Extracellular potassium changes in the spinal cord of the cat and their relation to slow potentials, active transport and impulse transmission.
1. By means of K-specific double-barrelled micro-electrodes the time course of changes in K+ concentration in the extracellular space of the lumbar spinal cord was examined after peripheral tetanic stimulation and after a single volley in a mixed peripheral nerve in non-anaesthetized, intercollicularly decerebrated and spinalized cats. 2. Tetanic stimulation (100 Hz) which increases the [K]e from 3 to 9 mM is followed by a phase of reduced [K]e during which [K]e decreases by 0.5 mM below resting level, lasting 1-2 minutes before returning to its original resting level. Evidence is presented that this subnormal phase of [K]e reflects active processes redistributing accumulated K+ from extracellular space. 3. The subnormal phase of [K]e can be registered only when the microelectrode is located in very close vicinity of discharging neurones and is not primarily dependent on the absolute level of increased [K]e. This can be considered as evidence that the neurones and not the glial cells are responsible for active reabsorption of K+ from the extracellular space. 4. Increased E1K]e is reflected in focally recorded potentials as a negativity and decreased [K]e as a positivity. The latency of focally recorded positivity is, however, shorter than the latency of reduced [K]e. This makes it likely that the positivity reflects not only passive hyperpolarization of glial elements, but also an active, electrogenic ion transport across neuronal membrane. 5. The shortest latency of increased [K]e induced by a single volley in a mixed peripheral nerve was found to be 9 msec; the peak, representing 0.5 mM, was attained after 40 msec and the total duration was 200 msec. A theoretical consideration is put forward that the time course of transient increase in [K]e is consistent with the suggestion that K+ which accumulates in the spinal cord after neuronal discharge is responsible for primary afferent depolarization. 6. Evidence is presented that increased [K]e, induced by a long lasting peripheral stimulation, is accompanied by decreased efficacy of impulse transmission.
D000818:Animals; D001693:Biological Transport, Active; D001794:Blood Pressure; D002415:Cats; D004558:Electric Stimulation; D005071:Evoked Potentials; D005110:Extracellular Space / Q000378:metabolism / Q000502:physiology*; D000860:Hypoxia; D011188:Potassium / Q000378:metabolism / Q000502:physiology*; D013116:Spinal Cord / Q000378:metabolism / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission; D013997:Time Factors
D011188:Potassium