You definitely want to avoid an encounter with a banded krait. A single bite from this snake delivers enough venom to spell the end for a dozen people. Working like a chemical brake, the active toxin finds its way to your neurons, and snuffs out the signals that would otherwise animate your muscles. It’s bad stuff.
Which makes it all the more surprising that the venom, or something very close, is found in our heads. Recent work from Professor Takao Hensch’s Harvard lab shows that a close molecular cousin of the krait’s toxin, called Lynx1, serves as a kind of brake in the brain. Rather than silencing neurons outright, molecules like Lynx1 help hold them in check, suppressing their tendency to grow and otherwise change with experience. In the absence of these brakes, our brains’ circuits are sprawling and adaptable, but also somewhat unstable.
When we are young, we live through a biological “critical period” -- a time when there is little braking, and the brain is extraordinarily adaptable. Certain kinds of learning seem to just happen without much special attention or practice. None of us learned our native tongue by memorizing rules and exceptions for juggling different parts of speech. Instead, our brains seemed somehow ready for the necessary information, and the information found its way in.
As the brain ages, it is much less willing to meet the world halfway. Instead of easily re-molding itself to accommodate new kinds of inputs, the older brain is more constrained - a biological truth known to anyone who’s struggled to pick up a new language later in life. While many processes contribute to this change in the brain’s learning potential, scientists believe that some of the changes are brought about by the gradual accumulation of molecules, like Lynx1, that limit the brain’s adaptability.
Of course, it might seem like a raw deal to be ‘bitten’ by your own brain, and have your neural prowess slowly snuffed out. But in fact, this is the necessary - if less exciting - second half of a process that stores knowledge in a format that’s accessible for life. Without some kind of insulation from change, the youthful neuronal clay would never set, making life’s lessons unstable and prone to degrade. So although Lynx1 and other molecules cut off our critical period by hitting the brakes on plasticity, they also help lock in knowledge for the long term.
Naturally, scientists have long been interested (reviewed here) in understanding the specifics of how these brakes work, and, perhaps one day, how to control them. With their investigation of Lynx1, the Hensch group has found what may be one of the major factors responsible for closing the door on plasticity after the critical period. In addition, they demonstrate a strategy for lifting the brake to enhance adult plasticity and repair wiring errors in the brain. This could have major implications for the treatment of developmental disorders and brain injuries, and may eventually provide ways to augment cognition in later life.
The first step in investigating Lynx1’s properties was to ask if it accumulated at the right time to function as a plasticity brake. By labeling and collecting samples of Lynx1 and its precursors from the brains of mice at different ages, the researchers tracked how its levels changed over time. Its concentration was low and steady at young ages - within the known critical period for mice -- and ramped up with age.