The study of memory is witnessing a spirited clash between proponents of traditional laboratory research and those advocating a more naturalistic approach to the study of “real-life” or “everyday” memory. The debate has generally centered on the “what” (content), “where” (context), and “how” (methods) of memory research. In this target article, we argue that the controversy discloses a further, more fundamental breach between two underlying memory metaphors, each having distinct implications for memory theory and assessment: Whereas traditional memory research has been dominated by the storehouse metaphor, leading to a focus on the number of items remaining in store and accessible to memory, the recent wave of everyday memory research has shifted toward a correspondence metaphor, focusing on the accuracy of memory in representing past events. The correspondence metaphor calls for a research approach that differs from the traditional one in important respects: in emphasizing the intentional –representational function of memory, in addressing the wholistic and graded aspects of memory correspondence, in taking an output-bound assessment perspective, and in allowing more room for the operation of subject-controlled metamemory processes and motivational factors. This analysis can help tie together soine of the what, where, and how aspects of the “real-life/laboratory” controversy. More important, however, by explicating the unique metatheoretical foundation of the accuracy-oriented approach to memory we aim to promote a more effective exploitation of the correspondence metaphor in both naturalistic and laboratory research contexts.

Research findings on addiction are contradictory. According to biographical records and widely used diagnostic manuals, addicts use drugs compulsively, meaning that drug use is out of control and independent of its aversive consequences. This account is supported by studies that show significant heritabilities for alcoholism and other addictions and by laboratory experiments in which repeated administration of addictive drugs caused changes in neural substrates associated with reward. Epidemiological and experimental data, however, show that the consequences of drug consumption can significantly modify drug intake in addicts. The disease model can account for the compulsive features of addiction, but not occasions in which price and punishment reduced drug consumption in addicts. Conversely, learning models of addiction can account for the influence of price and punishment, but not compulsive drug taking. The occasion for this target article is that recent developments in behavioral choice theory resolve the apparent contradictions in the addiction literature. The basic argument includes the following four statements: First, repeated consumption of an addictive drug decreases its future value and the future value of competing activities. Second, the frequency of an activity is a function of its relative (not absolute) value. This implies that an activity that reduces the values of competing behaviors can increase in frequency even if its own value also declines. Third, a recent experiment (Heyman & Tanz 1995) shows that the effective reinforcement contingencies are relative to a frame of reference, and this frame of reference can change so as to favor optimal or suboptimal choice. Fourth, if the frame of reference is local, reinforcement contingencies will favor excessive drug use, but if the frame of reference is global, the reinforcement contingencies will favor controlled drug use. The transition from a global to a local frame of reference explains relapse and other compulsive features of addiction.

We have been oversold on the base rate fallacy in probabilistic judgment from an empirical, normative, and methodological standpoint. At the empirical level, a thorough examination of the base rate literature (including the famous lawyer–engineer problem) does not support the conventional wisdom that people routinely ignore base rates. Quite the contrary, the literature shows that base rates are almost always used and that their degree of use depends on task structure and representation. Specifically, base rates play a relatively larger role in tasks where base rates are implicitly learned or can be represented in frequentist terms. Base rates are also used more when they are reliable and relatively more diagnostic than available individuating information. At the normative level, the base rate fallacy should be rejected because few tasks map unambiguously into the narrow framework that is held up as the standard of good decision making. Mechanical applications of Bayes's theorem to identify performance errors are inappropriate when (1) key assumptions of the model are either unchecked or grossly violated, and (2) no attempt is made to identify the decision maker's goals, values, and task assumptions. Methodologically, the current approach is criticized for its failure to consider how the ambiguous, unreliable, and unstable base rates of the real world are and should be used. Where decision makers' assumptions and goals vary, and where performance criteria are complex, the traditional Bayesian standard is insufficient. Even where predictive accuracy is the goal in commonly defined problems, there may be situations (e.g., informationally redundant environments) in which base rates can be ignored with impunity. A more ecologically valid research program is called for. This program should emphasize the development of prescriptive theory in rich, realistic decision environments.

The distinction that Koriat & Goldsmith have drawn between laboratory and naturalistic research is largely valid, but the metaphor they have chosen to characterize the latter may not be optimal. The “correspondence” approach is vulnerable on conceptual grounds and is not applicable to significant portions of empirical research.

Cognitive algebra strongly disproved the representativeness heuristic almost before it was published; and therewith it also disproved the base rate fallacy. Cognitive algebra provides a theoretical foundation for judgment-decision theory through its joint solution to the two fundamental problems – true measurement of subjective values, and cognitive rules for integration of multiple determinants.

