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How do shared circuits develop?

Published online by Cambridge University Press:  08 April 2008

Lindsay M. Oberman
Affiliation:
Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02215
Vilayanur S. Ramachandran
Affiliation:
Department of Psychology, University of California, San Diego, La Jolla, CA 92093-0109. loberman@bidmc.harvard.eduvramacha@ucsd.edu
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Abstract

The target article discusses a model of how brain circuits mediate social behaviors such as imitation and mindreading. Hurley suggests potential mechanisms for development of shared circuits. We propose that empirical studies can be designed to differentiate the influence of genetic and learning-based factors on the development of shared circuits. We use the mirror neuron system as a model system.

Type
Open Peer Commentary
Copyright
Copyright © Cambridge University Press 2008

The target article describes several possible scenarios for the development of “shared circuits.” For example, this mechanism could be “hardwired” by genes or acquired through learning, or a combination of both. We discuss the evidence for each claim and then suggest experiments that may disentangle the factors contributing to the development of shared circuits by using the mirror neuron system to illustrate our strategy.

As discussed in the target article, studies designed by Meltzoff and Moore (1977) provided evidence for neonatal imitation in infants as young as a few hours of age. Specifically, these infants imitated mouth opening, tongue protrusion, and hand opening. The researchers suggest that the pattern of imitation is not likely the result of conditioning or innate releasing mechanisms. They suggest that this early imitation implies that human neonates have an innate ability to equate their own unseen behaviors with gestures they see others perform. However, it is possible that the actions investigated by Meltzoff and Moore (1977) were not, as suggested, based on an innate shared circuit, but rather could have been a reflex in response to a smile – like a sneeze in response to pepper. One way to find out would be to test whether infants can mimic an asymmetrical smile or another uncommon action. This would eliminate the “reflex” explanation and implicate a more sophisticated hardwired mechanism based on preexisting rules of translating visual appearance of the body into motor output, leading to accurate imitation.

This type of shared circuit may also be based on a form of associative learning. For example, every time the monkey's motor command neuron fired to reach for a peanut, the visual appearance of the monkey's hand reaching activated visual neurons, such that the firing of the two neurons (motor and visual) become linked through Hebbian association. The net result is that the motor neuron itself is activated by the visual image of peanut grabbing, even if the visual image is of another monkey's hand.

This Hebbian association hypothesis has been suggested by those who argue against the claim that mirror neurons are performing a complex remapping of other's representations onto one's own motor system. There are reasons for rejecting this argument (Ramachandran & Oberman Reference Ramachandran and Oberman2007). First, given that only a portion of F5 neurons have “mirror” properties, why do these neurons “learn” while others do not? If mirror neurons were set up purely through Hebbian associations, one would predict that all neurons in that region would have mirror properties, but this is not the case. This shows that there are specialized mechanisms and hardwired constraints that characterize the subset of neurons we refer to as mirror neurons. Additionally, the Hebbian hypothesis cannot account for the facial mimicry literature, because, when an infant smiles, the brain receives no visual feedback on which to build an association. It is still possible that this behavior is reflexive and the mirror neuron system may not be mediating it; however, the Hebbian hypothesis is no better at explaining this behavior.

It is also possible that these shared circuits take time to develop. They may require pre-existing hardwired scaffolding that is then “educated” by learning before being fully functional. This does not speak to whether the development results in the motor neuron being converted into a “mirror neuron,” capable of doing a complex self-other algorithm, or whether a motor neuron is simply responding to the visual stimulus as a result of Hebbian associative processes. Thus, the question of innateness/learning and the question of the nature of the computation that is being performed are logically separable. Furthermore, the necessary empirical studies to answer these questions have yet to be conducted.

To answer the question of innateness, one could record from area F5 (a region already known to contain mirror neurons) in a newborn macaque and expose the monkey to several actions, including actions that he will likely be exposed to early in life (e.g., peanut breaking, grasping, etc.), as well as novel actions that are unlikely to be based on pre-existing hardwired mechanisms. If neurons in F5 respond to both the familiar and novel actions the first time they are presented, that would argue for an innate system that does not depend on Hebbian association mechanisms. If F5 neurons respond only to the familiar actions, then the same argument could be made for these findings as was made for the findings by Meltzoff and Moore, that the brain is hardwired to respond to certain evolutionarily relevant actions. Finally, if no F5 neurons respond to the observation of any actions in newborn monkeys, this would argue against mirror neurons being innate.

To test whether mirror neurons are capable of creating a self-other metarepresentation or simply a motor neuron that has made an associative link to a visual representation, a different type of study would need to be conducted. One possible study would be to record from an F5 mirror neuron in an adult macaque while he watches either another monkey grasp a peanut or himself reaching for a peanut. In the “self” condition, it would be important that the monkey not actually reach for the peanut (enlisting other motor and sensory systems), but instead that the monkey be presented with an optically reversed image so that the inactive monkey has the visual perception of its “own” hand moving. If it is true that these neurons are set up through Hebbian associative processes, the “self” condition should elicit a greater response than the other condition, as this “egocentric view” is what the association was built on. If the metarepresentation hypothesis is correct, however, the “other” condition should elicit a greater response.

There are currently several possible mechanisms for the development of a mirror neuron system. It is our prediction that, like other systems in the brain, these types of “shared circuits” are neither purely learned nor purely innate, but a result of both hardwired and learned processes. Indeed, the circuitry underlying mirror neurons may provide an ideal model system for exploring how nature and nurture interact to create the human body and mind.

References

Meltzoff, A. & Moore, M. (1997) Explaining facial imitation: A theoretical model. Early Development and Parenting 6:179–92.3.0.CO;2-R>CrossRefGoogle ScholarPubMed
Ramachandran, V. S. & Oberman, L. M. (2007) Broken mirrors: A theory of autism. Scientific American, June 2007, special edition.CrossRefGoogle Scholar