NEURON-SPECIFIC ENOLASE INCREASES IN CEREBRAL AND SYSTEMIC CIRCULATION FOLLOWING FOCAL ISCHEMIA

Citation
Fc. Barone et al., NEURON-SPECIFIC ENOLASE INCREASES IN CEREBRAL AND SYSTEMIC CIRCULATION FOLLOWING FOCAL ISCHEMIA, Brain research, 623(1), 1993, pp. 77-82
Citations number
34
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
623
Issue
1
Year of publication
1993
Pages
77 - 82
Database
ISI
SICI code
0006-8993(1993)623:1<77:NEIICA>2.0.ZU;2-S
Abstract
Neuron-specific enolase (NSE) is an isoform of the glycolytic enzyme, enolase, and is found in neurons and neuroendocrine cells. We evaluate d cerebral immunohistologic and plasma changes in NSE in rats from 2 h to 15 days following permanent or transient middle cerebral artery oc clusion (MCAO). At 1-2 days post-MCAO, loss bf NSE immunofluorescence from within neurons to the extracellular space was observed in the inf arcted areas of all MCAO animals. NSE also was identified intravascula rly throughout the brain following MCAO. NSE in plasma was determined by a specific radioimmunoassay. Plasma NSE following permanent or tran sient MCAO was increased significantly from that observed in controls (2.8 +/- 0.3 ng/ml) beginning at 2 h and persisting for 2.5 days post- MCAO (maximum levels of 8.8 +/- 0.9 to 9.6 +/- 0.5 ng/ml after 6-12 h; P < 0.05, n = 4-9). Quantified contralateral forelimb and hindlimb ne urological deficits in these animals were significant and persisted fo r at least 15 days following MCAO but were not observed following sham surgery. These data suggest that MCAO-induced cortical infarction and neurological dysfunction is associated with neuronal depletion and va scular redistribution of brain NSE resulting in a measurable increase in plasma NSE. Such diffusion of NSE into the cerebral vasculature and systemic circulation from ischemic tissue can be expected to serve as a marker for the incidence of cerebral damage in acute and chronic is chemic brain infarcts.