Sensory Conflict Neurons React and Help Us Readjust Our Balance In a Fall
Whether it is slipping on ice, tripping over an unseen bump on the sidewalk, or hitting a rock when skiing, sometimes you fall. But surprisingly you usually manage to recover your balance and walk on unharmed. So what’s going on in the brain when you manage to recover your balance in these situations it is not just a matter of good luck.
A distinctive and startlingly small cluster of cells deep within the brain that react within milliseconds to readjust our movements when something unexpected happens has been identified by McGill University researchers. Amazingly, each individual neuron in this tiny region that is smaller than a pin’s head displays the ability to predict and selectively respond to unexpected motion.
Science has known for a time that the sense system in the inner ear, called the vestibular system, helps keep our balance by stabilizing our visual field as we move around. And while researchers have already begun to have a basic understanding of how the brain constructs our perceptions of ourselves in motion, until now no one has understood the crucial step by which the neurons in the brain select the information needed to keep us in balance.
Sensory Conflicts Library
This new finding by Professor Kathleen Cullen overturns current theories about how we learn to maintain our balance as we move through the world. This also has important implications for our understanding of the neural basis of motion sickness.
It is theorized by neuroscientists that we fine-tune our movements and maintain our balance, due to a neural library of expected motions that we gain through “sensory conflicts” and errors. “Sensory conflicts” occur when there is a mismatch between what we think will happen as we move through the world and the sometimes contradictory information that our senses provide to us about our movements.
This type of “sensory conflict” could happen when our bodies detect motion that our eyes cannot see, like during plane, ocean or car travel, or when our eyes perceive motion that our bodies cannot detect, during an IMAX film, for example, when the camera swoops at high speed over the top of a roller coaster ride or deep into the Grand Canyon while our bodies remain sitting still. These “sensory conflicts” are also responsible for the feelings of vertigo and nausea that are associated with motion sickness.
Although the areas of the brain involved in judging spatial orientation have been identified for some time, until now, no one has been able to either show that distinct neurons signaling “sensory conflicts” existed, nor demonstrate exactly how they work.
“We’ve known for some time that the cerebellum is the part of the brain that takes in sensory information and then causes us to move or react in appropriate ways,” Prof. Cullen explained. “But what’s really exciting is that for the first time we show very clearly how the cerebellum selectively encodes unexpected motion, to then send our body messages that help us maintain our balance. That it is such a very exact neural calculation is exciting and unexpected.”
By demonstrating that these “sensory conflict” neurons not only in fact exist but also work by making choices spontaneously about which sensory information to respond to, Cullen and her team have made a significant contribution to the understanding of how the brain works to keep our bodies in balance as we move about.
In an earlier study, professor Cullen had shown for the first time that neurons in the vestibular nuclei in the brain instead decode incoming information nonlinearly as they respond preferentially to unexpected, sudden changes in stimuli.
The Primate Cerebellum Selectively Encodes Unexpected Self-Motion Jessica X. Brooks,Kathleen E. Cullen Current Biology, Volume 23, Issue 11, 947-955, 16 May 2013 10.1016 j.cub.2013.04.029
The Vestibular System Implements a Linear–Nonlinear Transformation In Order to Encode Self-MotionCorentin Massot, Adam D. Schneider, Maurice J. Chacron, Kathleen E. CullenResearch Article | published 24 Jul 2012 | PLOS Biology10.1371/journal.pbio.1001365