Mitochondrial dysfunction after experimental and human brain injury and its possible reversal with a selective N-type calcium channel antagonist (SNX-lll)

Verweij, Bon H.; Muizelaar, J. Paul; Viñas, Federico C.; Peterson, Pamela E.; Xiong, Ye; Lee, C. P.

doi:10.1080/01616412.1997.11740821

Cited by 133 publications

(5 citation statements)

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“…studies showed a decreased cytosolic phosphorylation ratio and an increased mitochondrial oxidative phosphorylation following fluid percussion injury , weight drop injury (Heath and Vink, 1995), and CCI injury (Verweij et al, 1997). An altered bioenergetic state leads to a disruption of cellular ionic gradients.…”

Section: Tbi Alters the Cerebral Bioenergetic State Recentmentioning

confidence: 99%

Traumatic Brain Injury Down‐Regulates Glial Glutamate Transporter (GLT‐1 and GLAST) Proteins in Rat Brain

Rao

Başkaya

Doğan

et al. 1998

Journal of Neurochemistry

190

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Excess activation of NMDA receptors is felt to participate in secondary neuronal damage after traumatic brain injury (TBI). Increased extracellular glutamate is active in this process and may result from either increased release or decreased reuptake. The two high‐affinity sodium‐dependent glial transporters [glutamate transporter 1 (GLT‐1) and glutamate aspartate transporter (GLAST)] mediate the bulk of glutamate transport. We studied the protein levels of GLT‐1 and GLAST in the brains of rats after controlled cortical impact‐induced TBI. With use of subtype‐specific antibodies, GLT‐1 and GLAST proteins were quantitated by immunoblotting in the ipsilateral and contralateral cortex at 2, 6, 24, 72, and 168 h after the injury. Sham‐operated rats served as control. TBI resulted in a significant decrease in GLT‐1 (by 20–45%; p < 0.05) and GLAST (by 30–50%; p < 0.05) protein levels between 6 and 72 h after the injury. d‐[3H]Aspartate binding also decreased significantly (by 30–50%; p < 0.05) between 6 and 72 h after the injury. Decreased glial glutamate transporter function may contribute to the increased extracellular glutamate that may mediate the excitotoxic neuronal damage after TBI. This is a first report showing altered levels of glutamate transporter proteins after TBI.

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Section: Tbi Alters the Cerebral Bioenergetic State Recentmentioning

confidence: 99%

Traumatic Brain Injury Down‐Regulates Glial Glutamate Transporter (GLT‐1 and GLAST) Proteins in Rat Brain

Rao

Başkaya

Doğan

et al. 1998

Journal of Neurochemistry

190

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“…After SCI, secondary neuronal death happens due to the glutamate-mediated excitotoxicity, leading to excessive intracellular calcium, mitochondrial dysfunction, acidosis, and the overproduction of free radicals [ 280 , 281 , 282 , 283 , 284 , 285 , 286 ]. This condition can be prevented by Prialt™ via inhibiting the release of glutamate [ 287 , 288 ] and calcium influx [ 276 ] and protecting mitochondria from traumatic brain injury [ 289 , 290 , 291 ]. Moreover, Prialt™ can reduce the expression of nNOS to inhibit apoptosis [ 178 ].…”

Section: Clinical Applications Of Neurotoxinsmentioning

confidence: 99%

Neurotoxins Acting at Synaptic Sites: A Brief Review on Mechanisms and Clinical Applications

Zhou

Luo

Liu

et al. 2022

Toxins

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Neurotoxins generally inhibit or promote the release of neurotransmitters or bind to receptors that are located in the pre- or post-synaptic membranes, thereby affecting physiological functions of synapses and affecting biological processes. With more and more research on the toxins of various origins, many neurotoxins are now widely used in clinical treatment and have demonstrated good therapeutic outcomes. This review summarizes the structural properties and potential pharmacological effects of neurotoxins acting on different components of the synapse, as well as their important clinical applications, thus could be a useful reference for researchers and clinicians in the study of neurotoxins.

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“…This idea has received further support from experimental TBI studies utilizing ketone bodies as an alternative substrate 48 and clinical studies that show increased brain uptake of lactate following TBI 49 . A Clinician's Guide to the Pathophysiology of Traumatic Brain Injury In addition to the glycolytic disturbances mentioned above, there is also increasing evidence for impairment of oxidative metabolism following brain trauma [50][51][52][53] . This may lead to depletion of high-energy phosphates (adenosine triphosphate, ATP) [54][55][56] , with a subsequent rise in anaerobic metabolism, and yet further accumulation of lactate 41,[57][58][59] .…”

Section: Pathophysiology Pathophysiology Pathophysiology Pathophysiolmentioning

confidence: 99%

A clinician's guide to the pathophysiology of traumatic brain injury

Madikians¹,

Giza²

2006

The Indian Journal of Neurotrauma

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Traumatic brain injury induces a complex pathophysiological cascade of cellular events. Central components of this response include increases in cerebral glucose uptake, reductions in cerebral blood flow, indiscriminate excitatory neurotransmitter release, ionic disequilibrium, and intracellular calcium accumulation. Acute glutamate release and nonspecific neuronal depolarization induce threatening perturbations in neuronal function. Restoration of homeostasis requires significant increases in glucose metabolism; however, there is often a concomitant reduction in cerebral blood flow, resulting in an uncoupling of supply and demand. Understanding the nature and timing of these processes provides the practicing clinician with a mechanistic rationale for acute physiological monitoring, aggressive interventions to address and minimize secondary injuries, implementation of advanced neuroimaging techniques, and careful monitoring return to normal activity in head injured patients.

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Mitochondrial dysfunction after experimental and human brain injury and its possible reversal with a selective N-type calcium channel antagonist (SNX-lll)

Cited by 133 publications

References 1 publication

Traumatic Brain Injury Down‐Regulates Glial Glutamate Transporter (GLT‐1 and GLAST) Proteins in Rat Brain

Traumatic Brain Injury Down‐Regulates Glial Glutamate Transporter (GLT‐1 and GLAST) Proteins in Rat Brain

Neurotoxins Acting at Synaptic Sites: A Brief Review on Mechanisms and Clinical Applications

A clinician's guide to the pathophysiology of traumatic brain injury

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