Contrary to argument that unique hues are undemonstrated, the World Color Survey shows that speakers of more than 100 minor and tribal languages focus color categories predominantly on 4 of the 40 hue columns of the ethnographic Munsell array. The pattern is not conditioned by saturation levels or other arbitrary structures among the color chips, nor is Western influence likely to be the cause. Moreover, all evidence suggests that color cognition is autonomous despite the connotations and polysemies of color terms.

The originality of Glenberg's theoretical account lies in the claim that memory works in the service of physical interaction with the three-dimensional world. Little consideration is given, however, to the role of memory in action. We present and discuss data on spatial memory for action. These empirical data constitute the first step of reasoning about the link between memory and action, and allow several aspects of Glenberg's theory to be tested.

A wealth of evidence supports the idea that the circuitry of the developing nervous system is gradually elaborated under the instructive influence of neural activity. Some care must be taken, however, not to handicap the acceptance of this useful perspective with too onerous a theoretical superstructure.

Negative feedback is an important mechanism whereby the organism maintains its balance in a complicated system. It may beregarded as a modern version of the ancient Eastern wisdom of Yin and Yang balance. Control of pain and analgesia, is no exception: CCK seems to serve as a built-in mechanism for the modulation of opioid analgesia system [dickenson].

The authors presume that activity in the dorsal horn or nociceptors is well correlated with pain sensations and behavior. This overlooks the myriad of interactions between cortex and our spinothalamic tract. It is better to think of our nociceptors, the dorsal horn, and the pain centers in our brain as all components in one larger and complex pain sensory system. [berkley; blumberg et al.; coderre & katz; dickenson; mcmahon; wiesenfeld-hallin et al.]

Although Glenberg's theory benefits from the incorporation of a suppression concept, a more differentiated view of suppression would be even more effective. We propose such a concept (based on the attention framework first developed by William James in the late nineteenth century), showing how it accounts for phenomena that Glenberg describes and also for phenomena that he ignores.

Saunders & van Brakel's criticism of Berlin & Kay's methodology misunderstands the fact that scientific hypotheses are tested by generating new, replicable data with novel explanatory power. Thus, although Berlin and Kay studied differences in colour words between languages, the same patterns are also present in colour word usage within languages, in a range of literary and other textual databases.

We argue that on logical grounds the constructivist algorithms mentioned by Quartz & Sejnowski (Q&S) do not resolve the learning paradox. In contrast, a neural network might acquire a more powerful structure by means of phase transitions. The latter kind of developmental mechanism can be in agreement with the constructivist manifesto.

Saunders & van Brakel's analysis of the phenomenal categorization and subsequent experimental research in unique hues fails to include contemporary methodological improvements. Alternative strategies are offered from the author's research that rely less on language and world knowledge and provide strong evidence for the general theoretical constructs of elemental hue, nonbasic, and basic color terms.

Glenberg offers two different accounts of embodied conceptualization. The first fails in cases where no direct bodily interaction is possible. The second fails in cases where the object in question cannot serve as a discriminative stimulus; moreover, it yields inappropriate content even in cases where it can be applied. Glenberg's disregard for the conceptual agenda set by the social world is also disquieting.

Plastic changes in spinal cord function like neuronal wind-up and increased receptive field are too short-lived to explain chronic pain without structural changes. It is possible that learning could be a mechanism for longlasting changes in nociceptive regulation. A learning process localized to the spinal cord has been shown to be important for the development of tolerance to the analgetic effect of ethanol, suggesting that nociceptive control systems may be changed by learning. Long term potentiation (LTP) is regarded as a useful model of learning and memory. LTP-like changes have been observed in in vitro preparations from the spinal cord and in spinal cord field potentials. Recently a long term increase in spinal A-β and C-fibre evoked responses after painful stimulation has been observed. [coderre & katz, dickenson, wiesenfeld-hallin et al.]

Quartz & Sejnowski (Q&S) find flaws in standard theories of neural selection, which they propose to repair by introducing Lamarckian mechanisms for anatomical refinement that are analogous to directed mutation in evolution. The reversal of cause and effect that these mechanisms require is no more plausible in an explanation of cognition than it is in an explanation of evolution.

Contrary to prevailing views, productivity and propositional construal are not problematic for perceptual views of representation. Glenberg's embodied representations contribute to our understanding of how these two important processes might be implemented perceptually.

Two points are made on the basis of (mainly) the cross-cultural psychological record. The first is that cross-cultural data indicate at least weak, nontrivial constraints on colour classification. The second is that exceptions to cross-cultural regularities as described by Saunders & van Brakel are compatible with the view that constraints on colour categories are probabilistic rather than deterministic.

Central sensitization and related neurochemical mechanisms are also induced in V nociceptive pathways after craniofacial injury or inflammation. Their characteristics raise additional possibilities that may explain some of the phenomena outlined by coderre& katz, dickenson, and wiesenfeld-hallin et al. They also underscore the need for therapeutic approaches to reduce nociceptive inputs to the CNS or their neuroplastic effects which can potentially enhance post-traumatic pain.

We suggest that neither selectionism nor constructivism alone are responsible for learning-based changes in the brain. On the basis of quantitative structural studies of human brain tissue it has been possible to find evidence of both increase and decrease in tissue mass at synaptic and dendritic levels. It would appear that both processes are involved in the course of learning-dependent changes.

While sharing the author's interest in the development of an action-based framework for memory research, I think the present version is neither new nor particularly productive. More differentiation is needed to describe memory functioning in a variety of domains and on the many levels of activity regulation. Above all, Glenberg's proposals seem to contradict empirical data.

Is (some) innate cognitive modularity consistent with a lack of innate neural modularity? Quartz & Sejnowski's (Q&S's) implicit negative answer to his question fuels their antinativist and antimodular cognitive conclusions. I attempt here to suggest a positive answer and to solicit discussion of this crucial issue.

The longevity of the Berlin and Kay theses results from the way in which they were formulated, contrasted with extreme relativism. Saunders & van Brakel need not reject colour opponency to reject universal colour categories. Colour opponency does not manifest itself in language, even when dealing directly with spectral colours.

This commentary provides experimental data in support of the critical role of capsaicin-sensitive primary afferent fibers in the initiation and maintenance of pathological pain. The demonstration of capsaicin-induced, centrally-evoked cutaneous hyperalgesia, and of neuroplastic changes elicited by the degeneration of C-fiber primary afferent terminals following peripheral nerve damage, indicates a significant contribution of capsaicin-sensitive sensory ganglion neurons in the development of pathological pain conditions. [coderre & katz]