Monday, November 23, 2009

A potassium channel blocker to restore nerve function in patients with spinal cord injuries..

The experimental compound, 4-aminopyridine-3-methyl hydroxide, has been shown to restore function to damaged axons, slender fibers that extend from nerve cells and transmit electrical impulses in the spinal cord.

The researchers subjected spinal cord tissue to stresses that mimic what happens in a compression injury, which stretches nerves. Then they treated the damaged axons with 4-aminopyridine-3-methyl hydroxide. The same drug is 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 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.

As per the claim by the researchers, the new compound is about 10 times more potent than 4-aminopyridine, meaning lower doses can be used to reduce the likelihood of serious side effects. Because myelin also is damaged in multiple sclerosis, the same drug might be used to restore nerve function in people stricken with the disease. Hope in the days to come patients suffering from Multiple sclerosis and spinal cord injuries will breathe a sigh of relief...

Ref : J Neurophysiol (November 18, 2009). doi:10.1152/jn.00154.2009.

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