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Journal Article[1]
Equipotentiality is a theory initially put forth by Karl Lashley in 1930. His theory suggested that the capacity of any part of a functional area in the brain could carry out functions lost by the destruction of other parts of the brain with or without a loss of efficiency. He stated that the capacity for equipotentiality can vary from one brain area to another, and that it is more applicable to association areas than other brain areas.[2] This suggests that the capacity for equipotentiality may not be activated until there has been some kind of damage to the brain. Lashley proposed that the cortex functions as a whole, and that the contributions of different parts of a specialized area are qualitatively the same, allowing for other parts of that area to compensate for any damage within the area.[3]
In support of his theory, Lashley presented data from his animal research. This research gave evidence that no singular sensation, memory, or skill was destroyed on its own by any lesion. Either a number of sensations, memories, or skills were affected by the lesion, or none were. This evidence led him to believe that the functional areas of the brain are equipotential for sensation, memory, and skills. Lashley did, however, suggest that this may not be possible for all parts of the brain, perhaps just the association areas.[4] Tied in with his theory of equipotentiality was the law of mass action, which states that the level of performance of a function is proportional to the amount of brain tissue damaged. Efficiency to perform a complex function is more severely affected as the damaged area may not be specialized for one specific aspect of a function but may play a role in that and other functions. A challenge to Lashley’s theory of equipotentiality came in the end of the 1930’s by Hunter.[5] He argued that Lashley did not present evidence to justify his claims, as the majority of his research was done in the maze habit. He considered this insufficient as evidence for a theory of equipotentiality.[6] He suggested that results from using a visual discrimination habit may disprove this theory. By the 1950's, researchers were seeing more and more data that Lashley’s theory of equipotentiality could not account for. Some suggested that animal research seems to continue to support his theory, but human research seemed to support the theory of cerebral localization.[7] However, some researchers suggested that the discrepancies in data did not necessarily mean the theory of equipotentiality was disproven. Instead, they proposed that the differences in animal research were due to the idea that lesions were general (or non-localized). However, it was suggested that lesions in humans are often both general and specific (or localized). If this were the case, there would be a different pattern of effects due to brain damage seen in animals as opposed to humans.[8] By the 1970’s, most research in neuroscience questioned the theory of equipotentiality, indicating that it was no longer a theory considered correct.[9]
In connection with the idea of the equipotentiality of functional areas in the brain, some put forth the idea of equipotentiality across cortical hemispheres for any function. The most definite time of hemispheric equipotentiality was considered to be in childhood, when the brain was still developing. This theory stands in opposition to the theory of cerebral dominance, which states that one hemisphere is more dominant than the other, especially for specific functions. For example, the left hemisphere has been considered to be the dominant hemisphere for language. However, one view of these theories suggested that the hemispheres were equipotential in humans until at least two years of age, when cerebral dominance began to develop. Even language was considered to be equipotential across hemispheres, but it was one of the earliest functions to become dominant in one hemisphere as there is a decrease of involvement in the lesser hemisphere.[10] This cerebral dominance does not necessarily eliminate the possibility of hemispheric equipotentiality. If the activation of the capacity for equipotentiality depends on damage, as stated above, functional cerebral dominance would be maintained so long as there is no damage. So the capacity for equipotentiality can be considered a latent capacity.[11] However, there is a competing view that the hemispheres are equipotential prior to full development, but lose their capacity for equipotentiality as the cortical areas become committed to specific functions. This would suggest that many areas are equipotential in childhood, but as the child develops into an adult, less and less of the brain has the capacity for equipotentiality because less brain areas are free from other functional commitments. So, as the brain matures, it becomes less equipotential.[12] Lashley did find evidence for hemispheric equipotentiality in his research and generally assumed it to be the case; however, he was more interested in overall equipotentiality, not just in the hemispheres.[13] A study by Samuel Kirk gave evidence for hemispheric equipotentiality in visual function and intelligence tests, but he found that handedness appeared to follow the theory of cerebral dominance. [14] Further research about hemispheric equipotentiality used a dichotic listening task to test the potential of either hemisphere for language. The researchers found that the left hemisphere dominance of language can be influenced by learning, both in children and in adults.[15]
In behaviorism, equipotentiality refers to the idea that any response an animal can make can be equally linked to any stimulus it can perceive.[16] In other words, according to the principle of equipontentiality, learning will not differ with the use of specific stimiuli, responses, or reinforcement.[17] The specific stimulus and response were not considered important, because any stimulus could be paired with any response. This view dominated throughout the 20th century.[18] However, most research investigating the principle of equipotentiality limited its studies to using a few species (rats and pigeons mainly) and a small number of experimental paradigms (for example, the Skinner box – see image).[19] Challenges to the principle of equipotentiality began to appear when researchers moved away from these limited species and paradigm experiments. For example, one study looked at several different species, including chickens, pigs, raccoons, rabbits, and ducks, only to find that the principle of equipotentiality was not as prevalent as initially thought. These previously untested species were not responding in the same way that the regularly used species did.[20] Evidence contrary to the principle of equipotentiality was also being observed in several studies that showed that responses were not equal with any given stimulus.[21] Equipotentiality was challenged as a principle in behaviorism as evidence started being observed that contradicted it. Several studies showed that there was an effect of “appropriateness” in the stimulus pairing relationships in conditioned learning.[22] Studies that involve conditioned taste aversion were a strong challenge against the principle of equipotentiality. Garcia and Koelling found that taste stimuli were much more easily associated with feelings of sickness (leading to taste aversion) than any other type of stimuli and similarly that audiovisual stimuli were much more easily associated with pain experienced on the skin.[23] Similarly, Jones and Macken used the equipotentiality theory to predict that speech tones and non-speech tones would have an equivalently disruptive effect on serial recall. [24]
The principle of equipotentiality has also been extended to dispositional motives. In this area, equipotentiality refers to the idea that one starting point can lead to many different endpoints. Specifically, one dispositional motive can be expressed through more than one behavior.[25] This has been demonstrated in research that has blocked a dispositional motive through one behavior, as that motive will then be expressed through another behavior.[26] This view goes as far as to explain the reason for why children with similar personality traits may have develop very different personality characteristics by adulthood.[27]
Lashley Article[28]
Holmes Article[29]
Hunter Article[30]
Piacentini Article[31]
Fletcher Article[32]
Bartley Article[33]
Harlow Article[34]
Joseph Article[35]
Aspden Article[36]
Unger Article[37]
Bishop Article[38]
Satz Article[39]
Sperry Article[40]
LeCompte Article[41]
Mettler Article[42]
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