Molecular brakes that affect brain plasticity identified
Even brain needs a set of molecular brakes that stabilize its circuitry during growth, according to researchers at the Stanford Univ School of Medicine.
Washington: Even brain needs a set of molecular brakes that stabilize its circuitry during development, according to researchers at the Stanford University School of Medicine.
In fact, the researchers also found that experimentally removing those brakes in mice enhanced the animals`` performance in a test of visual learning, suggesting a long-term path to therapeutic application.
In the study, Dr. Carla Shatz, professor of neurobiology and of biology, and her colleagues have implicated two members of a large family of proteins critical to immune function (collectively known as HLA molecules in humans and MHC1 molecules in mice) in brain development.
Until recently, these immune-associated molecules were thought to play no role at all in the healthy brain.
In previous studies, the researchers showed that MHC molecules are found on the surfaces of nerve cells in the brain, and that they temper "synaptic plasticity": the ease with which synapses are strengthened, weakened, created or destroyed in response to experience.
In a recent study, the researchers tied two specific members of the MHC1 family, called K and D, to the ability of circuits in a brain region responsible for motor learning to be refined by a learning experience.
For the current study, scientists looked at vision processing in the brain.
"We``d already found that K and D were located in brain regions we knew mattered: the visual cortex, and a relay station in the brain that sends its input to the visual cortex," said Shatz.
A good example of the "use it or lose it" manner in which experience-dependent circuit tuning shapes the brain is the ability of one eye to take over brain circuits that normally would be used by the other eye.
In order to map the roles of K and D in visual development, the researchers studied mice genetically engineered to lack these two molecules.
In the K- and D-deficient mice, the capacity of a more-used eye to dominate visual information-processing circuitry is abnormal, and in a surprising way, said Shatz.
"There``s too much of it. If one eye stops functioning, the other eye takes over more than its fair share of the cortical machinery devoted to the brain``s visual-information-processing territory," she said.
In a test of visual performance, they showed that the K- and D-deficient mice could see better through their remaining eye than could ordinary mice raised with a similarly blocked eye.
"This suggests there``s some kind of molecular brake on plasticity in the brain, and these molecules are involved in the braking system. Taking off the brake improved performance," she said.
The study has been published in Neuron.