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.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002463:Cell Membrane Permeability; D002540:Cerebral Cortex / Q000503:physiopathology*; D002712:Chlorides / Q000378:metabolism; D002534:Hypoxia, Brain / Q000503:physiopathology*; D008564:Membrane Potentials; D009830:Olfactory Bulb / Q000503:physiopathology*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D002712:Chlorides; D005680:gamma-Aminobutyric Acid; D011188:Potassium; D002118:Calcium