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Titolo:
HYPERTHERMIA DEPLETES ADENOSINE-TRIPHOSPHATE AND DECREASES GLUTAMATE UPTAKE IN RAT HIPPOCAMPAL SLICES
Autore:
MADL JE; ALLEN DL;
Indirizzi:
COLORADO STATE UNIV,DEPT ANAT & NEUROBIOL FT COLLINS CO 80523
Titolo Testata:
Neuroscience
fascicolo: 2, volume: 69, anno: 1995,
pagine: 395 - 405
SICI:
0306-4522(1995)69:2<395:HDAADG>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVOUS-SYSTEM; BRAIN; RELEASE; SYNAPTOSOMES; ASPARTATE; ISCHEMIA; NEURONS; ANOXIA; ACID; LOCALIZATION;
Keywords:
FEVER; GLUTAMATE CO-TRANSPORTERS; GLUTAMATE RELEASE; HEAT STROKE; ENERGY DEPLETION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
39
Recensione:
Indirizzi per estratti:
Citazione:
J.E. Madl e D.L. Allen, "HYPERTHERMIA DEPLETES ADENOSINE-TRIPHOSPHATE AND DECREASES GLUTAMATE UPTAKE IN RAT HIPPOCAMPAL SLICES", Neuroscience, 69(2), 1995, pp. 395-405

Abstract

The central nervous system is especially vulnerable to hyperthermia-induced dysfunction, yet the mechanism for this susceptibility is poorly understood. High levels of adenosine triphosphate are necessary to maintain normal re-uptake of glutamate and aspartate, the major excitatory amino acids, by excitatory amino acid co-transporters. We hypothesized that excitotoxic neurotransmitters accumulate extracellularly when hyperthermia depletes adenosine triphosphate, leading to decreased uptake or release of excitatory amino acids by these co-transporters. Incubation of hippocampal slices at 42 degrees C, a temperature that results in coma in vivo, reduced adenosine triphosphate to 70% of control values and decreased uptake of the transportable excitatory amino acid analogue, D,L threo-beta-hydroxyaspartate, to 50% of control values. The degree of adenosine triphosphate depletion induced by hyperthermia was highly correlated with decreases in excitatory amino acid uptake. Severe adenosine triphosphate depletion (less than or equal to 20% of control) induced by hyperthermia in combination:with metabolic insults was highly correlated with the release of endogenous glutamate andaspartate. Preloading slices with excitatory amino acid analogues potentiated hyperthermia-induced alterations of excitatory amino acid transport, strongly suggesting that the hyperthermia-induced changes werelargely due to altered excitatory amino acid co-transporter activity. Immunocytochemical studies suggested glutamate-like immunoreactivity was lost from axonal terminals during hyperthermia in a similar mannerto losses induced by metabolic toxins. Hyperthermia due to infectiousdiseases or heat stroke may induce disorientation and coma. These dysfunctions may be due, in part, to altered excitatory amino acid transport induced by adenosine triphosphate depletion.

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Documento generato il 15/07/20 alle ore 21:19:51