Abstract
We next trace implications of the detailed example from Chapter Two for two prominent issues in current philosophy of mind and one increasingly prominent area of current neuroscience. Reduction is central to all three. The first philosophical issue—the problem of mental causation—questions whether or how mental properties can exert causal effects on behavior. The second philosophical issue—the multiple realization argument—is widely thought to be one of two decisive arguments against the reduction of mind to brain or psychology to neuroscience. 1 We saw in the previous chapter that “reductionism” is alive and well in current cellular and molecular neuroscience. Now we’ll see whether that reduction-in-practice and its results carry helpful implications for issues that have attracted serious philosophical attention. The scientific issue concerns the status of cognitive neuroscience vis-à-vis the discipline’s cellular and molecular core. How do studies involving, e.g., neuron population dynamics or specific activations across neural regions, relate to ones exemplified by our detailed example from the previous chapter?
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Notes
The other is explaining consciousness. We’ll address it in Chapter Four.
Heil and Mele (1993) remains a good introduction to these issues and the philosophical exotica they have spawned. Trent Jerde pointed out to me that the cognitive neuroscientific empirical literature also contains work on “downward causation.” He cites Pardo, Pardo, and Raichle (1993) as an important contribution, as they study how self-control of mental states can direct neural responses. Jerde admits that a regress is looming. What about the neuronal processes constituting (or at least causally affecting) the self that is directing these responses? However, these empirical studies might hold promise for fruitful philosophical reflection, especially in light of the arcane concepts that have dominated purely philosophical discussions of mental causation.
Horgan presents the claims to follow in a slightly different order. I present them in this order to emphasize the conditional nature of claims 2 and 3 (in my numbering), with 4 asserting the antecedent of the implied conditionals.
We’ll investigate multiple realization in great detail in sections 4-6 of this chapter.
Horgan (2001) articulates and defends a version of causal compatibilism by applying David Lewis’s ([1973] 1983) observations about implicit, contextually variable discourse parameters to concepts like ‘cause’ and ‘causal explanation.’
Of course there remains a “psychology of memory/” Consolidation is not the only important feature of memory, just the one that first yielded to “ruthless” cellular/molecular reduction.
It seems reasonable to take “results published in Cell, Neuron, or similarly influential and respected mainstream neuroscience journals” as an adequate condition on “experimentally verified.” If you doubt this, pick up an issue yourself.
The “where to look” role is prominent in functional neuroimaging, using techniques that are prevalent in current cognitive neuroscience. I’ll discuss this point in the next section of this chapter.
It is worth noting that more than one century ago William James (1890) noticed similar sequential features in our “streams” of conscious experience. Given the apparent importance of frontal cortex in the neurobiology of consciousness, by discovering the cellular mechanisms of sequential features of cognition, we might also be drawing a bead on the ones underlying sequential features of consciousness, too. Bickle et al (2001) characterize these specific sequential features and emphasize these similarities across cognitive processes and our “Jamesian” conscious streams.
I describe the “dorsal” and “ventral” visual streams in some detail in Chapter Four, section 3 below. See especially Figures 4.2 and 4.3. That level of detail is not important for the current discussion.
For FEF location, see Figure 4.1 in Chapter Four below. For a good “textbook” overview of the primate oculomotor system, see Goldberg et al. (1991).
1 am skipping over many scientific details here because they have already appeared in print. See Bickle et al. (2000).
For the anatomical location of DLPFC, see Figure 4.1 in Chapter Four below. Sections 1 and 2 of that chapter contain a detailed discussion of Goldman-Rakic’s and her colleagues work. For current purposes, this paragraph will suffice.
In our complete model, we also developed a “Return to Fixation” mechanism that breaks off execution in the middle of a multiple-step saccade sequence and computes the dimensions of a saccade back to the original fixation point (Bernstein et al. 2000). We derived components of this additional feature directly from single-cell electrophysiology of “suppression site” neurons in FEFs (Burman and Bruce 1997) and structural MRI and neuropsychological assessment of two patients with anterior cingulate cortex (ACC) lesions encompassing the “cingulate eye fields” (Gaymard et al. 1998). Since we are just beginning to explore this component of our biological model with fMRI in behaving humans, I won’t discuss it here in any detail.
The next seven paragraphs describe the experimental task, fMRI data collection procedures, and preliminary data analysis first reported in Bickle et al. (2001). Since that report, we have fully processed and analyzed the preliminary data sets, so results reported here are new. I include some technical details to illustrate the complexity of even a quite simple functional neuroimaging task. A scientific manuscript describing the methods and results is currently in preparation. This project is completely collaborative, so the next seven paragraphs should be considered co-authored by Malcolm Avison, Vince Schmithorst, Anthony Landreth, and Scott Holland. Please note that co-authorship (and their full agreement with my arguments) does not extend to the final subsection of this chapter! I also thank Kathleen Akins for helpful written comments on a paper length treatment of the philosophical and scientific arguments of this section.
This timing was also designed to make the 4-step sequences very difficult, to begin probing activation in anterior cingulate cortex.
Both strategies also identified the anterior cingulate cortex.
