Babies’ brains are like sponges — highly tuned to incoming sensory information and readily rewiring their circuits. But when so-called critical periods close, our brains lose much of this plasticity. Classic experiments reveal this in the visual system: when kittens and mice had one eye covered shortly after birth, that eye was blind for life, even after the covering was removed. The brain never learned to interpret the visual inputs.
In 2010, a study led by Takao Hensch, PhD, of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital, showed that levels of a protein called Lynx1 rise just as the critical period for visual acuity closes. When the researchers deleted the Lynx1 gene in mice, the critical period reopened and mice recovered vision in the blind eye.
First in a two-part series on circadian biology and disease. Read part 2.
It’s long been known that a master clock in the hypothalamus, deep in the center of our brain, governs our bodily functions on a 24-hour cycle. It keeps time through the oscillatory activity of timekeeper molecules, much of which is controlled by a gene fittingly named Clock.
It’s also been known that the timekeeper molecules and their regulators live outside this master clock, but what exactly they do there remains mysterious. A new study reveals one surprising function: they appear to regulate the timing of brain plasticity—the ability of the brain to learn from and change in response to experiences.
“We found that a cell-intrinsic Clock may control the normal trajectory of brain development,” says Takao Hensch, PhD, a professor in the Departments of Molecular and Cellular Biology and Neurology at Harvard University and a member of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital. …
Say you’re a scientist in a movie, and you want to find out what gives a superhero his powers. You’d investigate any special suits he wears, whether he drinks any potions and what they are, right? Real-life scientists are following the same strategy to understand a powerful group of specialized brain cells.
Parvalbumin cells (PV-cells) are a population of inhibitory neurons found throughout the cerebral cortex. While small in number and size, they have the impressive capability to synchronize the electrical activities of other brain cells and orchestrate the timing of critical periods, interludes when the brain is more “plastic” and amenable to rewiring. Abnormalities in these pivotal cells are believed to make plasticity go awry, playing an important role in autism, schizophrenia and other neurodevelopmental disorders.
“The PV-cell is vulnerable in many mental illnesses,” says Takao K. Hensch, PhD, of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital and professor of molecular and cellular biology and neurology at Harvard University. “So if we can find a way to maintain its health and well-being, then we might have a way to treat neurodevelopmental disorders, even later in life.” …
What if blind eyes could see? What does that mean?
That’s the question neuroscientist Pawan Sinha and his team at MIT has begun to answer in a uniquely humanitarian and scientific endeavor.
Project Prakash (named for the Sanskrit word for “light”) intended, at first, to cure blind children in India. It’s a noble effort, given that India has the world’s highest population of blind people, less than half of whom survive to their third birthday and less than one percent of whom are employable.
Sinha’s team screened 20,000 blind Indian children and treated 700 of them for correctable problems such as cataracts. As Sinha recounted at last month’s One Mind for Research forum, these 700 children now can see.