"One of the fascinating abilities of the brain is the ability to compensate for loss of sensory input. You can learn a lot when you discover that a fairly simple nervous system is capable of realizing a sophisticated brain function like this." Dr. Itai Rabinovitch, who led the research in his work in the Department of Medical Neurobiology at the Faculty of Medicine of the Hebrew University, explains
The human brain has an impressive ability to respond to sensory loss by enhancing the remaining senses. through a compensatory mechanism, known as intermodal plasticity
(cross-modal plasticity), certain senses are sharpened following the loss of input from other senses, such as the sharpening of the sense of hearing in blind people.
To date, this mechanism has been studied in humans and other mammals. The assumption was that the mechanism is a product of a complex brain with billions of cells, like the human one. Now, a new international study, led by researchers from the Hebrew University of Jerusalem, reveals that the brain's compensatory mechanism is a fundamental characteristic even in much simpler nervous systems than those of humans. During the study, the researchers revealed how the mechanism works and the intersensory signaling system in the brain that enables it.
The research, published in the journal PLOS Biology, was carried out in combination at the Department of Medical Neurobiology at the Israel-Canada Medical Research Institute in the Faculty of Medicine of the Hebrew University, at the MRC Laboratory for Molecular Biology in Cambridge, England, and at the Fred Hutchinson Cancer Research Center in Seattle, United States.
"One of the fascinating abilities of the brain is the ability to compensate for loss of sensory input. A lot can be learned when you discover that a fairly simple nervous system is capable of realizing a sophisticated brain function like this. In such a case, a new threshold for the level of neural complexity required to maintain such a compensation mechanism is also revealed, and it is also much easier to discover and understand how it works from the molecular level to the behavioral level," explains Dr. Itai Rabinovitch, who led the research in his work in the Department of Medical Neurobiology at the Faculty of Medicine of the Hebrew University.
The international group of researchers checked whether the brain compensation mechanism also exists in a creature with a very simple nervous system. To do this, they studied a tiny worm called
C. elegans, which is a millimeter long, feeds on bacteria and its nervous system has only 302 nerve cells (compared to about 100 billion in the human brain).
The researchers examined the relationship between the loss of the sense of touch and the sharpening of the sense of smell in the C. elegans worm. They focused on worms with a genetic defect that causes them to lose their sense of touch.
In examining the worms, the researchers discovered a significant improvement in their ability to respond to the smells of food, meaning that their sense of smell was sharpened in the absence of their ability to feel touch to their bodies. The researchers were able to link the change in the sense of smell to a change in the strength of a certain synapse in the neural circuit that mediates the sense of smell.
In normal worms that do feel touch, the researchers found a process of suppressing the synapse. The nerve cells that sense touch transmit special signals that suppress the activity of other nerve cells responsible for smelling, thus weakening the ability to smell. The suppression of the synapse is done by a special signal, a neuropeptide, secreted by the neurons responsible for sensing touch.
On the other hand, in the absence of sensory input of touch, the suppressing signal - the neuropeptide - is secreted less, the synapse in the olfactory circuit is strengthened and thus the sense of smell is sharpened.
"We were able to reverse the changes that occurred following the loss of the sense of touch both by artificially activating the touch neurons and by engineering a new synapse in the neural circuits responsible for smelling," explains Rabinovitch. "There is still a long way to go, but we can think of future applications to treat unwanted side effects following the loss of sensory input."
The results of the study add to a series of studies regarding the role of neuropeptides in intersensory signaling, and expand the knowledge about the molecular and cellular processes that stand behind the brain compensation mechanism. Also, the research results may show that the brain compensation mechanism may have ancient evolutionary roots, as it was discovered in a nervous system much less developed than ours.
Link to the article: http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1002348
