Differential depression of spinal synaptic transmission in vitro by different hypoxic insults.

The effects of hypoxia (O2-free), aglycemia (glucose-free), ischemia (O2- and glucose-free) and chemical anoxia (by 3-nitropropionic acid; 3-NPA) were evaluated on the synaptic transmission in vitro. Stimulation of a dorsal root in hemisected spinal cord from neonatal rat, evoked monosynaptic (MSR) and polysynaptic reflexes (PSR) in the segmental ventral root. In all the hypoxic conditions, the reflexes were depressed in a time-dependent manner. Hypoxia took longer time (> 240 min) to abolish the reflexes where as, aglycemia and ischemia abolished them within 35 min. Recovery after wash was complete in hypoxia, 60-70% in aglycemia and 20-25% in ischemia. The time required for 50% depression of reflexes (T-50) was also in the same order (100, 23 and 13 min). The elimination of O2 in hypoxic or ischemic solution by N2 bubbling abolished the reflexes within 16 min. The T-50 values in both the conditions were between 5-8 min. Superfusion of 3-NPA (an irreversible inhibitor of succinate dehydrogenase) depressed the reflexes. The abolition time and T-50 values were shorter with the increasing concentrations of 3-NPA. The present results reveal that the energy production in hypoxic condition with normal glucose level can sustain the synaptic activity for a longer time while the glucose deficiency even in normoxic conditions drastically impair the synaptic activity. Further, aglycemia depressed the reflexes almost in a similar time as seen with ischemia.