July 14, 2014 | 3
Popular neuroscience books have made much in recent years of the possibility that the adult brain is capable of restoring lost function or even enhancing cognition through sustained mental or physical activities. One piece of evidence often cited is a 14-year-old study that that shows that London taxi drivers have enlarged hippocampi, brain areas that store a mental map of one’s surroundings. Taxi drivers, it is assumed, have better spatial memory because they must constantly distinguish the streets and landmarks of Shepherd’s Bush from those of Brixton.
A mini-industry now peddles books with titles like The Brain that Changes Itself or Rewire Your Brain: Think Your Way to a Better Life. Along with self-help guides, the value of games intended to enhance what is known as neuroplasticity are still a topic of heated debate because no one knows for sure whether or not they improve intelligence, memory, reaction times or any other facet of cognition.
Beyond the controversy, however, scientists have taken a number of steps in recent years to start to answer the basic biological questions that may ultimately lead to a deeper understanding of neuroplasticity. This type of research does not look at whether psychological tests used to assess cognitive deficits can be refashioned with cartoonlike graphics and marketed as games intended to improve mental skills. Rather, these studies attempt to provide a simple definition of how mutable the brain really is at all life stages, from infancy onward into adulthood.
One ongoing question that preoccupies the basic scientists pursuing this line of research is how routine everyday activities—sleep, wakefulness, even any sort of movement—may affect the ability to perceive things in the surrounding environment. One of the leaders in these efforts is Michael Stryker, who researches neuroplasticity at the University of California San Francisco. Stryker headed a group that in 2010 published a study on what happened when mice run on top of a Styrofoam ball floating on air. They found that neurons in a brain region that processes visual signals—the visual cortex—nearly doubled their firing rate when the mice ran on the ball.
The researchers probed further and earlier this year published on a particular circuit that acts as a sort of neural volume control in the visual cortex. It turns out that a certain type of neuron—the vasoactive intestinal peptide neurons (yes, they’re brain cells)— respond to incoming signals from a structure deep within the brain that signals that the animal is on the move. The VIP neurons then issue a call to turn up the firing of cells in the visual cortex. (As always with the brain, it’s not quite that straightforward: the VIP neurons squelch the activity of other neurons whose job is to turn down the “excitatory” neurons that rev up processing of visual information.)
“In the mouse the circuit happens to be hooked in the visual cortex to locomotion which puts it into a high-gain state,” Styker says. “That’s a sensible thing because when you move through the environment, you want the sensory system that tells you about things far away to be more active, to give a larger signal.” The researchers postulate that these neurons may form part of a general-purpose circuit able to detect an animal’s particular behavioral state and then respond to that input by regulating different parts of the cortex that process vision, hearing and other sensory information.
In late June, the investigators took their studies in a new direction with a publication that showed the possible clinical benefits of dialing up their newly identified neural knob. They did so in a study that demonstrated how the circuit that involves the VIP neurons plays a pivotal role in restoring visual acuity in a mouse that had been deprived of sight during a critical period in infancy when the animal must either use it or lose it. They sewed shut one eye in the young mouse for a time—effectively replicating amblyopia, a condition called “lazy eye” in human children that leads to vision loss. They waited until the mice had passed through the critical development stage, took out the stitches, and then switched on the VIP neurons in the behavioral plasticity circuit by having the mice go for a run. That restored vision to normal levels, but only if the animals were also exposed simultaneously to various forms of visual stimuli—either a grating pattern or random noise, similar to a television picture when a station is off the air.
The investigators have plans to see whether the same circuit in humans operates in a similar manner. One cautionary note to brain-game designers: the success in these experiments in eliciting plasticity—restoring vision, that is—was highly sensitive to the particular conditions under which the experiments were carried out. The visual cortex of a running rodent exposed to the grating pattern was better able to distinguish a similar geometric representation later, but not an image of snow-like noise.
What that means is that simply creating a game out of an n-back or Stroop test, or any other psychological assay for that matter, may not work that well in improving memory or self-control unless neuroscientists delve down with the same detailed level of analysis that Stryker and colleagues brought to bear. “We still don’t know what changes in circuitry are responsible for these phenomena of adult plasticity because we don’t have a really solid anatomical grasp of them,” Stryker says. Without the requisite insight, it may be that brain games make you into an ace at taking psychological tests designed to assess cognition, but these same tests may which have little or nothing to do with actually improving mental skills. You may spend all that time on sharpening cognition and end up as nothing more than a highly practiced test taker.
Stay tuned in coming years as brain science tries to sort out the plastic from the inelastic.
Image Source: National Eye Institute
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