K + changes in the brain and spinal cord measured by ion-selective microelectrodes

Abstract

Summary It is generally accepted that K+ accumulation in the extracellular space plays an important role in modifying impulse transmission. Using potassium-selective microelectrodes with liquid ion-exchanger further information was obtained in the CNS about dynamic changes in extracellular potassium concentration (Δ[K+]e) under various physiological and pathophysiological conditions. In the spinal cord the research was focused on the possible physiological role of K+ transients with respect to primary afferent depolarisation (PAD) which has been suggested to form the basis of presynaptic inhibition [I]. At present there are two major hypotheses about the genesis of PAD. It has been suggested that PAD results from the depolarizing action of a specific transmitter — GABA — released from axo-axonic synapses. On the other hand, PAD can be produced by Δ[K+]e which accompanies neuronal activity. We presented evidence that in the mammalian as well as in the amphibian spinal cord, K+ accumulates in the extracellular space during tetanic stimulation of the peripheral nerves and that the Δ[K+]e corresponds to 6–9 mmol/l [2]. In the isolated spinal cord of the frog, when all synaptic activity was blocked by high Mg2+, we demonstrated that an increase in [K+]e produces PAD. Less increase of [K+]e (0.1–0.5 mmol/l) was found in response to a single volley, to natural stimulation, or in the mesencephalic reticular formation of the rat during spontaneous neuronal activity. The possible discrepancies between the measurements of Δ[K+]e as obtained with potassium-selective microelectrodes and the actual changes which may occur in the close vicinity of neurones will be discussed. It is suggested that both the activation of axo-axonic synapses and Δ[K+]e participate in the mechanism of PAD.