Abstract
Most philosophers of mind and many cognitive psychologists still doubt that “genuinely cognitive” psychological theories will reduce to neurobiological counterparts. As I emphasized in Chapter One, this attitude contrasts starkly with the reductive aspirations of “mainstream” cellular and molecular neuroscientists. My first substantive task in this book is to characterize “reduction-in-practice,” as it is generating experiments, results, and explanations in current mainstream neuroscience. For reasons sketched in the previous chapter, I’ll ignore at first the concerns typically assumed by philosophers to occupy center stage in discussions of psychoneural reduction, namely philosophical anti-reductionist arguments and the problems of characterizing a concept of intertheoretic reduction for science generally. Instead, I’ll begin by presenting a detailed example, recent discoveries about the molecular mechanisms of long-term potentiation (LTP), an important type of experience-driven synaptic plasticity, and the behavioral data these mechanisms explain. This story is an accomplished neurobiological reduction of psychology’s “memory consolidation switch” that mediates the conversion of short-term to long-term memories. These recent scientific details show the nature of reduction at work and succeeding in current cellular and molecular neuroscience. Later in this chapter, as a piece of new wave metascience, I’ll generalize from this example, hopefully to provide a template for additional psychoneural reductions.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
Notes
It might seem strange to talk about the spinal cord and memory, but this has recently received some attention in the study of chronic peripheral pain. In fact, the same molecular mechanisms involved in cortical and hippocampal long-term potentiation underlie the experience-driven synaptic plasticity hypothesized to explain features of chronic pain. See Sufka (2001) for a clear exposition of this hypothesis.
lf these scientific details elude you now, fear not. Later in this chapter I’ll explain in detail the molecular mechanisms of LTP and experimental protocols and results in studies of this sort. For novices, I’ll even include a brief “primer” on basic cellular neuroscience.
Schouten and de Jong inform me that this argument in their (1999) was intended to reveal the cross-categorizations that obtain between psychological and neurobiological concepts, rendering any sort of “bottom-up” explanatory approach untenable. If so, then their argument rests upon issues I will take on in Chapter Three, namely, questions about methodology within neuroscience dominated by the search for cellular and molecular mechanisms and the issue of multiple realization.
Many readers will be familiar with well-known exceptions to the stimulus repetition feature. One-trial learning that remains stable for long periods has been studied for more than four decades. Typically, these are species-specific and evolutionarily prominent learning processes, e.g., conditioned taste aversions in rats. See, e.g., Garcia and Koelling (1966) (although most reputable learning theory textbooks will include a description of this phenomenon). For ease of exposition, I won’t be qualifying the “stimulus repetition” condition on consolidation in the discussion to follow. Fans of one trial learning can make the appropriate mental adjustments to my assertions, e.g., that stimulus repetition and rehearsal typically improves long-term memory recall and performance. Thanks to Carl Craver for pointing out the need to qualify some remarks I make in the discussion below.
This study is summarized nicely in Squire and Kandel 1999, 130–132.
Duncan also measured the latency of time spent in the test compartment after rats were placed there initially, but got little useful information from this behavioral measure and didn’t include it in his published results.
This point is not the only thing that “cognitivists” and “autonomists” could and do say. We’ll return to this point in earnest in the first two sections of Chapter Three. This discussion also foreshadows that about declarative memory, later in this chapter.
I’ll explain some of these biotechnological manipulations later in this chapter.
Cajal’s original publication is in French. Squire and Kandel (1999, 35-36) give a brief report of Cajal’s speculations.
Material presented in this subsection is abbreviated standard neurobiology textbook fare. Any reputable recent textbook will provide additional details. For those interested in a state-of-the art account of how neurons work, 1 recommend Levitan and Kaczmarek (2001).
The other type is neuroglia, a kind of connective tissue. The many roles of glial cells, and neuron-glial interactions, are targets of much current research. Much of this is beyond the scope of our concerns.
The “spike” metaphor describes the shape of the event recorded on an oscilloscope, as pictured in Figure 2.3.
Obviously, the “presynaptic terminal” of the primary synapse is postsynaptic to the modulatory neuron. More recently discovered complexities render the original “pre-” and “postsynaptic” terminology confusing.
Thanks to Carl Craver and Ken Sufka for reminding me of this point. Sufka points out in particular the new evidence of “pattern coding” in axons above and beyond rate/frequency coding of their action potentials (e.g., in Reichling and Levine 1999). I have not studied this literature carefully; nevertheless it is difficult for me to see how it escapes the general point I’m urging in this paragraph (and the next). At bottom, however, this is an empirical issue. If someone can show me specifically where or how this argument is wrong in light of some new, empirically confirmed coding discovery, I’ll give up this version.