Cerebellar long-term depression (LTD) is a form of synaptic plasticity, first described by Ito and co-workers, in which simultaneous activation of two excitatory inputs to a Purkinje neuron, parallel fibers (PFs) and climbing fibers (CFs), results in a sustained depression of PF synaptic drive. The purpose of this target article is not to assess the possible role of this synaptic alteration in motor learning, an issue which is addressed by other authors in this volume, nor is it to provide a detailed summary of the work on cerebellar LTD to this point (see Linden & Connor 1993; Crépel et al. 1993 for review) or to place cerebellar LTD within the context of other forms of persistent synaptic depression that occur within the mammalian brain (see Linden 1994b). Rather, it is to discuss results obtained using a very reduced preparation for the study of LTD, embryonic Purkinje neurons grown in culture and stimulated with exogenous excitatory amino acids, and to consider some advantages and limitations of this approach. Recent work using this preparation has suggested that three processes are necessary for the induction of cerebellar LTD: Ca influx through voltage-gated channels, Na influx through AMPA receptor-associated channels or voltage-gated Na channels, and protein kinase C activation - which is dependent upon activation of the metabotropic glutamate receptor mGluRl. In addition, input-specific induction of LTD has been demonstrated in this preparation Under conditions where both spontaneous and evoked neurotransmitter release are reduced or eliminated, indicating that postsynaptic alterations are sufficient to confer this important computational property.

The matching law accounts for both addictive behavior and the usefulness of a person's evaluating choices in overall categories. To explain why overall bookkeeping, once learned, does not easily win out over local bookkeeping, another implication of matching is needed: intertemporal bargaining. The role of melioration, though probably important for new addiction is separate.

Long-term depression (LTD) of synaptic transmission at parallel fibre-Purkinje cell synapses is thought to be a cellular substrate of motor learning in the cerebellum. This use-dependent change in synaptic efficacy is induced by conjunctive stimulation of Parallel fibres and climbing fibres. Researchers agree that the induction of LTD requires, as an initial step, a calcium influx via voltage-gated Ca2+ channels into a Purkinje cell, together with activation of ionotropic (AMPA) and probably metabotropic subtypes of glutamate receptors of this cell. Indeed, due to the lack of specific antagonist, the final demonstration of the contribution of metabotropic receptors in the LTD induction process, under functional conditions, remains unanswered. The debate is now focused on the second-messenger processes leading to LTD of synaptic transmission at parallel fibre-Purkinje cell synapses, after the calcium influx into the cell. All researchers agree that a calcium-dependent cascade of events including activation of protein kinase C is necessary for LTD induction. In contrast, the recruitment in the LTD induction of another cascade, also triggered by Ca2+, that is, through synthesis of nitric oxide and cyclic GMP, remains controversial.

On the other hand, growing evidence suggests that these chains of reaction underlying LTD might ultimately lead to a genuine change in the functional characteristics of AMPA receptors at the parallel fibre-Purkinje cell synapses.

Koehler's work will assist the effort to understand legal fact finding. It leaves two questions somewhat open: (i) the extent to which empirical research can measure correctness of fact-finding, a function that involves the resolution of normative questions and (ii) the standards judges should use in the absence of the research he advocates.

It is difficult to accommodate compulsive drug use that destroys regulation by consequences in a unitary framework of melioration or maximization, especially as both are strategies of behavioral regulation. The “contradiction” of addictive behavior despite aversive consequences is an illusory issue because consequences that do not decrease addictive behavior cannot be considered punishing.

The target article interprets current psychological research on everyday memory in terms of a correspondence metaphor. This metaphor is based on a reduction of everyday memory to autobiographical and eyewitness memory. This commentary focuses on everyday memory as it functions in activity. Viewed from this perspective, the joining of everyday memory to a correspondence metaphor is problematic. A more natural way to frame the processes of everyday memory is in terms of context, practice, and pragmatics.

The cellular basis of motor learning in the cerebellum has been attributed mostly to long-term depression (LTD) at excitatory parallel fiber (PF)-Purkinje cell (PC) synapses. LTD is induced when PFs are activated in conjunction with a climbing fiber (CF), the other excitatory input to PCs. Recently, by using whole-cell patch-clamp recording from PCs in cerebellar slices, a new form of synaptic plasticity was discovered. Stimulation of excitatory CFs induced a long-lasting (usually longer than 30 min) “rebound potentiation (RP)” of γ-amino-butyric acid A (GABAa)-receptor mediated inhibitory postsynaptic, currents (IPSCs). As in LTD, induction of RP requires transient elevation of intracellular calcium concentration ([Ca2+]1) due to activation of voltage-gated Ca2+ channels. Activity of inhibitory synapses seems also to be necessary for RP to occur. RP is mainly due to up-regulation of postsynaptic GABAa receptor function, since PC response to bath-applied exogenous GABA is also potentiated with a time course similar to RP. The difference in the time scale between the Ca2+ transients (10–30 sec) and the durations of RP (>30 min) strongly suggests that some intracellular biochemical machinery is involved. Pharmacological evidence suggests that protein kinases are involved in RP of inhibitory synapses and LTD of excitatory PF synapses. Besides the well-described LTD, RP could be a cellular mechanism that plays an important role in motor learning.

