Changes in Norepinephrine and Histamine in Monkey Spinal Cords Traumatized by Weight Drop and Compression

Kuruvilla, Anju; Theodore, Deepa R.; Abraham, Jacob

doi:10.1089/cns.1985.2.61

Cited by 5 publications

(8 citation statements)

References 24 publications

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“…Because Group A animals were used for model development, we did not collect complete velocity, force, and CSF pressure data for all animals (see Table 1); in all other respects Group A was identical to Group B. The weights used were higher than would be expected for a bone fragment associated with a burst fracture, but corresponded to the upper range previously used for large-animal experimental SCI 20,25,27,49,54,90 and were lower than the estimated wet weight of human thoracolumbar vertebra (250-550 g). 7 The height was selected to produce impact velocities within the range estimated for bone fragments during thoracolumbar vertebral burst fractures.…”

Section: Injury Devicementioning

confidence: 99%

Development of a large-animal model to measure dynamic cerebrospinal fluid pressure during spinal cord injury

Jones

Lee

Cripton

2012

SPI

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Object Spinal cord injury (SCI) often results in considerable permanent neurological impairment, and unfortunately, the successful translation of effective treatments from laboratory models to human patients is lacking. This may be partially attributed to differences in anatomy, physiology, and scale between humans and rodent models. One potentially important difference between the rodent and human spinal cord is the presence of a significant CSF volume within the intrathecal space around the human cord. While the CSF may “cushion” the spinal cord, pressure waves within the CSF at the time of injury may contribute to the extent and severity of the primary injury. The objective of this study was to develop a model of contusion SCI in a miniature pig and establish the feasibility of measuring spinal CSF pressure during injury. Methods A custom weight-drop device was used to apply thoracic contusion SCI to 17 Yucatan miniature pigs. Impact load and velocity were measured. Using fiber optic pressure transducers implanted in the thecal sac, CSF pressures resulting from 2 injury severities (caused by 50-g and 100-g weights released from a 50-cm height) were measured. Results The median peak impact loads were 54 N and 132 N for the 50-g and 100-g injuries, respectively. At a nominal 100 mm from the injury epicenter, the authors observed a small negative pressure peak (median −4.6 mm Hg [cranial] and −5.8 mm Hg [caudal] for 50 g; −27.6 mm Hg [cranial] and −27.2 mm Hg [caudal] for 100 g) followed by a larger positive pressure peak (median 110.5 mm Hg [cranial] and 77.1 mm Hg [caudal] for 50 g; 88.4 mm Hg [cranial] and 67.2 mm Hg [caudal] for 100 g) relative to the preinjury pressure. There were no significant differences in peak pressure between the 2 injury severities or the caudal and cranial transducer locations. Conclusions A new model of contusion SCI was developed to measure spinal CSF pressures during the SCI event. The results suggest that the Yucatan miniature pig is an appropriate model for studying CSF, spinal cord, and dura interactions during injury. With further development and characterization it may be an appropriate in vivo largeanimal model of SCI to answer questions regarding pathological changes, therapeutic safety, or treatment efficacy, particularly where humanlike dimensions and physiology are important.

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Section: Injury Devicementioning

confidence: 99%

Development of a large-animal model to measure dynamic cerebrospinal fluid pressure during spinal cord injury

Jones

Lee

Cripton

2012

SPI

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“…Within the complex molecular and cellular milieu that follows a traumatic spinal lesion, increases in the extracellular concentrations of biogenic amines, such as histamine (up to 0.9 mg/L; Kuruvilla et al, 1985), represent a relevant, and to a certain extent underestimated, neuromodulatory factor. Histamine concentrations stabilize at high levels for hours after spinal trauma at both the injury site and adjacent segments (Naftchi et al, 1974;Kobrine & Doyle, 1976;Kuruvilla et al, 1985;Panneerselvam, Cherian, Kuruvilla, Theodore, & Abraham, 1989). Histamine is one of the most potent endogenous vasodilators of the CNS (Burn & Dale, 1926) and contributes to development of hyperaemia and edema (Kobrine & Doyle, 1976;Kobrine, Doyle, & Rizzoli, 1976a;Kobrine, Doyle, & Rizzoli, 1976b;Winkler, Sharma, Stålberg, Olsson, & Nyberg, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…An additional effect of increased histamine levels is the progressive permeability of the blood-brain barrier that activates a positive feedback loop and thus promotes a further increase in the amount of histamine that "leaks" into the central hemorrhagic lesion (Gross, Teasdale, Angerson, & Harper, 1981;Gross, Teasdale, Graham, Angerson, & Harper 1982;Sharma, Vannemreddy, Patnaik, Patnaik, & Mohanty, 2006). After spinal trauma, the first surgical proceduressuch as anesthesia, laminectomy and decompression-have been shown to increase spinal levels of histamine within the first 5 h (Naftchi et al, 1974;Kuruvilla et al, 1985;Panneerselvam et al, 1989). In the future, it would be important to assess whether (and to what extent) increased levels of histamine, to which the spinal cord is exposed beyond the acute phases of the trauma, may contribute to the transient depression of spinal reflex activity (spinal shock; Ditunno, Little, Tessler, & Burns, 2004).…”

