Clark & Thornton's type-1/-2 distinction is not well-defined. The classes of type-1 and type-2 problems are too broad: many nocomputable functions are type-1 and type-2 learnable. They are also too narrow: trivial functions, such as identity, are neither type-1 nor type-2 learnable. Moreover, the scope of type-1 and type-2 problems appears to be equivalent. Overall, this distinction does not appear useful for machine learning or cognitive science.

The terms red, green, yellow, and blue are both necessary and sufficient to describe our chromatic experience. Their uniqueness and opponent nature is supported by evidence obtained under supra- threshold conditions, especially hue cancellation. These constraints are nontrivial. How some electrophysiologically identified mechanisms contribute to colour appearance is not known, but their complexities do not refute our experience of elemental hues.

It is argued by berkley that there are theoretical reasons why sex differences in pain may result from specific learning processes. I argue that Berkley has not gone far enough in pursuing this suggestion, and that the evidence that learning is a major determinant of pain behaviour is substantial. Moreover, sex differences in pain may represent only a special case of individual differences in pain resulting from learning processes.

This commentary argues that (1) arousal is not sufficient to induce LTP in the hippocampus, (2) learning can profoundly modulate synaptic plasticity in a state-dependent manner without affecting baseline synaptic efficacy, and (3) unilateral, synapse-specific LTP induction triggers an interhippocampal communication manifested as bilateral increases in gene expression at multiple sites in the hippocampal network.

Numerous mediators are involved in both the control and the transmission of nociceptive messages, and several lines of research have been developed in the management of pain. Complete enkephalin- degrading enzyme inhibitors, which produce naloxone-reversible analgesia in all tests where morphine has been found to be active, remains the most promising way. CCK compounds, especially the CCKB antagonists also may be interesting drugs. Indeed, they are able to strongly potentiate the antinociceptive effects of the opioids. [dickenson, wiesenfeld-hallin et al.]

Shors and Matzel's evaluation of approaches to the behavioural function of LTP is welcome, and should encourage a widening of conceptual approaches to this problem. In addition to their call for increased sophistication in thinking about LTP, there needs to be a parallel increase in sophistication in the study of behaviour. Changes in emotional state or tone may be a better function for LTP than attention mechanisms.

Uninformed learning mechanisms will not discover “type- 2” regularities in their inputs, except fortuitously. Clark & Thornton argue that error back-propagation only learns the classical parity problem – which is “always pure type-2” – because of restrictive assumptions implicit in the learning algorithm and network employed. Empirical analysis showing that back-propagation fails to generalise on the parity problem is cited to support their position. The reason for failure, however, is that generalisation is simply not a relevant issue. Nothing can be gleaned about back-propagation in particular, or learning in general, from this failure.

Evidence from molecular genetics bolsters the claim that color is not a perceptuolinguistic and behavioral universal. Neurobiology continues to fill in many details about the flow of color information from photon reception to central processing in the brain. Humans have the most acute color vision in the biosphere because of natural selection and adaptation, not coincidence.

Sections R1 to R3 attempt to take the sting out of hostile commentaries. Sections R4 to R5 engage Berlin and Kay and the World Color Survey to correct the record. Section R6 begins the formulation of a new theory of colour as an engineering project with a technological developmental trajectory. It is recommended that the colour space be abandoned.

Since learning emerges from a circuit mediating behavior it is unrealistic to require LTP to be a sufficient explanation of it; however, LTP is a necessary component of some learning circuits. The properties of that component bear a closer formal relationship to the acquisition of associative strength than to the modulation of attention.

Clark & Thornton's “superficially distinct ploys and mechanisms” are in fact very different: there is a deep difference between (a) filters and feature detectors, which “let the information in,” and (b) contentful representations and theories, which reconfigure it into a computationally tractable form. (a) is bringing abilities to experience whereas (b) is bringing content to experience. Both have well known problems. I outline an evolutionary story that avoids these problems and begins to explain how representations and theories developed out of feature detectors and filters.

Neuroplastic changes in the inhibitory systems contribute to pathological pains such as hyperalgesia. Activation or inhibition of the intrinsic inhibitory systems may depend on the pathophysiology which induces a sustained pain state. The mechanisms of hyperalgesia, opioid insensitivity following nerve injury, and opioid tolerance may be related to common neuroplastic changes. [wiesenfeld-hallin et al.]