The function of memory is to allow past experience to subserve present goal-oriented thought and action. The defining characteristic of goal-oriented approach/avoidance is value. Value lies beyond the reproductive conception of memory that is basic to both metaphors discussed in Koriat & Goldsmith's target article. Functional memory requires a quite different metaphor, for which a grounded theory is available.

Heyman explains useful ways to bring addictive drug use under environmental control. We doubt that relapse is explained by drug features such as immediate reinforcement, clouding of judgment, and so forth. Relapse may require explanation in terms of enduring sensitization of incentive neural substrates, but even if its causal assumptions are wrong, Heyman's model makes useful predictions for behavioral control.

There is a familiar risk of antinomy if from x is E and p(x is H/x is E) = r it is permissible to infer p(x is H) = r, and what Carnap (1950) called “The requirement of total evidence” will not prevent such antinomies satisfactorily. What is needed instead is a properly developed theory of evidential weight.

Heyman's view that addiction can be viewed as a natural outcome predictable by melioration and the matching law is provocative. Remaining to be explained more fully, however, are exactly how his view is an improvement on other reinforcement-based accounts. Included in these elaborations should be an account of how different “bookkeeping schemes” are developed and controlled and what new approaches to treatment and prevention of drug addiction are indicated.

Quantitative losses of memory content imply replicative processing; correspondence losses imply reconstructive processing. Research should focus on the relationship between these processes by obtaining accuracy- and quantity-based indicators of memory within the same framework. This approach will also yield information about the effects of task and individual-difference variables on loss and distortion, as well as the time course of each process.

The base rate fallacy is directly dependent on a particular judgment paradigm in which information may be unambiguously designated as either “base rate” or “individuating,” and in which subjects make two-stage sequential judgments. The paradigm may be a poor match for real world settings, and the fallacy may thus be undefined for natural ecologies of judgment.

Interest in the role of nitric oxide (NO) in the nervous system began with the demonstration that glutamate receptor activation in cerebellar slices causes the formation of a diffusible messenger with properties similar to those of the endothelium-derived relaxing factor. It is now clear that this is due to the Ca2+/calmodulin-dependent activation of the enzyme NO synthase, which forms NO and citrulline from the amino acid L-arginine. The cerebellum has very high levels of NO synthase, and although it has low levels of guanylyl cyclase, cerebellar cyclic guanosine monophosphate (cGMP) levels are an order of magnitude higher than in other brain regions. A transcellular metabolic pathway is also present in the cerebellar cortex to recycle citrulline back to arginine. The NO formed binds to and activates soluble guanylyl cyclase to elevate cGMP levels in target cells. Studies employing NADPH-diaphorase, a selective histochemical marker for NO synthase, together with immunohistochemistry, in situ hybridization and biochemical studies have indicated that NO production occurs in granule and basket cells in the cerebellar cortex, whereas cGMP formation appears to occur largely in other cells, including Purkinje cells. Given that a long-term depression of AMPA currents can be seen in isolated Purkinje cells, this anatomical localization suggests that NO cannot play an essential role in the induction of this form of synaptic plasticity.

In vitro studies using cerebellar slices or cultures, as well as in vivo studies, have demonstrated that NO formation and release occur in the cerebellar cortex in response to NMDA receptor activation. Using intracerebellar microdialysis in awake-behaving animals, we have found that this is associated with a large increase in extracellular cGMP levels in the cerebellar cortex. A similar increase in cGMP efflux is seen in response to activation of AMPA or metabotropic glutamate receptors, or to activation of the climbing fiber input. The increase in extracellular cGMP required the Ca2+-dependent activation of NO synthase, and was potentiated by inhibition of phosphodiesterases or organic anion transport. These results suggest a possible role for cGMP as an intercellular messenger in the cerebellar cortex.

In summary, stimuli that elevate Ca2+ levels in granule or in basket cells will activate NO synthase, which by binding to its receptor-soluble guanylyl cyclase – causes an increase in cGMP. cGMP may then act through protein kinases, phosphodiesterases, and ion channels or receptors to affect cerebellar function.