road to recovery? New ideas about how the brain repairs itself may help patients recover better after a stroke.
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A third of stroke survivors never recover enough brain function to live on their own. Now scientists think they know why. Once a stroke kills brain cells band, a neurotransmitter called GABA affects survival, brain tissue apparently healthy. GABA may help targeting a brain stroke-afflicted better overcome its damage, the researchers suggest.
When a stroke hits, doctors have few options. If they catch early enough, they can administer the drug tPA to keep more brain cells die, but tPA is not suitable for all types of stroke. Doctors may also prescribe physical therapy, which can sometimes help recover motor functions. Yet there are no approved drugs that help the brain to heal.
For its part, the brain seems to try a kind of natural drug therapy to limit the spread of damage. It releases additional amounts of GABA, which reduces the firing of neurons. GABA initially prevents stroke damaged brain tissue to become excited and dying. But the University of California, Los Angeles (UCLA), investigators led by Thomas Carmichael, a specialist of the race, and Istvan Mody, an expert in the inhibition, wonders if GABA could also interfere with brain plasticity the ability of the healthy areas take over for the injured.
Previous studies have tried to answer this question, but they have produced confusing results. The UCLA team hypothesized that others had failed to distinguish between two types of inhibition-phase, in which the GABA acts on specific receptors on nerve cell sites called synapses, and tonic, wherein the neurotransmitter acting on other receptors elsewhere on the nerve cell. "We looked at all the neural transmission properties after a stroke, and we found the biggest change was an increase in tonic form of inhibition in the cortical region adjacent to the stroke damage," says the graduate student and co-author Ben Huang study. Thus, the group gave rodents to stroke sufferers a drug that could specifically block the tonic inhibition of GABA but left intact phasic inhibition. Mice were damaged in areas that control movement, but they recovered about 50% more according to their members than similar rodents treated with control therapy, the team announced today online Nature .
The results suggest a new window, potentially therapeutic for the treatment of stroke, said Carmichael. Doctors may be able to give a GABA blocker medication after stroke, for example. The key would be good timing: after the tonic inhibition was initially protected as many brain cells as possible, but before it begins to interfere with the brain's recovery attempts. The class of medicines used by the UCLA team to block GABA receptors is currently in clinical development for other conditions such as memory loss, and was well tolerated in small studies. However, these drugs have not yet been tested in patients with stroke. Clinical trials are far warns Carmichael, because most animal studies by other laboratories should be performed first.
Nevertheless, other neuroscientists say the work offers a new direction for the stroke drug development. "The result is very rewarding because for many years, people have focused on excitatory synapses and excitatory connections in terms of brain plasticity," says Takao Hensch, a researcher of developmental plasticity in the department molecular and cellular biology at Harvard University. "It is only in the recent past we have begun to understand that the balance of excitation to inhibition is what is important."
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