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Changes in the extracellular levels of glutamate and aspartate during ischemia and hypoglycemia. Effects of hypothermia

Boris-Möller, Fredrik and Wieloch, Tadeusz LU (1998) In Experimental Brain Research 121(3). p.277-284
Abstract

Hypothermia (33°C) dramatically diminishes ischemic but not hypoglycemic brain damage. The beneficial effects of hypothermia in ischemia have been partly attributed to a reduction in the ischemia-induced increase in synaptic levels of glutamate or aspartate. With the microdialysis technique, we studied the effects of hypothermia (33°C) on the brain extracellular levels of glutamate and aspartate during hypoglycemia, ischemia, and their combination. In isoelectric hypoglycemia, striatal levels of glutamate and aspartate frequently show large transients of transmitter release occurring during both normothermia and hypothermia, whereas in the cortex levels of glutamate and aspartate are slightly lower during hypothermia compared with... (More)

Hypothermia (33°C) dramatically diminishes ischemic but not hypoglycemic brain damage. The beneficial effects of hypothermia in ischemia have been partly attributed to a reduction in the ischemia-induced increase in synaptic levels of glutamate or aspartate. With the microdialysis technique, we studied the effects of hypothermia (33°C) on the brain extracellular levels of glutamate and aspartate during hypoglycemia, ischemia, and their combination. In isoelectric hypoglycemia, striatal levels of glutamate and aspartate frequently show large transients of transmitter release occurring during both normothermia and hypothermia, whereas in the cortex levels of glutamate and aspartate are slightly lower during hypothermia compared with normothermia. In both regions studied, complete ischemia induced by i.v. KCl results in a progressive increase in glutamate and aspartate levels over time. In normoglycemic animals, hypothermia markedly attenuates the increase in glutamate and aspartate levels in the striatum but not in the cortex. Also in hypoglycemic animals, complete ischemia causes a progressive increase in the glutamate and aspartate levels. However, hypothermia affects only striatal glutamate levels. Since hypothermia protects both cortex and striatum against ischemic brain injury and not against hypoglycemic injury, presumably the protective effect of hypothermia is due to factors other than prevention of glutamate or aspartate overflow.

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author
organization
publishing date
type
Contribution to journal
publication status
published
keywords
Hypoglycemia, Hypothermia, Ischemia, Microdialysis, Rat, Transmitter release
in
Experimental Brain Research
volume
121
issue
3
pages
277 - 284
publisher
Springer
external identifiers
  • Scopus:0031853680
ISSN
0014-4819
DOI
10.1007/s002210050461
language
English
LU publication?
yes
id
9e99046a-5e58-45e8-b6d3-937cfa8d8352
date added to LUP
2016-10-05 16:06:16
date last changed
2016-11-29 08:33:32
@misc{9e99046a-5e58-45e8-b6d3-937cfa8d8352,
  abstract     = {<p>Hypothermia (33°C) dramatically diminishes ischemic but not hypoglycemic brain damage. The beneficial effects of hypothermia in ischemia have been partly attributed to a reduction in the ischemia-induced increase in synaptic levels of glutamate or aspartate. With the microdialysis technique, we studied the effects of hypothermia (33°C) on the brain extracellular levels of glutamate and aspartate during hypoglycemia, ischemia, and their combination. In isoelectric hypoglycemia, striatal levels of glutamate and aspartate frequently show large transients of transmitter release occurring during both normothermia and hypothermia, whereas in the cortex levels of glutamate and aspartate are slightly lower during hypothermia compared with normothermia. In both regions studied, complete ischemia induced by i.v. KCl results in a progressive increase in glutamate and aspartate levels over time. In normoglycemic animals, hypothermia markedly attenuates the increase in glutamate and aspartate levels in the striatum but not in the cortex. Also in hypoglycemic animals, complete ischemia causes a progressive increase in the glutamate and aspartate levels. However, hypothermia affects only striatal glutamate levels. Since hypothermia protects both cortex and striatum against ischemic brain injury and not against hypoglycemic injury, presumably the protective effect of hypothermia is due to factors other than prevention of glutamate or aspartate overflow.</p>},
  author       = {Boris-Möller, Fredrik and Wieloch, Tadeusz},
  issn         = {0014-4819},
  keyword      = {Hypoglycemia,Hypothermia,Ischemia,Microdialysis,Rat,Transmitter release},
  language     = {eng},
  number       = {3},
  pages        = {277--284},
  publisher    = {ARRAY(0xb1a33e0)},
  series       = {Experimental Brain Research},
  title        = {Changes in the extracellular levels of glutamate and aspartate during ischemia and hypoglycemia. Effects of hypothermia},
  url          = {http://dx.doi.org/10.1007/s002210050461},
  volume       = {121},
  year         = {1998},
}