Abstract：
:Deregulation of intracellular calcium homeostasis is widely considered as one of the underlying pathophysiological mechanisms of hypoxic-ischemic brain injury. Whether this alteration can result in cerebral calcification was investigated in basal ganglia, cerebral cortex, and hippocampus of human premature and term neonates together with glial reaction. In all samples nonarteriosclerotic calcifications were observed, their number and size were area-specific and increased in term neonates. Basal ganglia always presented the highest degree of calcification and hippocampus the lowest, located mainly in the CA1 subfield. In all cases, neuronal damage was associated with astroglial reaction and calcium precipitates, with microglial reaction only in basal ganglia and cerebral cortex, and argues for the participation of excitatory amino acid receptors in hypoxia-ischemia damage. These data correlate with hypoxia-ischemia vulnerability in the perinatal period. The clinical relevance of these precipitates and the neuroprotective interest of non-NMDA receptor manipulation are discussed in the light of our results.
journal_name
Neurobiol Disjournal_title
Neurobiology of diseaseauthors
Rodríguez MJ,Ursu G,Bernal F,Cusí V,Mahy Ndoi
10.1006/nbdi.2000.0332keywords:
subject
Has Abstractpub_date
2001-02-01 00:00:00pages
59-68issue
1eissn
0969-9961issn
1095-953Xpii
S0969-9961(00)90332-2journal_volume
8pub_type
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