Recent studies indicate a role of the sympathetic nervous system in acute and chronic pain. However, the terminology of the clinical sympathetically maintained pain (SMP) syndromes continues to be confusing and the criteria for diagnosis of SMP are being refined. (blumberg et al.) Despite significant progress in recent years, the mechanisms of the interaction between the sympathetic and sensory systems in SMP remain puzzling.

Analogical transfer in sequence learning is presented as an example of how the type-2 problem of learning an unbounded number of isomorphic sequences is reduced to the type-1 problem of learning a small finite set of sequences. The commentary illustrates how the difficult problem of appropriate analogical filter creation and selection is addressed while avoiding the trap of strong nativism, and it provides theoretical and experimental evidence for the existence of dissociable mechanisms for type-1 learning and type-2 recoding.

Gene targeting has generated a great deal of data on the molecular mechanisms of long-term potentiation and its potential role in learning and memory. However, the interpretation of some results has been questioned. Compensatory mechanisms and the contribution of genetic background may make it difficult to unequivocally prove the existence of a causal (genetic) link between LTP and learning.

Starting from macroscopic and microscopic facts of cerebellar histology, we propose a new functional interpretation that may elucidate the role of the cerebellum in movement control. The idea is that the cerebellum is a large collection of individual lines (Eccles's “beams”: Eccles et al. 1967a) that respond specifically to certain sequences of events in the input and in turn produce sequences of signals in the output. We believe that the sequence-in/sequence-out mode of operation is as typical for the cerebellar cortex as the transformation of sets into sets of active neurons is typical for the cerebral cortex, and that both the histological differences between the two and their reciprocal functional interactions become understandable in the light of this dichotomy. The response of Purkinje cells to sequences of stimuli in the mossy fiber system was shown experimentally by Heck on surviving slices of rat and guinea pig cerebellum. Sequential activation of a row of eleven stimulating electrodes in the granular layer, imitating a “movement” of the stimuli along the folium, produces a powerful volley in the parallel fibers that strongly excites Purkinje cells, as evidenced by intracellular recording. The volley, or “tidal wave,” has maximal amplitude when the stimulus moves toward the recording site at the speed of conduction in parallel fibers, and much smaller amplitudes for lower or higher “velocities.” The succession of stimuli has no effect when they “move” in the opposite direction. Synchronous activation of the stimulus electrodes also had hardly any effect. We believe that the sequences of mossy fiber activation that normally produce this effect in the intact cerebellum are a combination of motor planning relayed to the cerebellum by the cerebral cortex, and information about ongoing movement, reaching the cerebellum from the spinal cord. The output elicited by the specific sequence to which a “beam” is tuned may well be a succession of well timed inhibitory volleys “sculpting” the motor sequences so as to adapt them to the complicated requirements of the physics of a multijointed system.

Several types of amygdala-dependent learning can be blocked by local infusion of NMDA antagonists into the amygdala. This blockade shows anatomical, pharmacological, temporal, and behavioral specificity, providing a pattern of data more consistent with a role for NMDA receptors in learning than in arousal or attention, and supporting the contention that an “LTP-like” process is a neural substrate for memory formation.

Learning a mapping involves finding regularities in a training set and generalization to novel patterns. Clark & Thornton's type distinction has been discussed in terms of generalization, but has limited value in this respect. However, in terms of detection of regularities in the training set, the distinction is more valid, as it provides a measure of complexity and correlates with the size of search space.

We offer a critique of the role of the parallel fiber beam as the unit of cerebellar computation, with the “tidal wave” as its mode of operation. Instead we see the microcomplex linking cerebellar cortex and nuclei as the unit, with parallel fibers providing the means to coordinate the effects of microcomplexes in modulating various motor pattern generators (MPGs).

This commentary on blumberg et al. addresses complications associated with diagnostic testing for sympathetic dependence of pain that can lead to inappropriate positive and negative conclusions. In addition, it is suggested that their “ischemic” test be conceived as a test of the effect of local vascular pressure and that the two types of sensory disorders presented may differ primarily in the degree of sensitization of central pain pathways. Detailed reports with functionally-oriented testing like that done by blumberg are essential for an understanding the pathophysiological mechanisms.