The compound is a derivative of the drug 4-aminopyridine, used primarily as a research tool and also to manage symptoms of multiple sclerosis.
The axons of each nerve are sheathed in a thick insulating lipid layer, called myelin, which enables the transmission of signals without short circuiting, much like the insulation surrounding electrical wires. Spinal cord trauma damages the myelin sheath, exposing "fast potassium channels" that are embedded in the axons and are critical for transmitting nerve impulses.
The researchers confirmed previous circumstantial evidence suggesting injury causes the myelin insulation to recede, exposing the channels and impairing signal transmission. Laboratory and imaging techniques revealed the exposed channels in damaged axons.
The researchers also discovered that 4-aminopyridine-3-methyl hydroxide is a "potassium channel blocker," using a sophistic laboratory technique called "patch clamp" to measure signal conduction. Findings confirmed that the compound prevents the exposed channels from leaking electrical current and enhances nerve conduction in segments of the damaged spinal cord.
The compound could make it possible to sidestep spinal cord damage by enabling axons to transmit signals as though they were still sheathed in myelin, Shi said.
Nerves transmit signals through a series of rapid electrical pulses, or "action potentials." For proper nerve function, the time gap between pulses must be as brief as possible. However, 4-aminopyridine has been shown to lengthen the gap, or "refractory period," between pulses. The researchers found that 4-aminopyridine-3-methyl hydroxide restores function without affecting the refractory period. As a result, the damaged nerves perform more lik
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