Mechanisms of norepinephrine accumulation within sites of spinal cord injury

Vise, W. Michael; Yashon, David; Hunt, William E.

doi:10.3171/jns.1974.40.1.0076

Cited by 44 publications

(6 citation statements)

References 23 publications

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“…On the other hand, the concentration of 5HT in blood platelets is several orders of magnitude greater than in the cord (Da Prada and Picotti, 1979). Platelet aggregation (Assenmacher and Ducker, 1971), blood-brain barrier disruption (Vise et al, 1974), and hemorrhage (Assenmacher and Ducker, 1971) are well-documented correlates of spinal trauma. It is thus reasonable to attribute the rapid and marked posttraumatic elevation of 5HT in the cord to the extravasation of platelet-derived 5HT.…”

Section: Discussionmentioning

confidence: 98%

Serotonergic Response to Spinal Distraction Trauma in Experimental Scoliosis

Salzman¹,

Mendez²,

Dabney³

et al. 1991

Journal of Neurotrauma

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The effects of distraction injury to the spinal cord on serotonin (5HT) content and metabolism in a rat model of scoliosis were studied. Previous studies in this laboratory (Salzman et al., 1987a) have identified the 5HT response as a major component of the posttraumatic progression of spinal injury after impact trauma in the rabbit. The present study was designed to determine the universality of this response by examining a different model of injury in a different species. The results demonstrate that distraction trauma in the rat, like impact injury in the rabbit, is associated with a rapid and robust increase in the local spinal cord content and metabolism of 5HT and a long-term depletion of 5HT below the site of injury. The roles of the blood platelet and the raphe-spinal tract in the acute response and the disruption of axoplasmic transport during the chronic phase of injury are discussed.

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Section: Discussionmentioning

confidence: 98%

Serotonergic Response to Spinal Distraction Trauma in Experimental Scoliosis

Salzman¹,

Mendez²,

Dabney³

et al. 1991

Journal of Neurotrauma

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“…The data correlate well with earlier published reports. [7][8][9]12,[28][29][30] Loss or decrease of motor activity is the most prominent and the most functionally relevant result of the spinal cord injury. 31 Motor disturbances observed in the rabbits that experienced trauma in response to the force of 150 g cm were not the result of the laminectomy procedure.…”

Section: Discussionmentioning

confidence: 99%

Effect of indomethacin on motor activity and spinal cord free fatty acid content after experimental spinal cord injury in rabbits

et al. 2005

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Study design: Determination of functional and biochemical parameters as well as the effect of specific therapies on these parameters, in the experimental model of neurotrauma in rabbits. Objective: To assess the effect of indomethacin (0.1-3.0 mg/kg for 9 days), a potent inhibitor of endogenous prostaglandin synthesis, on the motor activity and on the spinal cord tissue concentration of free palmitic, stearic, oleic, arachidonic and docosahexaenoic acids in an experimental model of a spinal cord injury in rabbits. Setting: Faculty of Medicine, University of Rijeka, Croatia. Methods: The animals were randomly divided into nine experimental groups, four sham and/ or vehicle-treated and five indomethacin-treated (including one sham-operated and four injured groups). Laminectomy was followed by contusion of the spinal cord, using a modification of the technique of Albin. Motor activity was controlled daily during the course of the next nine postoperation days and scored using Tarlov's system. Spinal cord samples from the impact injury site were taken and frozen in liquid nitrogen. Total lipids were isolated and purified by a modification of the method of Folch. Free fatty acids (FFAs) were separated from the total lipid extract by preparative thin-layer chromatography, converted to the corresponding methyl esters and identified using gas chromatography, using nonadecanoic acid as the internal standard. Results: The concentrations of all analysed free fatty acids were increased in the spinal cord after neurotrauma, in comparison to control tissues. Treatment of injured rabbits with indomethacin resulted in a significant decrease in spinal cord FFAs and exerted a positive effect on neurotrauma-induced motor impairment. Conclusion: These results indicate a mechanism whereby indomethacin protects rabbits from the sequellae of neuronal damage caused by trauma, and suggests that it may be beneficial in the therapy of neurotrauma.

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“…Dobutamine [369] Propranolol [380,381], carvedilol [382,383], nadolol [384] β Adrenoreceptors' involvement in spinal cord neuromodulation is extensive. Traditionally, in conditions of early SCI, NE's activities are known to be involved in hemorrhagic necrosis [386][387][388][389], blood pressure/blood flow [390][391][392], and motor function [387,[393][394][395]. Nociception is regulated by α2-adrenergic receptors which inhibit activity of deep dorsal horn neurons [362,363], and in neuropathic pain models of SCI, catecholaminergic fibers have shown evidence of maladaptive plasticity and fiber sprouting after thoracic transection [396,397].…”

Section: Gsmentioning

confidence: 99%

Role of Descending Serotonergic Fibers in the Development of Pathophysiology after Spinal Cord Injury (SCI): Contribution to Chronic Pain, Spasticity, and Autonomic Dysreflexia

Fauss

Hudson

Grau

2022

Biology

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As the nervous system develops, nerve fibers from the brain form descending tracts that regulate the execution of motor behavior within the spinal cord, incoming sensory signals, and capacity to change (plasticity). How these fibers affect function depends upon the transmitter released, the receptor system engaged, and the pattern of neural innervation. The current review focuses upon the neurotransmitter serotonin (5-HT) and its capacity to dampen (inhibit) neural excitation. A brief review of key anatomical details, receptor types, and pharmacology is provided. The paper then considers how damage to descending serotonergic fibers contributes to pathophysiology after spinal cord injury (SCI). The loss of serotonergic fibers removes an inhibitory brake that enables plasticity and neural excitation. In this state, noxious stimulation can induce a form of over-excitation that sensitizes pain (nociceptive) circuits, a modification that can contribute to the development of chronic pain. Over time, the loss of serotonergic fibers allows prolonged motor drive (spasticity) to develop and removes a regulatory brake on autonomic function, which enables bouts of unregulated sympathetic activity (autonomic dysreflexia). Recent research has shown that the loss of descending serotonergic activity is accompanied by a shift in how the neurotransmitter GABA affects neural activity, reducing its inhibitory effect. Treatments that target the loss of inhibition could have therapeutic benefit.

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Mechanisms of norepinephrine accumulation within sites of spinal cord injury

Cited by 44 publications

References 23 publications

Serotonergic Response to Spinal Distraction Trauma in Experimental Scoliosis

Serotonergic Response to Spinal Distraction Trauma in Experimental Scoliosis

Effect of indomethacin on motor activity and spinal cord free fatty acid content after experimental spinal cord injury in rabbits

Role of Descending Serotonergic Fibers in the Development of Pathophysiology after Spinal Cord Injury (SCI): Contribution to Chronic Pain, Spasticity, and Autonomic Dysreflexia

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