scholarly journals Tamoxifen Promotes Axonal Preservation and Gait Locomotion Recovery after Spinal Cord Injury in Cats

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Braniff de la Torre Valdovinos ◽  
Judith Marcela Duenas Jimenez ◽  
Ismael Jimenez Estrada ◽  
Jacinto Banuelos Pineda ◽  
Nancy Elizabeth Franco Rodriguez ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Normal Values ◽  
Angular Displacement ◽  
Neuroprotective Effect ◽  
Ventral Horn ◽  
Tamoxifen Treatment ◽  
Myelinated Axons ◽  
Cord Injury ◽  
Hindlimb Kinematics

We performed experiments in cats with a spinal cord penetrating hemisection at T13-L1 level, with and without tamoxifen treatment. The results showed that the numbers of the ipsilateral and contralateral ventral horn neurons were reduced to less than half in the nontreated animals compared with the treated ones. Also, axons myelin sheet was preserved to almost normal values in treated cats. On the contrary, in the untreated animals, their myelin sheet was reduced to 28% at 30 days after injury (DAI), in both the ipsilateral and contralateral regions of the spinal cord. Additionally, we made hindlimb kinematics experiments to study the effects of tamoxifen on cat locomotion after the injury: at 4, 16, and 30 DAI. We observed that the ipsilateral hindlimb angular displacement (AD) of the pendulum-like movements (PLM) during gait locomotion was recovered to almost normal values in treated cats. Contralateral PLM acquired similar values to those obtained in intact cats. At 4 DAI, untreated animals showed a compensatory increment of PLM occurring in the contralateral hindlimb, which was partially recovered at 30 DAI. Our findings indicate that tamoxifen exerts a neuroprotective effect and preserves or produces myelinated axons, which could benefit the locomotion recovery in injured cats.

Neuroprotective Effect of Epidural Electrical Stimulation against Ischemic Spinal Cord Injury in Rats

2005 ◽  
Vol 103 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Manabu Kakinohana ◽  
Hideki Harada ◽  
Yasunori Mishima ◽  
Tatsuhiko Kano ◽  
Kazuhiro Sugahara
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Electrical Stimulation ◽  
Neuroprotective Effect ◽  
Spinal Cord Ischemia ◽  
Aortic Occlusion ◽  
Cord Injury ◽  
Optimal Setting ◽  
Transient Aortic Occlusion ◽  
Ischemic Spinal Cord Injury

Background Electroconvulsion therapy is likely to serve as an effective preconditioning stimulus for inducing tolerance to ischemic brain injury. The current study examines whether electrical stimuli on the spinal cord is also capable of inducing tolerance to ischemic spinal cord injury by transient aortic occlusion. Methods Spinal cord ischemia was induced by occlusion of the descending thoracic aorta in combination with maintaining systemic hypotension (40 mmHg) during the procedure. Animals implanted with epidural electrodes were divided into four groups according to electrical stimulation and sham. Two groups consisted of rapid preconditioning (RE group, n = 8) and sham procedure (RC group, n = 8) 30 min before 9 min of spinal cord ischemia. In the two groups that underwent delayed preconditioning, rats were exposed to 9 min of aortic occlusion 24 h after either pretreatment with epidural electrical stimulation (DE group, n = 8) or sham (DC group, n = 8). In addition, rats were exposed to 6-11 min of spinal cord ischemia at 30 min or 24 h after epidural electrical stimulation or sham stimulation. The group P50 represents the duration of spinal cord ischemia associated with 50% probability of resultant paraplegia. Results Pretreatment with electrical stimulation in the DE group but not the RE group protected the spinal cord against ischemia, and this stimulation prolonged the P50 by approximately 15.0% in the DE group compared with the DC group. Conclusions Although the optimal setting for this electrical preconditioning should be determined in future studies, the results suggest that epidural electrical stimulation will be a useful approach to provide spinal protection against ischemia.

Neuroprotective Effect of Vaccination with Autoantigen-Pulsed Dendritic Cells After Spinal Cord Injury

2012 ◽  
Vol 176 (1) ◽  
pp. 281-292 ◽  
Author(s):  
Yufu Wang ◽  
Ke Wang ◽  
Rui Chao ◽  
Jing Li ◽  
Lei Zhou ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Dendritic Cells ◽  
Neuroprotective Effect ◽  
Cord Injury

Neuroprotective Effect of Endogenous Pituitary Adenylate Cyclase-Activating Polypeptide on Spinal Cord Injury

2012 ◽  
Vol 48 (3) ◽  
pp. 508-517 ◽  
Author(s):  
Daisuke Tsuchikawa ◽  
Tomoya Nakamachi ◽  
Masashi Tsuchida ◽  
Yoshihiro Wada ◽  
Motohide Hori ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Adenylate Cyclase ◽  
Neuroprotective Effect ◽  
Cord Injury ◽  
Pituitary Adenylate Cyclase

scholarly journals EA Improves the Motor Function in Rats with Spinal Cord Injury by Inhibiting Signal Transduction of Semaphorin3A and Upregulating of the Peripheral Nerve Networks

