Boston, MA -- A protein once thought to play a role only in the immune system could hold a clue to one of the great puzzles of neuroscience: how do the highly malleable and plastic brains of youth settle down into a relatively stable adult set of neuronal connections? Harvard Medical School researchers report in the August 17 Science Express that adult mice lacking the immune system protein paired-immunoglobulin like receptor-B (PirB) had brains that retained the plasticity of much younger brains, suggesting that PirB inhibits such plasticity.
Intriguingly, brains of immature PirB-deprived mice also exhibited greater plasticity than brains endowed with the protein. Taken together, the results have important implications for the future study and repair of the brain. "Our study of mutant mice lacking PirB function reveals that at all ages, even during critical periods when circuits are prone to change, there are active molecular mechanisms that function to limit synaptic plasticity," said Josh Syken, HMS instructor in neurobiology and lead author of the study.
One way to promote new connections in brains damaged by disease or injury might be to target PirB. "The implications here should attract broad interest outside the field of developmental neuroscience because molecules and mechanisms that oppose neuronal plasticity represent new targets for therapy to re-establish damaged connections following spinal cord injury, head injury or stroke," said Syken, who carried out the study with Carla Shatz, Nathan Marsh Pusey professor of neurobiology at HMS, and colleagues.
Plasticity, the ability of functional brain circuits to change in response to experience-dependent neuronal activity, is largely restricted to critical periods of development. In their classic Nobel-prize winning experiments, David Hubel and Torsten Weisel showed that visual areas of the brain are responsive to environmental cues during a discrete period early in life, aft
Contact: John Lacey
Harvard Medical School