Brain May Be Less Plastic Than Hoped
Human Brain Flexibility
The visual cortex of the adult primate brain displays less flexibility in response to retinal injury than previously thought, according to a new study published in the May 19, 2005, issue of the journal Nature. This may have implications for other regions of the brain, and the approach the investigators used may be a key to developing successful neurological interventions for stroke patients in the future.
Stelios M. Smirnakis, a Howard Hughes Medical Institute physician-postdoctoral fellow in Nikos K. Logothetis' group at the Max Planck Institute for Biological Cybernetics, used functional magnetic resonance imaging (fMRI) to monitor cortical activity for seven and one-half months after injury to the retina of adult monkeys. They found limited reorganization in the primary visual cortex.
Their results contradict previous thinking. In a "News and Views" commentary published in the same issue of Nature, Martin I. Sereno, a neuroscientist at the University of California, San Diego, says the latest data indicate that adult brains may be less plastic than scientists had hoped.
In children, the brain's ability to compensate for injuries is well known. Children with severe epilepsy who lose an entire hemisphere during surgery can regain motor control on the affected side of their body and go on to develop normal language skills. But in adults, the case for brain plasticity has been less clear.
A series of studies in the 1980s and 1990s seemed to show that, in adult animals, neurons "filled in" blank spots in the motor and visual cortex after these areas fell silent from lack of sensory input due to injury. This led to speculation that adult brains could compensate for permanent damage to the eyes, ears, skin, or even to itself. In the case of damage to the retina, Smirnakis said, "the predominant-but by no means universal-view was that significant reorganization occurred as early as it does in the primary visual cortex."
But the latest imaging research from his team shows that, in monkeys, this is not the case. "We asked: Can visually driven activity in the region of the primary visual cortex that corresponds to the retinal injury recover to pre-lesional levels in the months following the lesion?" said Smirnakis. "The answer is, in that time interval the primary visual cortex did not achieve anything like normal responsivity."
To arrive at this conclusion, Smirnakis and his group first photocoagulated the retinas of four monkeys with a laser, creating small blind spots on the same sides of the field of vision. The retina sends signals that the brain interprets as light, color, or objects. Each section of the retina corresponds to a specific location in the primary visual cortex. Without any visual signal to interpret, the cortical area corresponding to each monkey's blind spot fell silent, generating no activity.