Distribution of hypoxia-induced calcium accumulation in gerbil hippocampal slice

Mitani, Akira; Kadoya, Fumito; Kataoka, Kiyoshi

doi:10.1016/0304-3940(90)90163-4

Cited by 41 publications

(15 citation statements)

References 8 publications

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“…Large accumulations of free calcium disrupt metabolic function and eventually cause neuronal death. 96 This massive increase in intracellular free calcium occurs preferentially in the cells that appear to be selectively vulnerable to ischemia. 97 ' 98 Neuronal injury from hypoxia can be prevented if calcium accumulation is blocked.…”

Section: Neuronal Cellsmentioning

confidence: 99%

Cognitive performance, mood, and neurological status at high terrestrial elevation

Banderet¹,

Shukitt-Hale²

2002

PsycEXTRA Dataset

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. ABSTRACT (Maximum 200 words)Cognitive and psychomotor performance and mood states, including many critical behavioral functions such as sleep, memory, ■ reasoning, and vigilance, are significantly impaired by ascent to HTE higher than 3,000 m. Impairments in behavior caused by HTE can degrade military operations because the judgment and rate and accuracy of performance of military personnel can be affected. Such adverse effects have distinct and measurable time courses; onset of some effects is immediate (cognitive performance), whereas the onset of others is delayed (symptoms of AMS or adverse moods). The behavioral consequences of HTE are primarily dependent on the level of altitude, the duration of exposure the rate of ascent, an individual's state of physiological acclimation or acclimatization, characteristics of the task performed, and characteristics of the individual such as hypoxic sensitivity. Military history documents that the adverse effects induced by HTE need to be considered when military operations at altitude are planned and undertaken. Current research indicates that some performance decrements induced by ascent to extremely high mountains (e.g., Mount Everest, 8,848 m) may persist for a year or longer after return to lower elevations. Psychological, operational, and medical strategies have been employed to minimize these adverse effects. Psychological strategies often involve training and familiarization with the adverse effects that will be experienced at high altitude. Operational strategies include staging at intermediate altitudes, acclimatizing, and using supplemental oxygen from tanks of oxygen generators. Medical strategies often involve the use of medications to improve functioning at altitude and techniques to avoid complications. In most situations, multiple strategies are employed. The strategies now available and new developments to come will ensure that high-altitude military operations in the future will be less affected by adverse changes in cognitive and psychomotor performance and mood.14. SUBJECT TERMS high altitude, hypoxia, cognitive performance, moods, symptoms, time course of altitude effects, behavior NUMBER OF PAGES 3516. PRICE CODE

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Section: Neuronal Cellsmentioning

confidence: 99%

Cognitive performance, mood, and neurological status at high terrestrial elevation

Banderet¹,

Shukitt-Hale²

2002

PsycEXTRA Dataset

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“…Studies using in vivo ischemic models of the retina have demonstrated that inner retinal neurons are more vulnerable to ischemia than outer retinal neurons (Hughes, 1991;Szabo et al, 1991;Peachey, Green and Ripps, 1993;Osborne, Larsen and Barnett, 1995;Larsen and Osborne, 1996;Rosenbaum et al, 1998). If in the retina there is a correlation between the rates of increase in [Ca 2 ] i and selective vulnerability to ischemia as is seen in the hippocampus (Mitani et al, 1990) …”

Section: Introductionmentioning

confidence: 95%

“…Biochemical and morphological studies have been conducted under ischemic conditions in the isolated retina of rat, rabbit or chick (Ames, 1983;Winkler, 1983;Doberstein et al, 1994;Neal et al, 1994;Romano et al, 1998). However, to date, intracellular Ca 2 responses to an in vitro ischemia have not been determined in retinal slice preparations, as has been performed using brain slices (Kass and Lipton, 1986;Mitani et al, 1990;Schurr et al, 1995;Laake et al, 1999). Studies using in vivo ischemic models of the retina have demonstrated that inner retinal neurons are more vulnerable to ischemia than outer retinal neurons (Hughes, 1991;Szabo et al, 1991;Peachey, Green and Ripps, 1993;Osborne, Larsen and Barnett, 1995;Larsen and Osborne, 1996;Rosenbaum et al, 1998).…”

Section: Introductionmentioning

confidence: 98%

“…Moreover, the development of imaging techniques using¯uor-escent probes for Ca 2 has enabled us to determine the temporal changes in the two-dimensional distribution of intracellular Ca 2 concentration {[Ca 2 ] i } in cultured cells or tissues. These techniques have been used to demonstrate the mobilization of [Ca 2 ] i under ischemic-like conditions (Mitani, Kadoya and Kataoka, 1990;Pisani et al, 1998) as well as in the presence of neurotransmitters or with activation of ion channels (Tank et al, 1988;Kudo, Nakamura and Ito, 1991;Yuste and Katz, 1991;Segal, 1995). Much attention has been focused on calcium due to its possible role in mediating neuronal cell death.…”

Section: Introductionmentioning

confidence: 99%

“…The CA1 region is the most susceptible, whereas the CA3 region and dentate gyrus are relatively resistant to ischemia (Kirino and Sano, 1984). Experiments in hippocampal slices demonstrated that a region-speci®c increase in [Ca 2 ] i , is elicited in the CA1 with glucose/oxygen deprived solution (Mitani et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Intracellular Ca2+Changes Induced by in vitro Ischemia in Rat Retinal Slices

Kuriyama

Nakagawa²,

Tsuda³

2001

Experimental Eye Research

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Species differences in fodrin proteolysis in the ischemic brain

Kitagawa¹,

Matsumoto²,

Saido³

et al. 1999

J. Neurosci. Res.

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There has been growing evidence that the breakdown of cytoskeletal proteins is an important biochemical change leading to ischemic neuronal death. In the present study, we investigated species differences in the susceptibility of fodrin to calpain activation induced by cerebral ischemia in gerbils, rats, and mice. In vivo fodrin proteolysis and degradation of microtubule-associated protein 2 after complete ischemia occurred more rapidly in the hippocampus and cerebral cortex of the gerbil brain than in the corresponding area of the rat and mouse brain. The N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 injected intraperitoneally before ischemia did not diminish fodrin degradation in the gerbil hippocampus. In vivo fodrin proteolysis was inhibited at 33 degrees C and enhanced at 41 degrees C compared with proteolysis at 37 degrees C during ischemia. However, in vitro fodrin proteolysis after addition of Ca2+ into the crude membrane fraction did not show any differences among three species. Although it is highly unlikely that the difference in the sensitivity of NMDA receptor or the sensitivity of calpain activation to calcium was the crucial determinant of susceptibility of fodrin degradation in the gerbil brain, the present study clearly demonstrated that fodrin in the gerbil brain was more susceptible to calpain activation induced by ischemia than that in the rat and mouse brains. Enhanced proteolysis may be one of the reasons neurons in the gerbil brain are highly vulnerable to ischemia.

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Distribution of hypoxia-induced calcium accumulation in gerbil hippocampal slice

Cited by 41 publications

References 8 publications

Cognitive performance, mood, and neurological status at high terrestrial elevation

Cognitive performance, mood, and neurological status at high terrestrial elevation

Intracellular Ca2+Changes Induced by in vitro Ischemia in Rat Retinal Slices

Species differences in fodrin proteolysis in the ischemic brain

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