Researchers at the Picower Institute for Learning and Memory at MIT report in the Feb. 13 issue of the Journal of Neuroscience that mice genetically engineered to lack a key protein used for building synapses-the junctions through which brain cells communicate-actually learned a spatial memory task faster and better than normal mice. But when tested weeks later, they couldn't remember what they had learned as well as normal mice, and they had trouble remembering contexts that should have provoked fear.
"These opposite effects on different types of learning are reminiscent of the mixed features of autistic patients, who may be disabled in some cognitive areas but show enhanced abilities in others," said Albert Y. Hung, a postdoctoral associate at the Picower Institute, staff neurologist at Massachusetts General Hospital and co-author of the study. "The superior learning ability of these mutant mice in a specific realm is reminiscent of human autistic savants."
Autism is one of a group of developmental disabilities known as autism spectrum disorders (ASDs), in which a person's ability to communicate and interact with others is impaired. The Centers for Disease Control and Prevention estimates that one in 150 American children has an ASD. Occasionally, an autistic person has an outstanding skill, such as an incredible rote memory or musical ability. Such individuals-like the character Dustin Hoffman played in the film Rain Man-may be referred to as autistic savants.
Hung said that while it seems counterintuitive that loss of an important synaptic scaffold protein would result in improved learning among the mice in this study, the absence of this protein may "trap" the mice's synapses in a more plastic state, which means the synapses are ready to respond to input but not maintain it in long-term memory.
Aberrant synapse development and faulty structure of dendritic spines-tiny protrusions on the surface of neurons that receive messages from other neurons-are often associated with neurodevelopmental disorders, including autism, in humans.Hung; Morgan H. Sheng, MIT's Menicon Professor of Neuroscience; and colleagues investigated the role in brain development and cognitive function of a protein called Shank1. Shank1 is one member of a family of proteins that act as structural scaffolds linking together different components of the synapse. In humans, mutations in the closely related protein Shank3 have been linked to the autism spectrum of disorders characterized by impaired social interaction, absent or delayed language development and repetitive behaviors.
In addition to Hung and Sheng, a Howard Hughes Medical Institute (HHMI) investigator, MIT authors are Picower Institute research scientist Kensuke Futai; MIT biology graduate student Jubin Ryu; MIT biology undergraduate Mollie A. Woodworth, Picower Institute postdoctoral fellow Fleur L. Kidd; Picower Institute research assistant Clifford Sung; and Mark F. Bear, Picower Professor of Neuroscience, HHMI investigator and director of the Picower Institute. Additional authors are from the University of Milan, the University of North Carolina at Chapel Hill, and Fujita Health University in Japan.
This work was supported by the RIKEN-MIT Neuroscience Research Center, the National Institutes of Health and HHMI.
Written by Deborah Halber, Picower Institute for Learning and Memory at MIT
Elizabeth A. Thomson | MIT News Office
Machine learning, imaging technique may boost colon cancer diagnosis
06.12.2019 | Washington University in St. Louis
The 136 Million Atom-Model: Scientists Simulate Photosynthesis
06.12.2019 | Jacobs University Bremen gGmbH
University of Texas and MIT researchers create virtual UAVs that can predict vehicle health, enable autonomous decision-making
In the not too distant future, we can expect to see our skies filled with unmanned aerial vehicles (UAVs) delivering packages, maybe even people, from location...
With ultracold chemistry, researchers get a first look at exactly what happens during a chemical reaction
The coldest chemical reaction in the known universe took place in what appears to be a chaotic mess of lasers. The appearance deceives: Deep within that...
Abnormal scarring is a serious threat resulting in non-healing chronic wounds or fibrosis. Scars form when fibroblasts, a type of cell of connective tissue, reach wounded skin and deposit plugs of extracellular matrix. Until today, the question about the exact anatomical origin of these fibroblasts has not been answered. In order to find potential ways of influencing the scarring process, the team of Dr. Yuval Rinkevich, Group Leader for Regenerative Biology at the Institute of Lung Biology and Disease at Helmholtz Zentrum München, aimed to finally find an answer. As it was already known that all scars derive from a fibroblast lineage expressing the Engrailed-1 gene - a lineage not only present in skin, but also in fascia - the researchers intentionally tried to understand whether or not fascia might be the origin of fibroblasts.
Fibroblasts kit - ready to heal wounds
Research from a leading international expert on the health of the Great Lakes suggests that the growing intensity and scale of pollution from plastics poses serious risks to human health and will continue to have profound consequences on the ecosystem.
In an article published this month in the Journal of Waste Resources and Recycling, Gail Krantzberg, a professor in the Booth School of Engineering Practice...
03.12.2019 | Event News
15.11.2019 | Event News
15.11.2019 | Event News
06.12.2019 | Ecology, The Environment and Conservation
06.12.2019 | Life Sciences
06.12.2019 | Medical Engineering