The fit function is a second order polynomial Y = A0 + A1X + A2X2, where Ys are the pixel values and X is the data point (frame) number (1, 2, …, 320). The linear and quadratic components subtracted away are A1X + A2X2.
And the anterior cingulate cortex.
We are conducting a follow-up study to explore these different time courses of activation in these two prominent frontal working memory regions during saccade sequencing.
We’ve now corrected this experimental flaw by introducing a fixation point during the control task!
Thanks to Huib Looren de Jong and Maurice Schouten for emphasizing to me the importance of these worries.
For nonphilosophers, Ludwig Wittgenstein ended his first major work, the Tractatus Logico-Philosophicus, with the following remark: “My propositions serve as elucidations in the following way: anyone who understands me eventually recognizes them as nonsensical, when he has used them—as steps—to climb up beyond them. (He must, so to speak, throw away the ladder after he has climbed up it.” ([1919] 1961). Please note that my appeal to Wittgenstein is metaphorical. As should be clear from the discussion in the text, I am not charging cognitive neuroscientists with literally asserting nonsense!
There is always the issue about how much scientific detail to include in a book addressed to an interdisciplinary audience. More detail, comparable to the amount presented in the last chapter, is coming in this chapter. But the details are necessary, first and foremost to show how Putnam’s empirical, scientific challenge has actually been met These details also speak to one of the general themes of this book, that impressive research and explanation of behavioral data is taking place in current cellular and molecular neuroscience, and philosophers of mind and cognitive science aren’t aware of it. Thanks to Trent Jerde and John Symons for advising me to remind readers of the “bigger picture” that all the “gory details” aim to illuminate.
In my (1998, chapter 5), I characterize this story as “combinatorial reduction.” My account is designed explicitly to incorporate Hawkins and Kandel’s evidence and arguments into a general theory of intertheoretic reduction.
Short sequences of amino acids determine which of a handful of DNA-binding domain motifs a given transcription factor possesses. Leucine zippers consist of a stretch of amino acids with a leucine residue in every seventh position. DNA binding occurs at a stretch of positively charged residues adjacent to each zipper. CREB proteins and C/EBP possess the leucine zipper motif.
However, Bartsch et al. (2000) have recently found another transcriptional activator in Aplysia neurons, Activating Factor (ApAF). ApAF is phosphorylated by PKA catalytic subunits and forms dimers with both ApCREB2 and ApC/EBP. These new results show that ApAF is a candidate memory enhancer gene further downstream from the CREB proteins. The (molecular) beat goes on …
Thanks to Huib Looren de Jong and Maurice Schouten for suggesting this standard example.
This section was improved by discussions with Marica Bernstein and Robert Skipper.
The next few paragraphs draw on Ridley (1998), chapter 7. This is a standard current textbook on evolutionary theory.
Another textbook example is the heme region of the hemoglobin molecule. See Ridley, chapter 7, for detailed discussion.
Though even here, most changes will be deleterious, since an amino acid replacement will typically affect the folded protein’s tertiary structure. The neutral theory can thus explain the slow rate of evolutionary change even in proteins’ functionally unimportant regions.
Note that this fact holds for all current theories of neural coding, not just for frequency/rate coding. (See Chapter Two, section 3.2 above.) The early chapters of Kandel, Jessell, and Schwartz (2000) are a good introduction to the full range of basic metabolic processes in neurons. Those in Shepherd (1994) provide a more compact presentation.
As discussed briefly in section 4 of this chapter, psychological differences across species are accounted for by different sequences and combinations of these cellular and molecular events—different sequences and combinations of the “cell biological alphabet” — made available by the more complex circuits and anatomies in “higher” cognitive species. However, I also repeat from that earlier discussion that psychological differences are not at issue in the multiple realization challenge; psychological similarities are.
See Shepherd (1994) for a good (though increasingly dated) primer on the shared molecular and molecular-genetic mechanisms of synapse plasticity and neuron development.
This nonexplanatory feature of current physics vis-à-vis psychology and behavior might be a reason why no one took seriously Paul Churchland’s (1982) attempt to undercut the multiple realization argument by arguing that “reductive unity” for psychological kinds will ultimately be found in thermodynamics. Churchland not only failed to offer any real empirical evidence for this possibility, but even more importantly it is difficult to see (now) how thermodynamics could explain (in any genuine sense) concrete behavioral data—like, e.g., that from the Kandel lab’s work with transgenic mice.
Ken Aizawa suggested this in a commentary at the 2002 Southern Society for Philosophy and Psychology annual meeting. He claimed that, e.g., “protein kinase A” is defined functionally and multiply realized physically. I demurred, on empirical grounds. We agreed to leave the question open, pending further discussion.
This work might be part of a general project that Jim Bogen suggests as a response to my arguments, that of developing a taxonomy of psychological kinds to see if anything systematic (and non-hand-waving) can be found that determines which kinds can and which cannot be “ruthlessly reduced.” I would look forward to grappling with any proposed taxonomy.
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Bickle, J. (2003). Mental Causation, Cognitive Neuroscience, and Multiple Realization. In: Philosophy and Neuroscience. Studies in Brain and Mind, vol 2. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-0237-0_3
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