Neurobiology of Stroke

Wd, Dietrich

doi:10.1016/s0074-7742(08)60608-x

Cited by 23 publications

(11 citation statements)

References 218 publications

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“…The early, diffuse damage identified is not consistent with focal ischemia that would have precipitated a more delayed and highly focal neuronal response (Dietrich et al, 1987;Dereski et al, 1993;Dietrich, 1998;Mennel et al, 2000;Bramlett and Dietrich, 2004). Although in this study, DTBI evoked elevated ICP, this elevation never exceeded 20 mmHg, suggesting no significant alteration in cerebral perfusion pressure with the normal arterial blood pressure described in this study.…”

Section: Membrane Disruption and Enduring Membrane Permeabilitycontrasting

confidence: 68%

Mechanoporation Induced by Diffuse Traumatic Brain Injury: An Irreversible or Reversible Response to Injury?

Farkas¹,

Lifshitz²,

Povlishock³

2006

J. Neurosci.

164

149

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Diffuse traumatic brain injury (DTBI) is associated with neuronal plasmalemmal disruption, leading to either necrosis or reactive change without cell death. This study examined whether enduring membrane perturbation consistently occurs, leading to cell death, or if there is the potential for transient perturbation followed by resealing/recovery. We also examined the relationship of these events to calpainmediated spectrin proteolysis (CMSP). To assess plasmalemmal disruption, rats (n ϭ 21) received intracerebroventricular infusion 2 h before DTBI of a normally excluded 10 kDa fluorophore-labeled dextran. To reveal plasmalemmal resealing or enduring disruption, rats were infused with another labeled dextran 2 h (n ϭ 10) or 6 h (n ϭ 11) after injury. Immunohistochemistry for the 150 kDa spectrin breakdown product evaluated the concomitant role of CMSP. Neocortical neurons were followed with confocal and electron microscopy.

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Section: Membrane Disruption and Enduring Membrane Permeabilitycontrasting

confidence: 68%

Mechanoporation Induced by Diffuse Traumatic Brain Injury: An Irreversible or Reversible Response to Injury?

Farkas¹,

Lifshitz²,

Povlishock³

2006

J. Neurosci.

164

149

View full text Add to dashboard Cite

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“…This vessel occlusion creates a region of severe focal ischemia in the brain area supplied by the affected vessel (Wolf & D'Agostino, 1998). Eventually, neurons and glia in this core region of ischemia die, creating a pan necrotic cerebral infarction (Dietrich, 1998). Surrounding this ischemic core of irreversible damage is a region that suffers only partially reduced blood supply.…”

Section: Stroke: Causes Neuronal Injury and Increased Glutamate And Cmentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

260

286

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Epilepsy is one of the most common neurological disorders. Although epilepsy can be idiopathic, it is estimated that up to 50% of all epilepsy cases are initiated by neurological insults and are called acquired epilepsy (AE). AE develops in 3 phases: (1) the injury (central nervous system [CNS] insult), (2) epileptogenesis (latency), and (3) the chronic epileptic (spontaneous recurrent seizure) phases. Status epilepticus (SE), stroke, and traumatic brain injury (TBI) are 3 major examples of common brain injuries that can lead to the development of AE. It is especially important to understand the molecular mechanisms that cause AE because it may lead to innovative strategies to prevent or cure this common condition. Recent studies have offered new insights into the cause of AE and indicate that injury-induced alterations in intracellular calcium concentration levels [Ca 2+ ] i and calcium homeostatic mechanisms play a role in the development and maintenance of AE. The injuries that cause AE are different, but they share a common molecular mechanism for producing brain damage -an increase in extracellular glutamate concentration that causes increased intracellular neuronal calcium, leading to neuronal injury and/or death. Neurons that survive the injury induced by glutamate and are exposed to increased [Ca 2+ ] i are the cellular substrates to develop epilepsy because dead cells do not seize. The neurons that survive injury sustain permanent long-term plasticity changes in [Ca 2+ ] i and calcium homeostatic mechanisms that are permanent and are a prominent feature of the epileptic phenotype. In the last several years, evidence has accumulated indicating that the prolonged alteration in neuronal calcium dynamics plays an important role in the induction and maintenance of the prolonged neuroplasticity changes underlying the epileptic phenotype. Understanding the role of calcium as a second messenger in the induction and maintenance of epilepsy may provide novel insights into therapeutic advances that will prevent and even cure AE.

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“…In stroke, tissue damage is most often caused by ischemia resulting from an occluded blood vessel (Dietrich 1998 ) . Neuroprotection by manipulation of brain nucleoside system may be bene fi cial in stroke victims.…”

Section: Strokementioning

confidence: 99%

Anatomical Distribution of Nucleoside System in the Human Brain and Implications for Therapy

Kovács

Dobolyi

2012

Adenosine

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Nucleosides have a wide range of physiological and pathophysiological roles in the human brain as modulators of a variety of neural functions. For example, adenosine, inosine, guanosine, and uridine participate in the mechanisms underlying memory, cognition, sleep, pain, depression, schizophrenia, epilepsy, Alzheimer's disease, Huntington's disease, and Parkinson's disease. Consequently, increasing attention is now being given to the speci fi c role of nucleosides in physiological and pathological processes in the human brain. Different elements of nucleoside system, including nucleoside concentrations, metabolic enzyme activity, and expression of nucleoside transporters and receptors, may be changed under normal and pathological conditions. The alterations suggest that interlinked elements of the nucleoside system are functioning in a tightly concerted manner.Nucleoside levels, activity of nucleoside metabolic enzymes, and expression of nucleoside transporters and receptors are unevenly distributed in the brain, suggesting that nucleosides have different roles in functionally distinct human brain areas. The aim of this chapter is to summarize our present knowledge of the anatomical distribution of nucleoside system in the human brain, placing emphasis on potential therapeutic pharmacological strategies.

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Neurobiology of Stroke

Cited by 23 publications

References 218 publications

Mechanoporation Induced by Diffuse Traumatic Brain Injury: An Irreversible or Reversible Response to Injury?

Mechanoporation Induced by Diffuse Traumatic Brain Injury: An Irreversible or Reversible Response to Injury?

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

Anatomical Distribution of Nucleoside System in the Human Brain and Implications for Therapy

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