Increased glucose improves recovery of neuronal function after cerebral hypoxia in vitro

Schurr, Avital; West, Catherine A.; Reid, Kenneth H.; Tseng, Michael T.; Reiss, Steven J.; Rigor, Benjamin M.

doi:10.1016/0006-8993(87)91283-2

Cited by 99 publications

(34 citation statements)

References 18 publications

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“…Our present study also confirmed our previous finding 7 regarding the protective effect of increasing glucose concentrations on synaptic function against hypoxia. In addition, this in vitro model allows one to screen drugs for their cytoprotective effects against ischemia/hypoxia.…”

Section: Discussionsupporting

confidence: 82%

“…In none of these studies was the combined partial deprivation of glucose and oxygen explored. In a recent study, 7 we tested the combined effects of lowered oxygen concentration and increased glucose concentration on hippocampal slices. We found that hypoxic brain slices benefited from higher levels of glucose as measured by the higher rate of recovery of synaptic function upon restoration of normoxic conditions.…”

Section: The Rat Hippocampal Slice Preparation As An In Vitro Model Omentioning

confidence: 99%

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The rat hippocampal slice preparation as an in vitro model of ischemia.

Dong

Schurr

Reid

et al. 1988

Stroke

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In vivo models of cerebral ischemia do not fully control for the interacting effects of many variables (e.g., anesthesia, temperature, cerebrovascular changes) and often do not clearly define the region affected. Numerous in vivo studies have indicated that hyperglycemia augments ischemic brain damage; this effect is often attributed to lactic acidosis. To separate the effects on neuronal tissue of ischemia from those due to actions on the cerebrovascular system, we used an in vitro blood-free system as an ischemic model. In our study we evaluated the effects of various combinations of oxygen and glucose levels on evoked synaptic activity in the CA1 region of the rat hippocampal slice preparation. A 50% inhibitory dose for both oxygen and glucose on neuronal synaptic function was determined. It is our intention to use this model for preliminary screening of antihypoxic/anti-ischemic drugs.

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Section: Discussionsupporting

confidence: 82%

Section: The Rat Hippocampal Slice Preparation As An In Vitro Model Omentioning

confidence: 99%

The rat hippocampal slice preparation as an in vitro model of ischemia.

Dong

Schurr

Reid

et al. 1988

Stroke

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“…In adult animals, hyperglycemia worsens neurologic outcome from ischemia (Siemkowicz and Hansen, 1978;Pulsinelli et al, 1982), whereas glucose supplement in neonate rats reduces hypoxic-ischemic brain damage (Hattori and Wasterlain, 1990). In the rat hippocampal slice, elevated glucose improves recovery of neuronal function after hypoxia (Schurr et al, 1987;Roberts and Sick, 1992). Neonate brain and brain slices may be less susceptible to glycemic state because they do not tend to accumulate lactate during hypoxia Hatton and Wasterlain, 1990).…”

Section: Discussionmentioning

confidence: 99%

Glucose Deprivation Results in a Lactate Preventable Increase in Adenosine and Depression of Synaptic Transmission in Rat Hippocampal Slices

Fowler

1993

Journal of Neurochemistry

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: The effect of glucose deprivation on adenosine levels and on synaptic transmission was investigated in rat hippocampal slices. Incubation of hippocampal slices either in glucose‐free medium or in the presence of the glucose transport inhibitor cytochalasin B (50 μM) increased bath adenosine levels and depressed the extracellularly recorded synaptic potential or population spike. The addition of lactate (10 mM), a precursor for mitochondrial ATP generation, prevented the elevation in adenosine and the depression of the population spike. These results indicate that the neuroinhibitory modulator adenosine is elevated during glucose deprivation and contributes to the hypoglycemic depression of synaptic transmission. The increase in adenosine during glucose deprivation can be prevented by providing substrate for mitochondrial ATP generation. The present results indicate an interaction between lactate and adenosine such that an increase in lactate may contribute to a decline in adenosine production.

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“…Because hyperglycemia also increases intraischemic lactic acid levels (27)(28)(29), it was reasonable to conclude that lactic acidosis itself exacerbates the ischemic brain damage during hyperglycemia. However, the role of glucose in brain injury in the adult as well as juvenile or fetal animals is far from resolved because many studies have failed to show detrimental effects resulting from glucose infusions and some have even shown beneficial effects of preischemic glucose infusions both in vitro (53)(54)(55)(56) and in vivo (21, 22, 31-33, 57, 58). In addition, several studies have demonstrated that lactate plays an important role in brain energy production (17,59,60) and, rather than exacerbating damage, it might actually attenuate the injury (17,61).…”

Section: Discussionmentioning

confidence: 99%