This subsection is not intended to be a comprehensive early history of LTP. Philosopher of neuroscience Carl Craver has a forthcoming manuscript (2003) that explores this history in excellent detail. Part of his history is based on interviews with key participants.
Notice that this is amplitude increase in population spike, not in individual spikes. (Recall the all-or-none law of the individual action potential.) This means that the single stimulating pulse to the perforant path caused more dentate neurons to reach threshold of excitation after the stimulus conditioning train had been delivered, compared with before.
I’ll say more about the hippocampus and declarative memory in the next section, with references to the recent literature.
The molecular genetic details are not crucial here, but will become so later in this section. I will then provide a brief primer on the molecular mechanisms of gene transcription.
A receptor antagonist blocks the transmitter’s effect, typically by competing with transmitter molecules for receptor binding sites but not initiating the transmitter’s activity when bound. On the other hand, a receptor agonist increases the efficiency of transmitter molecules at the receptor site.
This much molecular genetics is sufficient for our purposes in this section, but I’ll present more details in section 5.2 of this chapter when I turn to biotechnology’s contribution to the neurobiology of memory consolidation. For readers interested in pursuing this fascinating area more thoroughly, Lewin (1999) is a state-of-the-art textbook for current molecular genetics, but any reputable introduction to biology text will contain a discussion of molecular genetics in plenty of detail for the average non-scientist. Consult your local Biology department.
CREB proteins only have their transcriptional effects when phosphorylated. Recall from above that catalytic PKA subunits have translocated to the neuron’s nucleus. These translocated subunits phosphorylate CREB proteins.
Clayton (2000) is a useful recent review, although his “operational definition” of ‘immediate early gene’ does not square exactly with its usage by other molecular neuroscientists.
A detailed discussion of celebrated case H.M. with references to the primary literature can be found in any reputable neuropsychology textbook, e.g., Kolb and Whishaw (1996), 357–360.
Subsection 5.2 is co-authored by Marica Bernstein.
Recall from the brief description in subsection 4.2 of this chapter the basic dogma of molecular genetics: DNA→(transcription)→RNA→(translation)→protein.
This raises an interesting question, especially given CREB’s ubiquitous occurrence in all types of biological tissues. Why aren’t the knockouts more deficient? Hummler et al. (1994) argue that CREB operates in tandem with two other cAMP-driven transcriptional activators, cAMP response element modulation protein (CREM) and activating transcription factor 1 (ATF 1), which can compensate for each other. CREB mutants do in fact overexpress CREM in all tissue types.
More intensive training—three blocks of four trials per day over three training days— overcame these statistical differences between CREB-mutants and controls. Bourtcholadze et al. (1994) suggest that this is due to CREM compensation for the CREB deficiency (mentioned in the previous footnote).
This description constitutes an informal account of the structuralist program’s concept of a theory-element. Most structuralists find that set theory and category theory provide useful mathematical resources to characterize these concepts formally. See Balzer et al., (1987), Balzer and Moulines (1996), and Bickle (1998) for detailed presentations, including models of intcrtheoretic reduction (Balzer et al. 1987, chapter 5, Bickle 1998, chapter 3) and an application to earlier developments in the reduction of psychological theories of memory to neurobiological counterparts (Bickle 1998, chapter 6).
The relations making up this condition are called “ontological reduction links” by Moulines 1984.I adopt this terminology in Bickle 1998, chapter 3, and 2002).
That this is a case of reduction is very controversial in philosophy of biology. However, the molecular geneticists I know have no qualms about calling and treating it as such. Perhaps a reduction-in-practice of recent work in that discipline would be a useful contribution to philosophy of science.
To see these features developed in quasi-formal fashion, sec Bickle (2002).
I’ve used a “net” metaphor, across changing concerns and philosophy of science backgrounds, to express ideas about theory reduction in psychology and neuroscience since one of my earliest papers (Bickle 1992b). See elaborations in Bickle (1998, chapter six).
Thanks to Carl Craver for stressing this “normativity” worry.
Author information
Authors and Affiliations
Rights and permissions
Copyright information
© 2003 Springer Science+Business Media Dordrecht
About this chapter
Cite this chapter
Bickle, J. (2003). Reduction-In-Practice in Current Mainstream Neuroscience. In: Philosophy and Neuroscience. Studies in Brain and Mind, vol 2. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-0237-0_2
Download citation
DOI: https://doi.org/10.1007/978-94-010-0237-0_2
Publisher Name: Springer, Dordrecht
Print ISBN: 978-1-4020-1302-7
Online ISBN: 978-94-010-0237-0
eBook Packages: Springer Book Archive