Doctors may soon have a new weapon in their arsenal with which to combat strokes, which occur when the blood flow to part of the brain is interrupted.
Writing in Nature this week, UCLA-based researcher Tom Carmichael and his colleagues have found, using experimental mice, that surviving brain tissue surrounding an area affected by a stroke becomes electrically underactive. This occurs because the cells in this region increase their response to the inhibitory nerve transmitter GABA.
In the short term this is beneficial because, by suppressing the activity of these nerve cells the brain reduces their metabolic demands and therefore helps them to survive. But this state of electrical inexcitability seems to persist, which can hamper recovery in the long term. For instance, these brain regions can often take on some of the workload of the adjacent injured areas, helping to restore function.
Reasoning that re-enhancing the activity of these cells might therefore boost recovery, Carmichael and his colleagues administered an agent called L655,708, which was able to block the aberrant GABA signals in the brain.
Animals that received this treatment, which was best administered from three days after a stroke, showed dramatically improved motor function compared with untreated controls. This suggests that stroke rehabilitation in humans should perhaps also include a pharmacological component, rather than solely a physiotherapy-based regimen as is currently the status-quo.