Cellular learning theory: theoretical comment on Cole and McNally (2007)

Abstract

The idea that learning proceeds as a function of the discrepancy (or error) between expected and obtained outcomes is central to many theories of associative learning. However, remarkably little is known about the neurobiological mechanisms that underlie this learning of predictive errors in fear conditioning, a widely used preparation in studies of cellular and molecular mechanisms of memory. In this issue of Behavioral Neuroscience, S. Cole and G. P. McNally demonstrate an important dissociation between the establishment and regulation of predictive error at the cellular level. Their findings have added a level of complexity to currently established views of the function of NMDA and opioid receptors in learning and memory. This commentary discusses some of the implications of these findings for theoretical and neurobiological approaches to memory, as well as current thinking about the cellular circuitry involved in reward learning and drug abuse.

Figure 1.

Different roles for NMDA and opioid receptors in learning. A CS-US conditioning trial activates NMDA and opioid receptors. Opioid receptors code the predictive error between the US that occurs (λ) and the US that is expected based on the total available cues in the environment (ΣV); NMDA receptors act on the product of this predictive error. In the terms of the Rescorla-Wagner equation, NMDA receptors may act on the rate parameters associated with the CS (α) or the US (β), and opioid receptors may act on the predictive error itself, placing a ceiling on the magnitude and direction of associative change (ΔV). These two receptor systems interact to produce changes in associative learning, which ultimately result in changes in behavior.