Brain plasticity refers to the brain’s ability to change throughout life. When young, the brain is highly plastic, but becomes less so as we age. Too much plasticity can be a problem, but it’s necessary for the brain’s ability to repair itself or reorganize itself after injury or when learning new things.
Researchers at Tufts University and Yale University School Of Medicine have identified a new molecular mechanism that could restore plasticity in aged brains. The research was conducted on mice and published in the journal Cell Reports. The research has implications for a range of disorders, including autism and stroke.
Brain plasticity refers to the brain’s ability to change throughout life. When young, the brain is highly plastic but becomes less so as we age. Too much plasticity can be a problem, but it’s necessary for the brain’s ability to repair itself or reorganize itself after injury or when learning new things.
“It’s been known for a while that maturation of inhibitory nerve cells in the brain controls the onset of critical period plasticity, but how this plasticity wanes as the brain matures is not understood,” stated Adema Ribic, researcher at Tufts School of Medicine and first author of the study. “We’ve had some evidence that a set of molecules called SynCAMs may be involved in this process, so we decided to dig deeper into those specific molecules.”
They focused on the visual cortex in mice. This part of the brain oversees the processing of visual scenes. They utilized viral tools and electrophysiological techniques to measure activity of neurons in awake mice that were freely responding to visual stimuli. When they removed the SynCAM 1 molecule from the brain, it increased plasticity in the visual cortex of the mice, independent of their age.
For example, loss of vision in one eye cuts cortical responses to stimulus from that eye during the critical periods, but not in adulthood. The researchers showed that SynCAM 1 is regulated by visual experience while also limiting visual cortex plasticity.
They further found that SynCAM 1 controls a specific neuronal connection called synapses, specifically long-distance synapses between the visual thalamus, which is located beneath the cerebral cortex, and inhibitory neurons in the cortex. The molecule was required in order to form synapses between thalamus and inhibitor neurons, which then helps inhibitory neurons mature and actively restrict critical period plasticity.
“Our study identified a fundamental mechanism that controls brain plasticity, and perhaps most exciting, we can show that a process in the adult brain actively suppresses plasticity,” stated Thomas Biederer, associate professor of neuroscience at Tufts and senior author of the study. “Therefore, the limited ability of the mature brain to change is not simply a consequence of age but is directly enforced by the SynCAM 1 mechanism. This allows us to target the mechanism to re-open plasticity in the mature brain, which could be relevant for treating disorders like autism.”
When human beings are young, their brains are very plastic. They all have a “critical period” where different parts of their brains are able to remodel neural connections in response to external stimuli. They believe autism may involve disruption of those critical periods.
It’s also known that antidepressants may restore plasticity, but they also have other effects. Ribic stated, “Our study found a way to increase plasticity in a very controlled way, both spatially and temporally. Combined with the latest approaches in genetic manipulation, this may prove to be a new path to tackle both childhood disorders and brain injury in adults.”
Work needs to be done to determine if the plasticity mechanism works in humans and whether it can be activated repeatedly.