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Rong Hu ◽  
Haipeng Xu ◽  
Yaheng Jiang ◽  
Yi Chen ◽  
Kelin He ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Peripheral Nerve ◽  
Motor Function ◽  
Gray Matter ◽  
Ventral Horn ◽  
Damage Site ◽  
Central Tube ◽  
Spinal Cord Segment ◽  
Cord Injury

Peripheral nerve networks (PNNs) play a vital role in the neural recovery after spinal cord injury (SCI). Electroacupuncture (EA), as an alternative medicine, has been widely used in SCI and was proven to be effective on neural functional recovery. In this study, the interaction between PNNs and semaphrin3A (Sema3A) in the recovery of the motor function after SCI was observed, and the effect of EA on them was evaluated. After the establishment of the SCI animal model, we found that motor neurons in the ventral horn of the injured spinal cord segment decreased, Nissl bodies were blurry, and PNNs and Sema3A as well as its receptor neuropilin1 (NRP1) aggregated around the central tube of the gray matter of the spinal cord. When we knocked down the expression of Sema3A at the damage site, NRP1 also downregulated, importantly, PNNs concentration decreased, and tenascin-R (TN-R) and aggrecan were also reduced, while the Basso-Beattie-Bresnahan (BBB) motor function score dramatically increased. In addition, when conducting EA stimulation on Jiaji (EX-B2) acupoints, the highly upregulated Sema3A and NRP1 were reversed post-SCI, which can lessen the accumulation of PNNs around the central tube of the spinal cord gray matter, and simultaneously promote the recovery of motor function in rats. These results suggest that EA may further affect the plasticity of PNNs by regulating the Sema3A signal and promoting the recovery of the motor function post-SCI.

scholarly journals The Effects of Local Cooling on Canine Spinal Cord Blood Flow

1985 ◽  
Vol 12 (2) ◽  
pp. 83-87 ◽  
Author(s):  
Robert R. Hansebout ◽  
R. Neil Lamont ◽  
M. Venkatraya Kamath
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Cord Blood ◽  
Normal Values ◽  
Local Cooling ◽  
Spinal Cord Blood Flow ◽  
Central Temperature ◽  
Cord Injury

ABSTRACT:The internal spinal cord blood flow was measured in dogs at the site of local cooling using hydrogen polarography. Blood flow decreased to 50% of the normothermic values during cooling of the cord to a central temperature of 16 degrees Celsius. Upon cessation of cooling internal blood flow rapidly returned to normal values. Implications of this finding for the treatment of spinal cord injury are discussed.

Neuroprotective Effect of Prophylactic Intrathecal Methylprednisolone in Spinal Cord Injury in Rat Model

2014 ◽  
Vol 14 (11) ◽  
pp. S86-S87 ◽  
Author(s):  
Thomas Cheriyan ◽  
Hiroyuki Yoshihara ◽  
Stephen P. Maier ◽  
Devon J. Ryan ◽  
Jeffrey H. Weinreb ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Rat Model ◽  
Neuroprotective Effect ◽  
Cord Injury

scholarly journals B-RAFV600E Inhibitor Dabrafenib Attenuates RIPK3-Mediated Necroptosis and Promotes Functional Recovery after Spinal Cord Injury

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1582 ◽  
Author(s):  
Takehiro Sugaya ◽  
Haruo Kanno ◽  
Michiharu Matsuda ◽  
Kyoichi Handa ◽  
Satoshi Tateda ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Tissue Damage ◽  
Neuroprotective Effect ◽  
Neural Tissue ◽  
Injured Spinal Cord ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Cord Injury

The receptor-interacting protein kinase 3 (RIPK3) is a key regulator of necroptosis and is involved in various pathologies of human diseases. We previously reported that RIPK3 expression is upregulated in various neural cells at the lesions and necroptosis contributed to secondary neural tissue damage after spinal cord injury (SCI). Interestingly, recent studies have shown that the B-RAFV600E inhibitor dabrafenib has a function to selectively inhibit RIPK3 and prevents necroptosis in various disease models. In the present study, using a mouse model of thoracic spinal cord contusion injury, we demonstrate that dabrafenib administration in the acute phase significantly inhibites RIPK3-mediated necroptosis in the injured spinal cord. The administration of dabrafenib attenuated secondary neural tissue damage, such as demyelination, neuronal loss, and axonal damage, following SCI. Importantly, the neuroprotective effect of dabrafenib dramatically improved the recovery of locomotor and sensory functions after SCI. Furthermore, the electrophysiological assessment of the injured spinal cord objectively confirmed that the functional recovery was enhanced by dabrafenib. These findings suggest that the B-RAFV600E inhibitor dabrafenib attenuates RIPK3-mediated necroptosis to provide a neuroprotective effect and promotes functional recovery after SCI. The administration of dabrafenib may be a novel therapeutic strategy for treating patients with SCI in the future.

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