Anoxia increases potassium conductance in hippocampal nerve cells.
The effect of anoxia on nerve cell function was studied by intra- and extracellular microelectrode recordings from the CA1 and CA3 region in guinea pig hippocampal slices. Hyperpolarization and concomitant reduction of the nerve cell input resistance was observed early during anoxia. During this period the spontaneous activity first disappeared, then the evoked activity gradually disappeared. The hyperpolarization was followed by depolarization and an absence of a measurable input resistance. All the induced changes were reversed when the slice was reoxygenated. Reversal of the electro-chemical gradient for Cl- across the nerve cell membrane did not affect the course of events during anoxia. Aminopyridines blocked the anoxic hyperpolarization and attenuated the decrease of membrane resistance, but had no effect on the later depolarization. Blockers of synaptic transmission. Mn++, Mg++ and of Na+-channels (TTX) were without effect on the nerve cell changes during anoxia. It is suggested that the reduction of nerve cell excitability in anoxia is primarily due to increased K+-conductance. Thus, the nerve cells are hyperpolarized and the input resistance reduced, causing higher threshold and reduction of synaptic potentials. The mechanism of the K+-conductance activation is unknown at present.
D000818:Animals; D002463:Cell Membrane Permeability; D004558:Electric Stimulation; D005071:Evoked Potentials; D005110:Extracellular Space / Q000032:analysis; D006168:Guinea Pigs; D006624:Hippocampus / Q000502:physiology*; D000860:Hypoxia / Q000503:physiopathology*; D008564:Membrane Potentials; D009474:Neurons / Q000502:physiology; D010100:Oxygen; D011188:Potassium / Q000032:analysis / Q000502:physiology*; D011312:Pressure; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects
D011188:Potassium; D010100:Oxygen