Effects of calcium and calcium antagonists against deprivation of glucose and oxygen in guinea pig hippocampal slices

Amagasa, Masataka; Ogawa, Akira; Yoshimoto, Takashi

doi:10.1016/0006-8993(90)90242-4

Cited by 27 publications

(6 citation statements)

References 35 publications

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“…It may also be significant that the CAl neurones were subjected to only 2-4 min of anoxia. After this time, and thus at times comparable with our study, there is a decrease in extracellular Ca2+ concentration (Hansen, 1985;Silver & Erecin'ska, 1990) and neuronal depolarization (Silver & Erecinska, 1990) which is suggestive of an increase in ICa Both NMDA receptor activation (Choi, 1988;Silver & Ereciniska, 1990) and voltage-dependent Ca2+ channels may be involved (Choi, 1988;Amagasa, Ogawa & Yoshimoto, 1990).…”

Section: Inward Currents During Anoxiasupporting

confidence: 81%

Ionic basis of membrane potential changes induced by anoxia in rat dorsal vagal motoneurones.

Cowan

Martin

1992

The Journal of Physiology

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SUMMARY1. The effects of anoxia on membrane properties of 119 dorsal vagal motoneurones (DVMs) were investigated in an in vitro slice preparation of the rat medulla.2. Membrane potential was unaffected by anoxia in 11 % of DVMs. An hyperpolarization accompanied by a decrease in input resistance occurred in 44 % of DVMs; the remaining 45 % depolarized with either an increase (60 %) or decrease in input resistance (40 %). TTX at a concentration of 0-3-1 /M did not significantly affect these responses.3. Anoxic artificial cerebrospinal fluid (ACSF) containing 20 mM-TEA reversed the response of DVMs that hyperpolarized in standard ACSF to reveal a depolarization of 7-4 + 2 1 mV, and increased the anoxic depolarization from 5'0 + 0-7 to 8'7 + 1 4 mV. 5. In anoxic ACSF containing TEA, the action potential width was increased from 0 92 + 0'04 to 841 + 1 1 ms in hyperpolarizing DVMs, and from 0'85 + 0-01 to 2 4 + 1 0 ms in depolarizing DVMs. The increase in width was prevented by 2-3 mMMn2+ 6. The long after-hyperpolarization (AHP) of DVMs, which is contributed to by both an apamin-sensitive IK(ca) and an apamin, charybdotoxin and TEA insensitive IK(Ca) was decreased in duration from 2-59+0-14 to 1P94+0'12 s during anoxia.

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Section: Inward Currents During Anoxiasupporting

confidence: 81%

Ionic basis of membrane potential changes induced by anoxia in rat dorsal vagal motoneurones.

Cowan

Martin

1992

The Journal of Physiology

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“…Substrate depletion-induced injury in our cultures presumably resulted from a loss of ATP in both neurons and astrocytes that could be attenuated by glucose. Why energy depletion kills astrocytes is not known precisely, but in neurons a decline in ATP leads to depolarization, the expression of the "excitotoxic" action of glutamate, and the lethal accumulation of intracellular calcium (Goldberg et al, 1987;Rothman et al, 1987;Novelli et al, 1988;Erecihska and Silver, 1989;Amagasa et al, 1990;Kohmura et al, 1990). In our system, CORT may have impaired energy metabolism in neurons, further enhancing their sensitivity to excitotoxic injury.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids Exacerbate Hypoxic and Hypoglycemic Hippocampal Injury In Vitro: Biochemical Correlates and a Role for Astrocytes

Tombaugh

Yang

Swanson

et al. 1992

Journal of Neurochemistry

138

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The acute secretion of glucocorticoids is critical for responding to physiological stress. Under normal circumstances these hormones do not cause acute neuronal injury, but they have been shown to enhance ischemic and seizure-induced neuronal injury in the rat brain. Using fetal rat hippocampal cultures, we asked whether hypoxic and hypoglycemic cell damage in vitro could be exacerbated by direct exposure to corticosterone (CORT). Each of these insults alone damaged neuronal cells, whereas 4-6 h of hypoxic treatment could damage age-matched astrocytes if glucose was reduced or omitted. Ischemic-like injury to both cell types could be attenuated by pretreatment with high (30 mM) glucose. Exposure to 100 nM CORT did not affect cell viability under control conditions but enhanced both hypoxic and hypoglycemic neuronal injury. In both cases, pretreatment with high glucose abolished this CORT-mediated synergy. In astrocyte cultures, CORT exacerbated both hypoxic and hypoglycemic injury and this effect was also attenuated by high-glucose pretreatment. Identical 24-h CORT treatment caused a 13% reduction in glucose uptake in astrocytes and a 38% reduction in glycogen content, without affecting the level of intracellular glucose. Thus, CORT could endanger both neurons and astrocytes in mixed hippocampal cultures and this effect emerged only under conditions of substrate depletion. The metabolic disruption in astrocytes by CORT further suggests that the ability of CORT to exacerbate neuronal injury may be due in part to impaired glial cell function.

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“…In the case of hypoxia/ischemia, mitochondria sequester the calcium, but become damaged once the levels of Ca 2+ are in excess of their buffering capacity. The reduction or removal of calcium from the experimental media in adult rat hippocampal slice preparations during both brief and prolonged hsd improved the recovery of rat hippocampal slices compared to slices perfused with normal concentrations of calcium (Amagasa et al, 1990;Balestrino and Somjen, 1986;Roberts and Sick, 1988;Young et al, 1991). In addition, a relationship has been demonstrated between the mitochondrial redox status (i.e.…”

Section: Influence Of Calciummentioning

confidence: 94%

NADH hyperoxidation correlates with enhanced susceptibility of aged rats to hypoxia

Foster¹,

Margraf²,

Turner³

2008

Neurobiology of Aging

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Aging increases mitochondrial dysfunction and susceptibility to hypoxia. Previous reports have indicated an association between post-hypoxic hyperoxidation of intra-mitochondrial enzymes and delayed neuronal injury. Therefore we investigated the relationship between NADH fluorescence and neuronal function during and after hypoxia across the lifespan. Hippocampal slices were prepared from adult (1 to >22 months) F344 rats. NADH fluorescence, extracellular voltage and tissue PO 2 were recorded from the CA1 region during hypoxia (95% N 2 ) of various lengths following onset of hypoxic spreading depression (hsd). Slices from younger rats recovered evoked neuronal responses to a greater degree and exhibited less hyperoxidation after a hypoxic episode, than slices from older rats. However, the use of Ca 2+ free-media in slices from >22 month old rats improved recovery and delayed NADH hyperoxidation (2.5 min hypoxia after hsd). Post-hypoxic decrease of NADH fluorescence (hyperoxidation) was age dependent and correlated with decreased neuronal recovery. Slices exposed to repeated hypoxic episodes yielded data suggesting depletion of the NAD + pool, which may have contributed to the deterioration of neuronal function.

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Effects of calcium and calcium antagonists against deprivation of glucose and oxygen in guinea pig hippocampal slices

Cited by 27 publications

References 35 publications

Ionic basis of membrane potential changes induced by anoxia in rat dorsal vagal motoneurones.

Ionic basis of membrane potential changes induced by anoxia in rat dorsal vagal motoneurones.

Glucocorticoids Exacerbate Hypoxic and Hypoglycemic Hippocampal Injury In Vitro: Biochemical Correlates and a Role for Astrocytes

NADH hyperoxidation correlates with enhanced susceptibility of aged rats to hypoxia

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