Sunday, 1 September 2013

The Sodium Switch And Neuropathic Pain

Today's post from link below) is a technically, difficult to grasp description of how sodium acts as an on/off switch for neurotransmitters in the brain. The Kainate receptor plays a role in receiving pain signals and as such, if it can be switched off in isolation from other receptors, there's a chance that pain information can be blocked without affecting other brain functions. Sodium might be able to do just that. These sorts of snippets of information are not going to mean much to most people but they do show how deeply researchers are looking in trying to come up with solutions to irregular nerve behaviour that causes neuropathy patients so much discomfort. We may not understand what's going on but we should be grateful for it, especially if one day, they come up with a really effective treatment for the pain we have to put up with.

New Pharmacological Drug Target Identified in the Brain

A research team says it has found that sodium serves as a unique on/off switch for a major neurotransmitter receptor in the brain. The kainate receptor is fundamental for normal brain function and is implicated in numerous diseases, such as epilepsy and neuropathic pain, according to the investigators.

Derek Bowie, Ph.D., and his colleagues in McGill University’s department of pharmacology and therapeutics worked with University of Oxford scientists to make the discovery. They believe that by offering a different view of how the brain transmits information, their research highlights a new target for drug development. Their findings are published in the Nature Structural & Molecular Biology.

Balancing kainate receptor activity is the key to maintaining normal brain function, explained Dr. Bowie. For example, in epilepsy, kainate activity is thought to be excessive. Thus, drugs which would shut down this activity are expected to be beneficial.

“It has been assumed for decades that the ‘on/off’ switch for all brain receptors lies where the neurotransmitter binds,” continued Dr. Bowie, who also holds a Canada Research Chair in Receptor Pharmacology. “However, we found a completely separate site that binds individual atoms of sodium and controls when kainate receptors get turned on and off.”

The sodium switch is unique to kainate receptors, which means that drugs designed to stimulate this switch should not act elsewhere in the brain. This would be a major step forward, since drugs often affect many locations, in addition to those they were intended to act on, producing negative side-effects as a result.

“Now that we know how to stimulate kainate receptors, we should be able to design drugs to essentially switch them off,” said Dr. Bowie, who added that Philip Biggin, D.Phil., and his lab group at Oxford University used computer simulations to predict how the presence or absence of sodium would affect the kainate receptor.

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