Outwardly rectifying deflections in threshold electrotonus due to K+ conductances

Area of Science:

• Neuroscience
• Electrophysiology
• Axonal physiology

Background:

• A transient decrease in excitability, known as the S1 notch, occurs during threshold electrotonus.
• This phenomenon has been linked to fast potassium (K+) channel activity, especially in demyelinating diseases.

Purpose of the Study:

• To investigate the underlying mechanisms of the S1 notch in healthy sensory and motor axons.
• To determine if fast K+ channels contribute to the notch in non-demyelinated axons.

Main Methods:

• Recording threshold electrotonus in human median nerve sensory and motor axons using various test stimulus durations.
• Analyzing the notch's characteristics (latency, amplitude) in response to varying conditioning stimuli and temperature.
• Investigating notch behavior with brief current pulses triggering EMG and examining low-threshold axons.

Main Results:

• The notch occurred more with briefer stimuli and in sensory axons.
• In motor axons, notch latency decreased and amplitude increased with stronger stimuli or cooling.
• No evidence for fast K+ channel outward rectification was found; the notch in normal motor axons arises from exceeding threshold, more pronounced in sensory axons due to their stimulus-response properties.

Conclusions:

• The S1 notch in healthy axons is primarily caused by the conditioning stimulus crossing the action potential threshold, not fast K+ channel outward rectification.
• Sensory axons exhibit the notch more readily due to their lower stimulus-response curve slope and longer strength-duration time constant.
• These findings offer an alternative explanation for the notch observed in demyelinating conditions.