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Titolo:
CALCIUM, ENERGY-METABOLISM AND THE DEVELOPMENT OF SELECTIVE NEURONAL LOSS FOLLOWING SHORT-TERM CEREBRAL-ISCHEMIA
Autore:
SIMS NR;
Indirizzi:
FLINDERS UNIV S AUSTRALIA,SCH MED,DEPT MED BIOCHEM,GPO BOX 2100 ADELAIDE SA 5001 AUSTRALIA
Titolo Testata:
Metabolic brain disease
fascicolo: 3, volume: 10, anno: 1995,
pagine: 191 - 217
SICI:
0885-7490(1995)10:3<191:CEATDO>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSIENT FOREBRAIN ISCHEMIA; FREE FATTY-ACIDS; PROTEIN-KINASE-C; PYRUVATE-DEHYDROGENASE ACTIVITY; D-ASPARTATE ANTAGONIST; RAT-BRAIN INVIVO; GLOBAL-ISCHEMIA; BLOOD-FLOW; GERBIL HIPPOCAMPUS; MITOCHONDRIAL RESPIRATION;
Keywords:
ISCHEMIA; ENERGY METABOLISM; CALCIUM; EXCITOTOXICITY; MITOCHONDRIA;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
167
Recensione:
Indirizzi per estratti:
Citazione:
N.R. Sims, "CALCIUM, ENERGY-METABOLISM AND THE DEVELOPMENT OF SELECTIVE NEURONAL LOSS FOLLOWING SHORT-TERM CEREBRAL-ISCHEMIA", Metabolic brain disease, 10(3), 1995, pp. 191-217

Abstract

Short-term cerebral ischemia results in the delayed loss of specific neuronal subpopulations. This review discusses changes in energy metabolism and Ca2+ distribution during ischemia and recirculation and considers the possible contribution of these changes to the development ofselective neuronal loss. Severe ischemia results in a rapid decline of ATP content and a subsequent large movement of Ca2+ from the extracellular to the intracellular space. Similar changes are seen in tissue subregions containing neurons destined to die and those areas largely resistant to short-term ischemia, although differences have been observed in Ca2+ uptake between individual neurons. The large accumulation of intracellular Ca2+ is widely considered as a critical initiating event in the development of neuronal loss but, as yet, definitive evidence has not been obtained. The increased intracellular Ca2+ content activates a number of additional processes including lipolysis of phospholipids and degradation or inactivation of some specific proteins, all of which could contribute to altered function on restoration of blood flow to the brain. Reperfusion results in a rapid recovery of ATP production. Cytoplasmic Ca2+ concentration is also restored during early recirculation as a result of both removal to the extracellular space and uptake into mitochondria. Within a few hours of recirculation, subtle increases in intracellular Ca2+ and a reduced capacity for mitochondrial respiration have been detected in some ischemia-susceptible regions. Both of these changes could potentially contribute to the development of neuronal loss. More pronounced alterations in Ca2+ homeostasis,resulting in a second period of increased mitochondrial Ca2+, developwith further recirculation in ischemia-susceptible regions. The available evidence suggests that these increases in Ca2+, although developing late, are likely to precede the irreversible loss of neuronal function and may be a necessary contributor to the final stages of this process.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/04/20 alle ore 11:59:54