Abstract
Explanations of how psychological capacities are carried out often invoke functional brain areas. I argue that such explanations cannot succeed. Psychological capacities are carried out by identifiable entities and their activities in the brain, but functional brain areas are not the relevant entities. I proceed by assuming that if functional brain areas did carry out psychological capacities, then these brain areas could be included in descriptions of mechanisms. And if functional brain areas participate in mechanisms, then they must engage in activities. A number of ways in which we might understand the claim that functional brain areas engage in activities are examined. None are successful, and so one conclusion is that functional brain areas do not participate in mechanisms. Consequently, they are not the entities that carry out psychological capacities.
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Notes
I will occasionally refer to levels in this paper. Since levels will not carry much of the explanatory burden, I will not spend too much time introducing them. By levels I mean levels of organization (see, for instance, Wimsatt 1976). And, in addition to a level occupied by functional brain areas, I will refer to a level occupied by neurons (the cellular level) and a level occupied by molecules (the molecular level). Furthermore, my view—which I do not defend in this paper—is that the cellular level and the molecular level are the levels at which the entities and activities that carry out psychological capacities occur.
The membrane potential is a measure of the electrical charge on the inside of the cell membrane relative to the electrical charge on the outside of the membrane. (The charge on the outside of the membrane is, by convention, set at zero, and so the membrane potential is a measure of the charge on the inside of the cell membrane.) At rest the membrane potential for a neuron is typically around −70 mV.
The charged sodium ions (Na+) are drawn into the neuron because of the concentration gradient that is created by the small amount of Na+ inside the neuron compared to outside of it when in the resting state (i.e., when the membrane potential is −70 mV). There is also an electrical driving force that pulls Na+ into the neuron until its equilibrium potential is reached (about 61.5 mV; Kingsley 2000).
The inactivation of the sodium channel—when the channel is blocked by the portion of the protein that has swung into the mouth of the pore—is not the same as deactivation, which occurs when this part of the protein moves away and parts of the protein that form the channel itself are drawn together on the intracellular side. What should count as the termination conditions for this mechanism—inactivation or deactivation—is an interesting question, but it will not be pursued here.
Machamer et al. are somewhat wary of the term interaction. They say, “Terms like ‘cause’ and ‘interact’ are abstract terms that need to be specified with a type of activity and are often so specified in typical scientific discourse. Anscombe (1981, p. 137) noted that the word ‘cause’ itself is highly general and only becomes meaningful when filled out by other, more specific, causal verbs” (2000, p. 6). Nevertheless, for our present purposes, interaction seems like a good place to start.
The optic nerves designate the axons between the retinae and the optic chiasm (where some of the axons cross from the right eye to the left hemisphere of the brain, and from the left eye to the right hemisphere) and the optic tracks are the continuation of these axons from the optic chiasm to the LGN.
That is to say, V1 (qua brain area) is equally active when a bar of light at a 70° orientation is hitting the retina and when a bar of light at a 45° orientation is hitting the retina. The relevant differences in activity only show up when we drop down to the level of neurons.
Machamer et al. (2000, p. 2) do not devote much attention to this distinction, but they do say, “Mechanisms are sought to explain how a phenomenon comes about or how some significant process works.” Craver (2002) calls the process that the mechanism carries out the role, and Craver and Bechtel (2005) call it the phenomenal aspect of the mechanism.
Bechtel (2005) has a very useful example concerning investigations into the mechanism that carries out fermentation. Researchers in the late nineteenth century were not in a position to make a distinction between the role that the mechanism performs and the activities of the mechanism itself. Without having the correct biochemical framework to discover the mechanism, researchers were, as Bechtel says, stuck asking “whether methylglyoxal, for example, would ferment as rapidly as sugar” (p. 318). But, Bechtel continues, “decomposing fermentation into fermentations simply invoked the vocabulary designed to explain the overall behavior to describe the operation of its components. It did not explain the process in terms of something more basic” (p. 318).
One of the most well known examples of this type of lesioning occurred to Phineas Gage who had a rod driven through the ventromedial prefrontal region of his brain (Damasio 1994). Another well known case is H.M. who underwent the bi-lateral removal of his medial temporal lobes in a procedure performed to reduce the occurrence of epileptic seizures (Scoville and Milner 1957; Corkin 2002).
In these studies some animals have a particular brain area removed—often bilaterally—while control animals do not. All animals are then given tests of one type or another in order to measure the deficiency created by the lesioning. See, for example, Zola-Morgan and Squire (1984).
Most types of temporary lesioning, for example, transcranial magnetic stimulation (Amassian et al. 1989), injection of muscimol (Robinson 2000), or injection of sodium amobarbital into the carotid artery (Binder et al. 1996), are better analyzed, not as lesioning studies, but as cellular or molecular interventions.
See also the argument made earlier about activity within a brain area (at the end of the section titled “Additive Effects of the Activity of Neurons”).
