Monday, December 10, 2012

The Similarities Between Alcohol and Spinal Cord Injury: On a Cellular Level


                Recent research (from separate groups) into both Spinal Cord injuries (SCI) as well as the base mechanisms of alcohol’s effects has yielded surprising findings – the surprise being that the two unrelated issues show similar mechanic results.

                Large-conducting potassium channels – or BK channels – are found in nerve, muscle, and gland cells. Activated mostly by voltage-dependent calcium channels, the BK channel opens to allow and efflux of potassium out of the cell – causing a hyperpolarization of the cellular membrane. Previous research has already shown that activated BK channels may play a big role in regulating action potentials in neurons, resulting in decreases not only in the frequency of conduction (the amount of times the neuron can fire in a period of time), but also the size of the action potential. Research by both Ye, Buttigieg, et al. and McIntire have shown that this might be important in understanding both SCI mechanisms and treatment targets, but also in understanding the effects of alcohol on the body.

                As those who have ever been intoxicated may well know, intoxication affects mobility and the general speed of cognitive processing. McIntire and his team at the University of California at San Francisco have shown the BK channel to be important in mediating this effect. Alcohol causes the channel to be open more often than is normal – making it harder for the cells to fire action potentials because they have a higher threshold. This is similar to SCI patients in the cellular mechanics aspect of it. SCI has been shown to cause not only axon cell death, but also demyelination of the remaining axons. The myelination usually prevents the majority of BK channels on the axon from becoming active – they are never exposed to changes in calcium levels or voltage because that only occurs at the Nodes of Ranvier. Once the myelin sheath is removed, however (caused by oligodendrocyte cell death), these channels become active at a much higher rate, yielding negative effects for the firing of action potentials. All of this cumulates to hinder mobility and neuronal signaling in both SCI patients as well as people who are intoxicated.

                Research into targeting BK channels in treatment of SCI patients, and in the understanding of how alcohol affects the body could go a long way for many people today. Approximately 11,000 people in the United States receive spinal cord injuries per year, and the number of people who are affected by alcohol is astronomically high. This new area of research is quite exciting – keep your eye out for future developments of drug targets and other findings! 

Citations: 

- http://www.scientificamerican.com/article.cfm?id=sobering-shift
Ye H, Buttigieg J, et al. Expression and functional role of BK channels in chronically injured spinal cord white matter. J Neur Disease.2012; 47: 225-236. DOI 10.1016/j.nbd.2012.04.006

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