Opioid overdose antidote naloxone nasal spray promotes stroke recovery in rats

The life-saving drug used to treat opioid overdose, naloxone, reduces brain inflammation in the aftermath of stroke in male rats. The preclinical research by the researchers from the University of Helsinki and National Institute on Drug Abuse in the USA lays the groundwork for developing the first drug to promote recovery from a leading cause of adult disability.

Naloxone has been used for decades to prevent death from drug overdose and has become widely used in recent years in response to the unrelenting opioid crisis. Although the therapeutic potential of naloxone in stroke has been explored, research in this area is limited to a few case studies from the 1980s and inconclusive clinical trials.

Mikko Airavaara from Institute of Biotechnology (UH, Finland) and Brandon Harvey from NIDA, NIH and colleagues expanded on this work by showing in a rat model of stroke that one week of treatment with naloxone, beginning one day after the stroke, tempered the brain’s immune response and improved neurological function in the second week.

As with the naloxone nasal spray Narcan, the researchers administered the drug to rats though the nose at doses similar to those that have been shown to be safe in humans.

Together, these initial findings warrant further study of naloxone in different populations of animals and over a longer recovery period to investigate its potential for promoting recovery from stroke in humans.

Airavaara’s group will further study (+)-naloxone, which is an optical isomer i.e. a molecular reflection of the (-)-naloxone (Narcan), which is already on the market. The advantage of the (+)-form is that it does not inhibit the opioid receptors but it can in a similar way promote the recovery from a brain stroke as Narcan. The (+)-form could be used to avoid the side effects caused by opioid blockage.

Original article:

Post-stroke intranasal (+)-naloxone delivery reduces microglial activation and improves behavioral recovery from ischemic injury

DOI: https://doi.org/10.1523/ENEURO.0395-17.2018

Corresponding authors:

Brandon K. Harvey (National Institute on Drug Abuse, Baltimore, MD, USA), bharvey@intra.nida.nih.gov and Mikko Airavaara (University of Helsinki, Finland), mikko.airavaara@helsinki.fi



Airavaara research group's web page