ABSTRACT
K+ accumulates in the intercellular space as a result of neuronal activity. The changes in extracellular K+ concentration, Δ [K]e (estimated by K+-selective microelectrodes), depends on neuronal activity, on the density of discharging neurones and the removal of the accumulated K+ by diffusion, active transport and current flow through cells. In the mammalian as well as the amphibian spinal cord a single volley in a peripheral nerve increases [K]e by 0·2–0·5 mmol.1−1, while tetanic stimulation (100 Hz) by 7–8 m-mol.l−1, with a maximum in the lower dorsal horn. Increased [K]e was also found in lumbar segments when the somatosensory cortex of the cat and medulla of the frog were stimulated. In the frog spinal cord, the tactile stimulation of the hindlimb evoked Δ [K]e by about 0·1 mmol.1−1, nociceptive stimulation by 0· 2–1·0 mmol.1−1. Spontaneous Δ [K]e and dorsal root potentials (DRPs) were observed at various intervals after stimulation, associated with the decay phase of Δ [K]e.
It was shown that primary afferent depolarization (PAD) consists of two components: the ‘early’ component (mediated by GABA and depressed by picrotoxin or bicuculline) and the ‘late’ K+ component (potentiated by picrotoxin and bicuculline). Even when increased [K]e produces PAD, this does not mean that it also results in presynaptic inhibition. It was found that the Δ [K]e produced depolarization of motoneurones and neuroglia and there is every reason to believe that this also applies to the interneurones. Evidence is available that an increase of [K]e up to 6 mmol. 1−1 facilitates impulse transmission in the spinal cord while higher levels result in its inhibition.
