During childhood the human brain is very plastic, all young mammals have a critical period when different areas of the brain can remodel neural connections in response to external stimuli; disruption of this developmental sequence results in serious damage such as autism. Maturation of inhibitory nerve cells within the brain controls onset of critical period plasticity, how plasticity wanes with age is not fully understood, but evidence suggests SynCAM molecules may be involved in the process.
Focussing on the visual cortex using advanced viral tools and electrophysiological techniques the team was able to measure activity of neurons in awake mice freely responding to visual stimuli; removal of SynCAM 1 molecules from the brain was observed to increase plasticity in the visual cortex of young and adult mice. Further investigations revealed SynCAM 1 to control specific neuronal connection synapses, being necessary for the formation of synapses between the thalamus and inhibitory neurons, which helps inhibitory neurons to mature and actively restrict critical period plasticity.
The team suggests they have identified a fundamental mechanism that controls brain plasticity, and have shown that a process in the adult brain actively suppresses plasticity. Limited ability of the mature brain to change is not a consequence of age, rather it is directly enforced by SynCAM 1 mechanisms which allowed the team to target the mechanism to reopen plasticity in the mature brain; findings may be relevant for treating disorders such as autism explains Thomas Biederer, Ph.D.
Potential for side effects in developing treatment should be reduced by focusing on a single molecule and synapse type to induce heightened plasticity; combined with latest approaches in genetic manipulation this may prove to be a new path towards tackling childhood disorders and brain injury in adults, although further study is needed to determine if this plasticity mechanism will work in humans and if results seen in mice can be activated repeatedly.
