Abstract：
:While exposure of cultured spinal neurons to mild hypothermia provides some protection from physical trauma (dendrotomy), profound cooling (< 17 degrees C) causes unrelated neuronal injury and death, which can be prevented by treatment with NMDA receptor antagonists. To investigate the mechanism of hypothermic neuronal injury we examined the ultrastructure of cultured spinal neurons after 2 h of cooling to 17 degrees C or 10 degrees C, with or without the presence of the NMDA receptor antagonist D-2-amino-5-phosphonovalerate, and with or without rewarming to 37 degrees C. These groups were compared to cultures exposed to NMDA or to the calcium ionophore A23187. Patterns of ultrastructural change, involving cytoskeletal disruption, mitochondrial abnormalities and vacuolization of the cytoplasm, suggest a common mechanism of injury in all treatment groups, involving an elevation of intracellular calcium. Some neurons exposed to hypothermia, NMDA or ionophore developed beaded dendrites. Microtubules were fragmented in varicosities but not in the intervening constrictions; other organelles were largely excluded from the constrictions. Varicosities may form when organelles and cytoplasm accumulate as the result of disruption of transport and membrane stabilizing proteins by proteases activated by calcium influx via NMDA mediated channels. The periodic nature of the swellings may reflect inherently discontinuous distribution of molecular subunits of the cytoskeleton.
journal_name
Brain Resjournal_title
Brain researchauthors
Emery DG,Lucas JHdoi
10.1016/0006-8993(95)00726-7subject
Has Abstractpub_date
1995-09-18 00:00:00pages
161-73issue
1-2eissn
0006-8993issn
1872-6240pii
0006-8993(95)00726-7journal_volume
692pub_type
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