For many people, scratching an itch is still one of the fastest and easiest ways to alleviate a crawling and irritating feeling on their skin. However, there are those who just can't seem to get rid of the itchy sensation no matter how much scratching they do.
These individuals are known to suffer from a hard-to-treat condition called chronic intractable itch, in which the sensation stems from renal failure and dialysis. This chronic illness is what inspired a team of scientists from The Scripps Research Institute (TSRI) in Florida to find a treatment for.
In a recent study featured in the journal Neuropharmacology, Professor Laura Bohn and her colleagues at TSRI identified a compound class that has the ability to prevent chronic itch without triggering any of the adverse side effects typically associated with treating the illness.
Bohn said that they have been studying compounds that can help preserve the positive properties of opioids while also eliminating many of the known side effects.
She explained that the new research describes how they were able to refine the signaling aspect of medicines at the receptor, allowing them to suppress the itchy sensation without the need for sedation. Producing compounds capable of activating the receptors in this manner could provide scientists with the means to enhance the therapeutic potential of drugs.
Bohn and her team made use of a compound known as isoquinolinone 2.1 in order to target the kappa opioid receptor. This receptor is most visible in the central nervous system, and it helps moderate an individual's perceptions of pain and responses to stress.
Through the use of mouse models afflicted with the chronic intractable itch, the researchers found that the isoquinolinone 2.1 compound was effective in preventing an irritant-induced itch from occurring without triggering sedation on the animals.
The Scripps researchers noted that the isoquinolinone 2.1 is just one of a newly discovered class of "biased" kappa agonists that can avoid many side effects on the central nervous system. This is done by specifically activating a signaling cascade mediated by G proteins without compromising other systems based on β-arrestin-related protein responses.
Photo: Jo Jakeman | Flickr
