The effects of hypothermia on amino acid neurotransmitter release from the cerebral cortex

Simpson, Richard E.; Walter, Gary A.; Phillis, John W.

doi:10.1016/0304-3940(91)90827-g

Cited by 28 publications

(9 citation statements)

References 15 publications

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“…An increase in extracellular glycine was observed during and after ischemia in rabbits, and this elevation was attenuated by hypothermia (Baker et al, 1991). Simpson et al . (1991) did not find extracellular glycine elevated in normothermic rat brain ischemia but observed that hypothermia reduced glycine to be- low basal levels .…”

Section: Discussionmentioning

confidence: 98%

Neuroprotective Effect of Hypothermia in Cortical Cultures Exposed to Oxygen‐Glucose Deprivation or Excitatory Amino Acids

Bruno

Goldberg

Dugan

et al. 1994

Journal of Neurochemistry

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We examined the effect of moderate hypothermia (30°C) on neuronal injury in murine cortical cell cultures . Lowering the temperature during and after a period of oxygen-glucose deprivation reduced both the release of glutamate to the bathing medium and accompanying neuronal degeneration . Hypothermia immediately after brief exposure to high concentrations of NMDA or glutamate also reduced the resulting neuronal degeneration . This protective effect was not eliminated when MK-801 and 6-cyano-7-nitroquinoxaline-2,3-dione were added immediately after washout of the exogenously added excitotoxin, suggesting that it was mediated by actions additional to reduction of endogenous late glutamate release . Hypothermia applied only during exposure to NMDA or glutamate, whether brief or prolonged, did not reduce subsequent cytosolic calcium accumulation or neuronal degeneration, suggesting that the postsynaptic induction of NMDA receptor-mediated excitotoxicity is not sensitive to temperature reduction . However, hypothermia during prolonged S-a-amino-3-hydroxy-5methyl-4-isoxazolepropionic acid or kainate exposure did reduce neuronal degeneration . Key Words: Glutamate-NMDA-Kainate-S-a-Amino-3-hydroxy-5-methyl-4isoxazolepropionic acid (AMPA)-Excitotoxicity-Stroke-Hypoxia-Ischemia .

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Section: Discussionmentioning

confidence: 98%

Neuroprotective Effect of Hypothermia in Cortical Cultures Exposed to Oxygen‐Glucose Deprivation or Excitatory Amino Acids

Bruno

Goldberg

Dugan

et al. 1994

Journal of Neurochemistry

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“…A decreased pH, however, has been shown to be protective against NMDA-mediated toxicity (Giffard et al, 1990) and thus would contrast with the effects of lowered temperature on intracellular pH. Elevations in extracellular gluta-mate levels during anoxia or ischemia, which could turn on NMDA receptors, can be attenuated by mild hypothermia (Busto et al, 19896; but see Simpson et al, 1991). Whether decreased glutamate release during hypothermia is causally related to protection remains to be seen.…”

Section: Discussionmentioning

confidence: 99%

Hypothermia, Metabolic Stress, and NMDA‐Mediated Excitotoxicity

Zeevalk

Nicklas

1993

Journal of Neurochemistry

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Isolated embryonic retinas were metabolically stressed by inhibition of glycolysis either with iodoacetate (IOA) or by glucose withdrawal plus 10 mM 2-deoxy-D-glucose, and the effects of hypothermia were examined. Incubation at 30 versus 37 degrees C during 30 min of hypoglycemia with IOA completely reduced the rapid swelling-related GABA release [6 +/- 2 vs. 68 +/- 10 nmol/100 mg of protein (mean +/- SEM) for 30 and 37 degrees C, respectively]. Histology of the retina immediately following 30 min of metabolic stress at 30 degrees C appeared normal, whereas that at 37 degrees C showed a pattern of acute edema, characteristic of NMDA-mediated acute excitotoxicity. Coincubation with a competitive or noncompetitive NMDA antagonist, respectively, CGS-19755 (10 microM) or MK-801 (1 microM), during 30 min of hypoglycemia at 37 degrees C completely prevented tissue swelling, whereas extracellular GABA content remained at basal levels, indicating that the cytotoxic effects of IOA treatment for 30 min at 37 degrees C were NMDA receptor mediated. Longer periods of hypoglycemia at 37 degrees C produced acute toxicity that was only partially NMDA receptor mediated. Hypothermia delayed the onset of NMDA-mediated toxicity by 30-60 min. At 30 degrees C, the rate of loss of ATP was slowed during the first several minutes of hypoglycemia (82 and 58% of maximal tissue levels at 30 and 37 degrees C, respectively, at 5 min, but by 10 min, ATP levels were comparably reduced. After a transient exposure of retina to 50 microM NMDA in Mg(2+)-free medium, hypothermia significantly attenuated acute GABA release by 30%.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…5,37 Following global ischemia, glutamate levels increase within 10 to 20 minutes after onset of ischemia and then decrease by 30 to 50 minutes. 2,6,22,35,39 Following focal cerebral ischemia, glutamate levels typically peak within 60 minutes of onset of ischemia and return to baseline 19,20 or decrease substantially 3 by 90 to 120 minutes. Mild hypothermia appears to blunt this peak and, in some instances, delays it by 20 minutes.…”

Section: J Neurosurg / Volume 94 / January 2001mentioning

confidence: 99%

Delayed induction and long-term effects of mild hypothermia in a focal model of transient cerebral ischemia: neurological outcome and infarct size

Maier

Sun²,

Kunis³

et al. 2001

Journal of Neurosurgery

162

109

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Mild hypothermia conferred significant degrees of neuroprotection in terms of survival, behavioral deficits, and histopathological changes, even when its induction was delayed by 120 minutes after onset of MCA occlusion (p < 0.05) compared with normothermic conditions. Furthermore, the neuroprotective effect of mild hypothermia (2-hour duration) that was induced during the ischemia period was sustained over 2 months. These studies lend further support to the use of mild hypothermia in the treatment of stroke.

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The effects of hypothermia on amino acid neurotransmitter release from the cerebral cortex

Cited by 28 publications

References 15 publications

Neuroprotective Effect of Hypothermia in Cortical Cultures Exposed to Oxygen‐Glucose Deprivation or Excitatory Amino Acids

Neuroprotective Effect of Hypothermia in Cortical Cultures Exposed to Oxygen‐Glucose Deprivation or Excitatory Amino Acids

Hypothermia, Metabolic Stress, and NMDA‐Mediated Excitotoxicity

Delayed induction and long-term effects of mild hypothermia in a focal model of transient cerebral ischemia: neurological outcome and infarct size

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