Abstract
This two-part investigation explored the parameters and mechanisms of: (1) injury to spinal cord (SC) neurons by nonfreezing low temperatures, and (2) hypothermic protection of SC neurons subjected to a defined, physical injury (dendrite transection). Conclusions from the studies of hypothermic injury were: (1) morphologic and ultrastructural signs of stress developed in SC neurons as the temperature was decreased below 17°C; (2) most neurons showing stress during cooling died upon rewarming to 37°C; (3) spontaneous SC network activity was not significantly changed by cooling to 17°C for 2 hours and rewarming, but cooling to 10°C for 1 hour caused a reduction of burst frequency after rewarming, and cooling to 10°C for 2 hours resulted in electrical silence after rewarming; and (4) application of N-methyl-D-aspartate (NMDA) antagonists before cooling prevented neuronal death, ultra-structural damage, and loss of activity upon rewarming, but application after cooling (before rewarming) was not protective. Conclusions from the studies of hypothermic protection were: (1) cooling at 17°C for 2 hours followed by rewarming to 37°C significantly increased lesioned neuron survival, but protection was lost when the period at 17°C was increased to 6 hours; (2) NMDA blockade under normothermic (37°C) or hypothermic (17°C or 10°C for 2 hours) conditions was not more protective of lesioned neurons than cooling to 17°C (no NMDA antagonist); and (3) 200 μM thiopental or 100 μM pentobarbital increased lesioned neuron survival to a degree comparable to cooling for 2 hours at 17°C.
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