Abstract
The effects of in vitro aglycemia (glucose-free) and ischemia (glucose-free and O 2-free) were examined on the dorsal root-evoked ventral root spinal monosynaptic and polysynaptic reflexes in neonatal rat spinal cords. Aglycemia and ischemia depressed the reflexes in a time-dependent manner and abolished them by 35 min. The depression by ischemia began immediately while that by aglycemia began after 15 min. The NMDA receptor antagonist, dl-2-amino-5-phosphonovaleric acid (APV), blocked the depression induced by aglycemia completely and that by ischemia partially. Strychnine (glycine A receptor antagonist) or bicuculline (GABA A receptor antagonist) blocked the aglycemia-induced depression of the reflexes. In the case of ischemia, strychnine but not bicuculline, blocked the depression partially. The results indicate that aglycemia and ischemia depress the synaptic transmission involving NMDA receptors. Aglycemia involves both γ-aminobutyric acid-ergic and glycinergic inhibitory transmission while ischemia involves other additional mechanisms.
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