References
Amassian, V. E., Cracco, R. Q., Maccabee, P. J., Cracco, J. B., Rudell, A., & Eberle, L. (1989). Suppression of visual perception by magnetic coil stimulation of human occipital cortex. Electroencephalography and Clinical Neurophysiology, 74, 458–462.
Anderson, M. (2007). The massive redeployment hypothesis and the functional topography of the brain. Philosophical Psychology, 20, 143–174.
Anscombe, G. E. M. (1981). Metaphysics and the Philosophy of Mind. Minneapolis, MN: University of Minnesota Press.
Armstrong, C. M., & Hille, B. (1998). Voltage-gated ion channels and electrical excitability. Neuron, 20, 371–380.
Bechtel, W. (2005). The challenge of characterizing operations in the mechanisms underlying behavior. Journal of the Experimental Analysis of Behavior, 84, 313–325.
Binder, J. R., Swanson, S. J., Hammeke, T. A., Morris, G. L., Mueller, W. M., Fischer, M., et al. (1996). Determination of language dominance using functional MRI: A comparison with the Wada test. Neurology, 46, 978–984.
Cavanagh, P. (1999). Top-down processing in vision. In R. A. Wilson & F. C. Keil (Eds.), The MIT encyclopedia of the cognitive sciences (pp. 839–840). Cambridge, MA: The MIT Press.
Churchland, P. S., & Sejnowski, T. J. (1990). Neural representation and neural computation. Philosophical Perspectives, 4, 343–382.
Corkin, S. (2002). What’s new with the amnesic patient H.M.? Nature Reviews Neuroscience, 3, 153–160.
Craver, C. F. (2002). Interlevel experiments and multilevel mechanisms in the neuroscience of memory. Philosophy of Science, 69, S83–S97.
Craver, C., & Bechtel, W. (2005). Mechanism. In S. Sarkar & J. Pfeifer (Eds.), The philosophy of science: An encyclopedia (pp. 469–478). New York: Routledge.
Damasio, A. R. (1994). Descartes’ error: Emotion, reason, and the human brain. New York: Putnam.
Fodor, J. (2000). The mind doesn’t work that way. Cambridge, MA: MIT Press.
Hubel, D. H., & Wiesel, T. N. (1962). Receptive fields, binocular interaction and functional architecture in the cat’s visual cortex. Journal of Physiology, 160, 106–154.
Kingsley, R. E. (2000). Concise text of neuroscience. Philadelphia: Lippincott Williams & Wilkins.
Lewis, M. D. (2005). Bridging emotion theory and neurobiology through dynamic systems modeling. Behavioral and Brain Sciences, 28, 169–194.
Lycan, W. G. (1981). Form, function, and feel. The Journal of Philosophy, 78, 24–50.
Lycan, W. G. (1987). Consciousness. Cambridge, MA: MIT Press.
Machamer, P., Darden, L., & Craver, C. (2000). Thinking about mechanisms. Philosophy of Science, 67, 1–25.
Mishkin, M. (1982). A memory system in the monkey. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, 298, 85–95.
Mishkin, M., Ungerleider, L. G., & Macko, K. A. (1983). Object vision and spatial vision: Two cortical pathways. Trends in Neurosciences, 6, 414–417.
Robinson, F. R. (2000). Role of the cerebellar posterior interpositus nucleus in saccades. I. Effect of temporary lesions. Journal of Neurophysiology, 84, 1289–1302.
Saper, C. B., Iverson, S., & Frackowiak, R. (2000). Integration of sensory and motor function: The association areas of the cerebral cortex and the cognitive capabilities of the brain. In E. R. Kandel, J. H. Schwartz, & T. M. Jessell (Eds.), Principles of neural science (pp. 349–380). New York: McGraw-Hill.
Scoville, W. B., & Milner, B. (1957). Loss of recent memory after bilateral hippocampal lesions. Journal of Neurology, Neurosurgery, and Psychiatry, 20, 11–21.
Wimsatt, W. C. (1976). Reductionism, levels of organization, and the mind-body problem. In G. G. Globus, M. Grover, & I. Savodnik (Eds.), Consciousness and the brain: A scientific and philosophical inquiry (pp. 205–267). New York: Plenum Press.
Yu, F., & Catterall, W. (2003). Overview of the voltage-gated sodium channel family. Genome Biology, 4, 207.
Zola-Morgan, S., & Squire, L. (1984). Preserved learning in monkeys with medial temporal lesions: Sparing of motor and cognitive skills. Journal of Neuroscience, 4, 1072–1085.
Acknowledgments
Thanks to Tom Polger, John Bickle, Bob Richardson, and Jenefer Robinson for comments on earlier versions of this material.
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Johnson, G. Mechanisms and Functional Brain Areas. Minds & Machines 19, 255–271 (2009). https://doi.org/10.1007/s11023-009-9154-6
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DOI: https://doi.org/10.1007/s11023-009-9154-6