[Potassium activity in the cat cortex: experimental epilepsy].
Two mechanisms are discussed which link extracellular potassium accumulation and epileptogenic neuronal hyperactivity in the cortex. The potassium concentration (aK) of the environment of a repetitively discharging membrane can increase sufficiently for a supra-threshold depolarization at afferent erminals. This can explain the finding of ectopic spike generation and the antidromic breakthrough in thalamo-cortical projections after a primary cortical discharge. Spread and recurrent enhancement of excitatory drives may be the result of this mechanism. Initiation and termination of seizure is not explained by potassium accumulation. There is a ceiling level in potassium of about 10 mequ/1 which is strictly maintained during normal as well as epileptiform activity. This level is probably not high enough for depolarizing inactivation of neuronal membranes. Stimulation of cortical afferents can have a dual effect on aK. After a primary shortlasting increase, aK can reach subnormal values. This is possibly brought about by a stimulated re-uptake of K+. Seizures can be initiated at these subnormal levels. The effect of the re-uptake e.g. hyperpolarization of terminal afferents and increase of evoked transmitter release is discussed for the initiation for paroxysmal activity.
D000818:Animals; D002415:Cats; D002540:Cerebral Cortex / Q000503:physiopathology*; D004195:Disease Models, Animal; D004827:Epilepsy / Q000503:physiopathology; D005110:Extracellular Space / Q000032:analysis; D008564:Membrane Potentials; D008839:Microelectrodes; D009474:Neurons / Q000503:physiopathology; D011188:Potassium / Q000032:analysis / Q000134:cerebrospinal fluid / Q000502:physiology*; D012640:Seizures / Q000503:physiopathology*; D011984:Sensory Receptor Cells
D011188:Potassium
Kaliumaktivität im Cortex der Katze: Untersuchungen zur experimentellen Epilepsie