Terminal anoxic depolarization proceeds more slowly in the olfactory bulb than in the cerebral cortex of rats.

The time course of terminal anoxic depolarization and of the concomitant [K+]e increase was compared in the cerebral cortex and olfactory bulb of rats anesthetized with pentobarbital. Respiration arrest elicited by (+)-tubocurarine induced a negative slow potential shift which reached 50% of maximum after 90 s in the cortex and after 180 s in the olfactory bulb (n = 10). Bulbar [K+]e increased slowly to 16 mmol/l, then more rapidly to 40 60 mmol/l and reached 90 mmol/l after 10 min asphyxia (n = 10). While the resting and maximal [K+]e levels were the same in the cortex and olfactory bulb, the fast [K+]e rise started in the olfactory bulb at a higher level (16 mmol/l) and proceeded at a slower rate (doubling time 14 s) than in the cortex, where the same values were 11 mmol/l and 5 s, respectively. It is argued that the olfactory bulb resistance to asphyxia is due to a powerful GABAergic inhibition which counteracts the autoregenerative ionic shift and accounts for the absence of spreading depression in this structure.