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Published on: May 25, 2011
Axonal and glial currents activated during the post-tetanic hyperpolarization in non-myelinated nerve
1Département de Pharmacologie, Centre Médical Universitaire, 1 rue Michel Servet, CH-1211 Geneva 4, Switzerland.
Electrical activity in rabbit vagus nerves causes extracellular potassium ([K+]e) increases and depolarization. Post-tetanic hyperpolarization is enhanced when specific inward currents are blocked, revealing their role in regulating nerve potential and potassium levels.
Area of Science:
- Neuroscience
- Cellular Physiology
- Ion Channel Research
Background:
- Nerve activity alters extracellular potassium ([K+]e) and membrane potential.
- The Na+-K+ pump generates post-tetanic hyperpolarization (PTH).
- The role of inward currents in short-circuiting Na+-K+ pump activity is not fully understood.
Purpose of the Study:
- To simultaneously measure membrane potential and [K+]e changes during nerve activity and recovery.
- To investigate the contribution of inward currents to Na+-K+ pump activity and extracellular potassium regulation.
Main Methods:
- Utilized a modified sucrose-gap method and potassium-sensitive microelectrodes in rabbit vagus nerve preparations.
- Stimulated nerves and recorded electrical activity and [K+]e.
- Blocked inward currents using Cl– removal, Cs+, or Ba2+ to assess their impact on PTH.
Main Results:
- Nerve stimulation at 15 Hz for 15 s caused a significant [K+]e increase (16.9 mM) and depolarization.
- PTH amplitude increased substantially when inward currents (I h and I KIR) were blocked.
- The inwardly rectifying I KIR current was identified as originating from Schwann cells.
Conclusions:
- Inward currents (I h and I KIR) normally short-circuit the axonal Na+-K+ pump.
- Schwann cell-derived I KIR plays a role in regulating extracellular potassium.
- These ionic channels collectively maintain optimal membrane potential and facilitate K+ removal after nerve activity in non-myelinated nerves.
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