Cell Damage in the Brain: A Speculative Synthesis

Siesjö, Bo K.

doi:10.1038/jcbfm.1981.18

Cited by 1,724 publications

(141 citation statements)

References 202 publications

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“…This seems to correlate with their selective vulnerability to ischemic, epileptic, and hypoglycemic cell death through calciummediated necrosis (13).…”

Section: Discussionmentioning

confidence: 99%

“…An elevated intracellular concentration of free calcium is considered a primary neurotoxic mechanism in brain damage induced by different means, including ischemia (13,14). The increased concentrations of cytoplasmic free calcium after hypoxia are derived both from an influx and a release from intracellular stores, such as mitochondria and endoplasmic reticulum (27).…”

Section: Discussionmentioning

confidence: 99%

“…Mobilization and influx of calcium has long been considered a major mechanism of ischemic cell death (13)(14)(15)(16). Our histochemical stainings revealed the most prominent STC expression in the pyramidal cells of the cerebral cortex and hippocampus and in the Purkinje cells of the cerebellum (12), i.e., brain neurons known to be highly sensitive to ischemia (13). Given this, we hypothesized that STC may be involved in the protection against hypoxic damage.…”

mentioning

confidence: 90%

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Stanniocalcin: A molecular guard of neurons during cerebral ischemia

Zhang

Lindsberg

Tatlısumak

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

142

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“…This seems to correlate with their selective vulnerability to ischemic, epileptic, and hypoglycemic cell death through calciummediated necrosis (13).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 90%

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Stanniocalcin: A molecular guard of neurons during cerebral ischemia

Zhang

Lindsberg

Tatlısumak

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

142

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“…Alteration of calcium homeostasis is hypothesized to contribute to neuronal death following ischemia-reperfusion (1)(2)(3)(4)(5) or neurodegenerative diseases like Alzheimer's disease (6 -11). An overload of neuronal Ca 2ϩ may activate a number of pathological processes like disruption of the mitochondrial membrane potential, free radical production, stimulation of catabolic enzymes, and enhancement of excitatory amino acid release that will lead to cell death (12).…”

mentioning

confidence: 99%

Calcium Entry through L-type Calcium Channels Causes Mitochondrial Disruption and Chromaffin Cell Death

Cano‐Abad¹,

Villarroya²,

Garcı́a³

et al. 2001

Journal of Biological Chemistry

127

112

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] m and caused mitochondrial membrane depolarization. Cyclosporin A, a blocker of the mitochondrial transition pore, and superoxide dismutase prevented the apoptotic cell death induced by Ca 2؉ overload through L-channels. These results suggest that Ca 2؉ entry through L-channels causes both calcium overload and mitochondrial disruption that will lead to the release of mediators responsible for the activation of the apoptotic cascade and cell death. This predominant role of L-type Ca 2؉ channels is not shared by other subtypes of high threshold voltage-dependent neuronal Ca 2؉ channels (i.e. N, P/Q) expressed by bovine chromaffin cells.

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“…The choices of attempting to enhance glucose transport and using the hippocampus were not random. The brain is exquisitely dependent upon glucose; nervous tissue has extremely high metabolic rates, utilizes little other than glucose, and stores it poorly (34). Moreover, neurological insults such as hypoxia-ischemia, hypoglycemia, and sustained seizure disrupt energy charge in the brain and preferentially damage the hippocampus; in the case of sustained seizure, glucose transport can become the rate-limiting step determining whether there is a damaging mismatch between energy delivery and utilization (32).…”

Section: Construction Of Amplicons and Generation Of Defectivementioning

confidence: 99%

Altering central nervous system physiology with a defective herpes simplex virus vector expressing the glucose transporter gene.

Mocarski

Sapolsky

1993

Proc. Natl. Acad. Sci. U.S.A.

143

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Because of their postmitotic nature, neurons are difficult subjects for gene transfer. To circumvent this, we have used a defective herpes simplex virus vector to overexpress the rat brain glucose transporter (GT) gene under the control of the human cytomegalovirus iel promoter. This vector, designated vIElGT, was propagated using a herpes simplex virus type 1 temperature-sensitive mutant, ts756. GT expressed from vIElGT was readily immunoprecipitated from membrane fractions of vIElGT-infected Vero cells. By using indirect double immunofluorescence techniques, vIElGT was shown to be capable of enhancing GT expression in cultured hippocampal neurons and glia. Glucose transport in such vIElGT-infected cultures was increased -2-fold relative to controls. The efficacy of this system in vivo was then tested by microinjection of vIElGT into adult rat hippocampus. When examined 2 days later, GT expression from vIElGT was demonstrated in hippocampal neurons by in situ hybridization; a small but significant increase in glucose transport was detected in tissue immediately surrounding the injection site by 2-deoxy[14C]glucose uptake and autoradiography. Such iinjections did not cause marked cytopathology. Thus, this approach can be used to alter central nervous system physiology in vitro and in vivo.

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Cell Damage in the Brain: A Speculative Synthesis

Cited by 1,724 publications

References 202 publications

Stanniocalcin: A molecular guard of neurons during cerebral ischemia

Stanniocalcin: A molecular guard of neurons during cerebral ischemia

Calcium Entry through L-type Calcium Channels Causes Mitochondrial Disruption and Chromaffin Cell Death

Altering central nervous system physiology with a defective herpes simplex virus vector expressing the glucose transporter gene.

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