Neuroprotective effects of a novel NMDA antagonist, Gacyclidine, after experimental contusive spinal cord injury in adult rats

Gaviria, Moisés; Privat, Alain; D’Arbigny, Pierre; Kamenka, Jean-Marc; Haton, Henri; Ohanna, F

doi:10.1016/s0006-8993(00)02581-6

Cited by 87 publications

(48 citation statements)

References 52 publications

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“…1,2 A variety of agents, for example, neurotrophic factors, methylprednisolone, ganglioside, and NMDA antagonist gacyclidine have been investigated for protecting the injured spinal cord from secondary pathological processes, [3][4][5][6] but there is not a satisfactory therapeutic answer to spinal cord injury yet. Animal experiments have shown that extracts of Ginkgo biloba (EGb 761) can prevent neuronal damage in brain ischemia through inhibition of nitric oxide synthesis, 7 and clinical studies have shown some beneficial effects of EGb 761 in the treatment of patients with Alzheimer's disease and other types of dementia.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of extract of Ginkgo biloba (EGb 761) on nerve cells after spinal cord injury in rats

Sun

Wang

et al. 2006

Spinal Cord

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Study design: An experimental animal model was used to assess spinal cord injury following lateral hemitransection at thoracic spinal cord level. Objective: To determine whether extract of Ginkgo biloba (EGb) could have a neuroprotective effect in spinal cord injury (SCI) in rats. Setting: Department of Biological Sciences and Biotechnology, Tsinghua University, China. Methods: A total of 72 adult rats were divided randomly into three groups: the EGb group, normal saline (NS) group, and sham operation group (sham group). After thoracic spinal cord hemitransection was performed at the level of the 9th thoracic vertebra (T9), rats in the EGb group were given 100 mg/kg EGb 761 daily, while rats in the NS group received NS. The rats in the sham group only underwent laminectomy without spinal cord hemitransection. At various time points after surgery, thoracic spinal cords were sampled and sliced for histochemistry, immunohistochemistry of inducible nitric oxide synthase (iNOS), and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) of apoptotic cells. Results: Myelin staining showed that the area of cavities was small and the demyelinated zones were limited at and around the injury site of the spinal cord in the EGb group, while the area of cavities was large and the demyelinated zones were serious in the NS group. Nissl staining showed that the ratio of bilateral ventral horn neurons (transection side/uninjured side) in the EGb group was higher than that in the NS group (Po0.05). The apoptotic index and the percentage of iNOS-positive cells were lower in the EGb group than in the NS group. Furthermore, the percentage of iNOS-positive cells positively correlated with the apoptotic index (r 2 ¼ 0.729, Po0.01) after SCI. Conclusion: This study demonstrated that EGb 761 could inhibit iNOS expression and have neuroprotective effect by preventing nerve cells from apoptosis after SCI in rats.

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Section: Introductionmentioning

confidence: 99%

Protective effects of extract of Ginkgo biloba (EGb 761) on nerve cells after spinal cord injury in rats

Sun

Wang

et al. 2006

Spinal Cord

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“…Therefore, the development of clinical treatment of NMDA antagonists has become difficult. Besides considerably better tolerability than other N-methyl-Daspartate antagonists, gacyclidine has improved function, histology and electrophysiology in a rat model [61,63] .…”

Section: Gacyclidine (Gk11)mentioning

confidence: 96%

“…Like gacyclidine (GK11), NMDA also has shown that receptor antagonists have significant neuroprotective effects after SCI in animal studies [61] . With the distribution of glutamate into each side of the central nervous system in humans, significant adverse effects of the systematic treatment may be seen.…”

Section: Gacyclidine (Gk11)mentioning

confidence: 99%

Current and future medical therapeutic strategies for the functional repair of spinal cord injury

Yılmaz¹

2015

WJO

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Spinal cord injury (SCI) leads to social and psychological problems in patients and requires costly treatment and care. In recent years, various pharmacological agents have been tested for acute SCI. Large scale, prospective, randomized, controlled clinical trials have failed to demonstrate marked neurological benefit in contrast to their success in the laboratory. Today, the most important problem is ineffectiveness of nonsurgical treatment choices in human SCI that showed neuroprotective effects in animal studies. Recently, attempted cellular therapy and transplantations are promising. A better understanding of the pathophysiology of SCI started in the early 1980s. Research had been looking at neuroprotection in the 1980s and the first half of 1990s and regeneration studies started in the second half of the 1990s. A number of studies on surgical timing suggest that early surgical intervention is safe and feasible, can improve clinical and neurological outcomes and reduce health care costs, and minimize the secondary damage caused by compression of the spinal cord after trauma. This article reviews current evidence for early surgical decompression and nonsurgical treatment options, including pharmacological and cellular therapy, as the treatment choices for SCI.

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“…For instance, Vitamin C and E are strong antioxidant, which can provide best protection against cord ischemia [18][19][20]. A novel N-methyl-D-aspartate (NMDA) antagonist, Gacyclidine, owns its capacity for reducing the extent of an ischemic lesion and may promise its future use [21,22]. If medical managements don't reveal significant improvement of delayed neurologic compromise, surgery that return spinal cord to its former kyphotic position by releasing part of the correction may be considered [4,23].…”

Section: Disscussionmentioning

confidence: 99%

Delayed Neurologic Deficit after Thoracolumbar Kyphosis Correction: One Case Report

Rong¹

2015

J Spine

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Study design: Case Report.Objective: To present one case suffering from delayed neurologic deficit after kyphosis deformity correction and analyze its potential etiological factors, how to identify and treat it.Summary of background data: Tardive neurologic deficits occur much less than acute ones after corrections of spinal deformities. Currently some risk factors, such as postoperative hypotension, deformity severity, and intraoperative haemorrhage are considered to be related with its occurrence and worsening though the true mechanisms are not clear. Extrinsic cord compression should be excluded by radiographic examinations before conservative treatments, such as improving blood perfusion, eliminating cord edema, suppressing local inflammation; promoting neurite outgrowth can be applied. If these don't lead to functional recovery of spinal cord, emergency operation returning the cord to its former kyphotic position can also be considered. Methods:This 44 year-old female patient demonstrated thoracolumbar kyphosis of 136.9° combined with incompetence of spinal cord before operation, and underwent posterior vertebra column resection with the kyphotic correction of 68.8°. No neurologic dysfunction was found during operation.

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Neuroprotective effects of a novel NMDA antagonist, Gacyclidine, after experimental contusive spinal cord injury in adult rats

Cited by 87 publications

References 52 publications

Protective effects of extract of Ginkgo biloba (EGb 761) on nerve cells after spinal cord injury in rats

Protective effects of extract of Ginkgo biloba (EGb 761) on nerve cells after spinal cord injury in rats

Current and future medical therapeutic strategies for the functional repair of spinal cord injury

Delayed Neurologic Deficit after Thoracolumbar Kyphosis Correction: One Case Report

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