Elsevier

Experimental Neurology

Volume 37, Issue 1, October 1972, Pages 164-178
Experimental Neurology

Unit activity in experimental epileptic foci during focal cortical hypothermia

https://doi.org/10.1016/0014-4886(72)90233-6Get rights and content

Abstract

The change in neuronal firing frequency was measured by extracellular microelectrode recordings during focal cooling of several experimental epileptic foci, using a Peltier cooling device. The experimental epileptic foci studied included foci in cat sensory motor cortex secondary to tungstic acid, strychnine, and freezing, and foci in monkey sensory motor cortex secondary to alumina. Cooling of tungstic acid and strychnine foci was associated with changes in neuron firing that were similar to those seen in normal cortex similarly cooled. By contrast, cooling of alumina foci exhibiting spontaneous seizures was invariably associated with a single seizure after only a 1–3 C drop in cortical temperature followed by electrical silence persisting until rewarming. Initial cooling of alumina foci without spontaneous seizures was similar to normal cortex; however, repeated cooling cycles were associated with changes similar to those seen in alumina foci exhibiting spontaneous seizures. Frozen foci showed variable changes with cooling; occasional cells responding in a manner similar to alumina foci exhibiting spontaneous seizures, others more like normal cortex. These findings were interpreted as suggesting that there are pathophysiologic differences between the various experimental epileptic foci under normothermic conditions. Membrane potentials of neurons in tungstic acid and strychnine foci are likely normal. Neurons in alumina foci may be partially depolarized under normothermic conditions as may some but not all units in foci secondary to freezing.

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Cited by (15)

  • Rapid focal cooling attenuates cortical seizures in a primate epilepsy model

    2017, Experimental Neurology
    Citation Excerpt :

    The mechanism by which cooling controls seizures is still unclear. Some proposed mechanisms involving effects on ion transport across the cell membrane, such as alterations in passive Na2 + exchange (Moseley et al., 1972; Reynolds et al., 1975), increase of resting input resistance (Volgushev et al., 2000), or inhibition of Na+-K+-ATP enzyme were discussed (Aihara et al., 2001). Reversible reduction of neurotransmitter release and diffusion during cooling has also been reported (Boucher et al., 2010; Yang et al., 2005).

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Supported by NIH Grant NS 04053.

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