink Encephalopathy within Descending Motor Tracts

2002 ◽  
Vol 76 (11) ◽  
pp. 5759-5768 ◽  
Author(s):  
Jason C. Bartz ◽  
Anthony E. Kincaid ◽  
Richard A. Bessen
Keyword(s):  
Spinal Cord ◽  
Sciatic Nerve ◽  
Neuronal Damage ◽  
Red Nucleus ◽  
Disease Onset ◽  
Retrograde Transport ◽  
Lumbar Spinal Cord ◽  
Transmissible Mink Encephalopathy ◽  
Lumbar Spinal ◽  
The Brain

ABSTRACT The spread of the abnormal conformation of the prion protein, PrPSc, within the spinal cord is central to the pathogenesis of transmissible prion diseases, but the mechanism of transport has not been determined. For this report, the route of transport of the HY strain of transmissible mink encephalopathy (TME), a prion disease of mink, in the central nervous system following unilateral inoculation into the sciatic nerves of Syrian hamsters was investigated. PrPSc was detected at 3 weeks postinfection in the lumbar spinal cord and ascended to the brain at a rate of approximately 3.3 mm per day. At 6 weeks postinfection, PrPSc was detected in the lateral vestibular nucleus and the interposed nucleus of the cerebellum ipsilateral to the site of sciatic nerve inoculation and in the red nucleus contralateral to HY TME inoculation. At 9 weeks postinfection, PrPSc was detected in the contralateral hind limb motor cortex and reticular thalamic nucleus. These patterns of PrPSc brain deposition at various times postinfection were consistent with that of HY TME spread from the sciatic nerve to the lumbar spinal cord followed by transsynaptic spread and retrograde transport to the brain and brain stem along descending spinal tracts (i.e., lateral vestibulospinal, rubrospinal, and corticospinal). The absence of PrPSc from the spleen suggested that the lymphoreticular system does not play a role in neuroinvasion following sciatic nerve infection. The rapid disease onset following sciatic nerve infection demonstrated that HY TME can spread by retrograde transport along specific descending motor pathways of the spinal cord and, as a result, can initially target brain regions that control vestibular and motor functions. The early clinical symptoms of HY TME infection such as head tremor and ataxia were consistent with neuronal damage to these brain areas.

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