Section: Discussionmentioning

confidence: 99%

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Histamine modulates spinal motoneurons and locomotor circuits

Coslovich

Brumley

D’Angelo

et al. 2017

J of Neuroscience Research

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Spinal motoneurons and locomotor networks are regulated by monoamines, among which, the contribution of histamine has yet to be fully addressed. The present study investigates histaminergic regulation of spinal activity, combining intra- and extracellular electrophysiological recordings from neonatal rat spinal cord in vitro preparations. Histamine dose-dependently and reversibly generated motoneuron depolarization and action potential firing. Histamine (20 µM) halved the area of dorsal root reflexes and always depolarized motoneurons. The majority of cells showed a transitory repolarization, while 37% showed a sustained depolarization maintained with intense firing. Extracellularly, histamine depolarized ventral roots (VRs), regardless of blockage of ionotropic glutamate receptors. Initial, transient glutamate-mediated bursting was synchronous among VRs, with some bouts of locomotor activity in a subgroup of preparations. After washout, the amplitude of spontaneous tonic discharges increased. No desensitization or tachyphylaxis appeared after long perfusion or serial applications of histamine. On the other hand, histamine induced single motoneuron and VR depolarization, even in the presence of tetrodotoxin (TTX). During chemically induced fictive locomotion (FL), histamine depolarized VRs. Histamine dose-dependently increased rhythm periodicity and reduced cycle amplitude until near suppression. This study demonstrates that histamine induces direct motoneuron membrane depolarization and modulation of locomotor output, indicating new potential targets for locomotor neurorehabilitation.

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“…With respect to other subcortical substrates, there are few brainstem or spinal cord results on the acute effects of spinal cord injury in monkeys. Nonetheless, acute changes in neurochemistry and structure have been reported at the spinal and brainstem levels [21,54,55]. At the cellular level, acute SCI leads to immediate cell necrosis, lipid peroxidation, lysosomal enzyme release, and cell membrane damage [54].…”

Section: Experimental Animal Studies After Acute Scimentioning

confidence: 99%

Neural Plasticity After Spinal Cord Injury

Ding

Kastin²,

Pan³

2005

CPD

101

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Spinal cord injury (SCI) has devastating physical and socioeconomical impact. However, some degree of functional recovery is frequently observed in patients after SCI. There is considerable evidence that functional plasticity occurs in cerebral cortical maps of the body, which may account for functional recovery after injury. Additionally, these plasticity changes also occur at multiple levels including the brainstem, spinal cord, and peripheral nervous system. Although the interaction of plasticity changes at each level has been less well studied, it is likely that changes in subcortical levels contribute to cortical reorganization. Since the permeability of the blood-brain barrier (BBB) is changed, SCI-induced factors, such as cytokines and growth factors, can be involved in the plasticity events, thus affecting the final functional recovery after SCI. The mechanism of plasticity probably differs depending on the time frame. The reorganization that is rapidly induced by acute injury is likely based on unmasking of latent synapses resulting from modulation of neurotransmitters, while the long-term changes after chronic injury involve changes of synaptic efficacy modulated by long-term potentiation and axonal regeneration and sprouting. The functional significance of neural plasticity after SCI remains unclear. It indicates that in some situations plasticity changes can result in functional improvement, while in other situations they may have harmful consequences. Thus, further understanding of the mechanisms of plasticity could lead to better ways of promoting useful reorganization and preventing undesirable consequences.

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Changes in Norepinephrine and Histamine in Monkey Spinal Cords Traumatized by Weight Drop and Compression

Cited by 5 publications

References 24 publications

Development of a large-animal model to measure dynamic cerebrospinal fluid pressure during spinal cord injury

Development of a large-animal model to measure dynamic cerebrospinal fluid pressure during spinal cord injury

Histamine modulates spinal motoneurons and locomotor circuits

Neural Plasticity After Spinal Cord Injury

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