Elsevier

Experimental Neurology

Volume 42, Issue 2, February 1974, Pages 248-263
Experimental Neurology

Extracellular potassium activity during epileptogenesis

https://doi.org/10.1016/0014-4886(74)90023-5Get rights and content

Abstract

Direct measurements of extracellular potassium concentration ([K+]0) changes in penicillin epileptogenic foci of cat cortex were made using potassium-sensitive microelectrodes. Interictal EEG events were accompanied by increases in [K+]0 lasting several seconds. The amplitudes and rise rates of these increases varied with cortical depth, distance from the center of the focus, and the [K+]0 at which they occurred. During ictal events, [K+]0 consistently reached 9–10 mm. The patterns of ictal [K+]0 changes also showed variations with depth in the cortex and distance from the focus. There was an upper limit for [K+]0 during both interictal and ictal epileptiform activity at about 10 mm. The role of these [K+]0 changes in modulating neuronal excitability in the epileptogenic focus is discussed. The [K+]0 level did not appear to be a critical factor in initiation or termination of ictal episodes.

References (34)

  • G.F. Ayala et al.

    Excitability changes and inhibitory mechanisms in neocortical neurons during seizures

    J. Neurophysiol.

    (1970)
  • R. Birks et al.

    Acetylcholine metabolism of a sympathetic ganglion

    Can. J. Biochem. Physiol.

    (1961)
  • J.D. Cooke et al.

    The specific effect of potassium on transmitter release by motor nerve terminals and its inhibition by calcium

    J. Physiol.

    (1973)
  • M. Dichter et al.

    Silent cells during interictal discharges and seizures in hippocampal penicillin foci. Evidence for the role of extracellular K+ in the transition from the interictal state to seizures

    Brain Res.

    (1972)
  • J.C. Eccles
  • B. Frankenhaeuser et al.

    The after-effects of impulses in the giant nerve fibres of Loligo

    J. Physiol.

    (1956)
  • K.J. Futamachi et al.

    Potassium activity in rabbit cortex

    (1973)
  • Cited by (223)

    • Glia-mediated modulation of extracellular potassium concentration determines the sexually dimorphic output frequency of a model brainstem oscillator

      2019, Journal of Theoretical Biology
      Citation Excerpt :

      Although the simulations conducted as part of the present study clearly support the notion of an astrocytic syncytium-mediated regulation, via [K+]o, of the oscillatory activity of the pacemaker nucleus, and thus provide a plausible model for the development of the sexually dimorphic EOD, its validity is contingent upon the changes in [K+]o that can be accommodated in the pacemaker nucleus. While the intracellular concentration of K+ of the pacemaker and relay cells, as well as the extracellular concentration of this ion species, in the pacemaker nucleus are unknown, studies employing various methods to determine potassium concentrations suggest that [K+]o is, with 1.7–3.6 mM (Nilsson et al., 1993; Rice and Nicholson, 1988), rather constant across different fish species, and similar to the resting potassium concentration in the extracellular fluid of the mammalian brain, which has been reported to be approximately 3 mM (Lux and Neher, 1973; Moody et al., 1974; Prince et al., 1973). Assuming that the intracellular concentration of potassium in the pacemaker and relay cells is similar to the typical concentration found in mammalian neurons, approximately 140 mM (Lodish et al., 2000), in the model pacemaker neural network a lowering of [K+]o from 4.2 mM to 1.0 mM results in a decrease of the oscillation frequency from 526 Hz to 442 Hz, and is thus of similar relative magnitude as the difference between the mean male and female EOD frequencies in adult fish (880 Hz vs. 740 Hz, respectively).

    View all citing articles on Scopus
    1

    These experiments were supported in part by USPHS Grant NS 06477 from the National Institute of Neurological Diseases and Stroke (David A. Prince); an NSF predoctoral fellowship (William J. Moody, Jr.); and a research grant from the Epilepsy Foundation of America (David A. Prince). We gratefully acknowledge the secretarial assistance of Ms. Pamela Vario.

    View full text