With some help from the commentators, a few adjustments to the characterizations of A-consciousness and P-consciousness can avoid some trivial cases of one without the other. But it still seems that the case for the existence of P without A is stronger than that for A without P. If indeed there can be P without A, but not A without P, this would be a remarkable result that would need explanation.

Inactivation of the Ca2+ extrusion mode of the retinal rod Na- Ca + K exchanger is suggested to be the mechanism that prevents lowering of cytosolic free Ca2+ to < 1 nM when rod cells are saturated for a prolonged time under bright light conditions. Under these conditions, Ca2+ fluxes across disk membranes can contribute significantly to Ca2+ homeostasis in rods.

Over the past two decades, research on neural transplantation in animal models of neurodegeneration has provided provocative in sights into the therapeutic use of grafted tissue for various neurological diseases. Although great strides have been made and functional benefits gained in these animal models, much information is still needed with regard to transplantation in human patients. Several factors are unique to human disease, for example, age of the recipient, duration of disease, and drug interaction with grafted cells; these need to be explored before grafting can be considered a safe and effective therapeutic tool.

Because consciousness has an organizational, or functional, center, Gray supposes that there must be a corresponding physical center in the brain. He proposes further that since this center generates consciousness, ablating it would eliminate consciousness, while leaving behavior intact. But the center of consciousness is simply the product of the functional linkages among sensory input, memory, inner speech, and so on, and behavior.

A lesion to the brain is not necessary for a successful neural transplantation. Embryonic Purkinje cells placed on the surface of an uninjured adult cerebellum can develop and migrate into the host molecular layer. Both the Purkinje cells that migrated into the host cerebellum and those that remained in the graft were innervated by collateral sprouting of adult intact climbing fibers.

Magic angle spinning (MAS) NMR methods provide a means of obtaining high resolution structural data on rhodopsin and its photoin termediates. Current work has focused on the structure of the retinal chromophore and its interactions with surrounding protein charges. The recent development of MAS NMR methods for measuring internuclear distances with a resolution of ∼0.2 will complement diffraction methods for addressing key mechanistic questions.

Gray has expanded his account of schizophrenia to explain consciousness as well. His theory explains neither phenomenon adequately because he treats individual minds (and brains) in isolation. The primary function of consciousness is to permit high level interactions with other conscious beings. The key symptoms of schizophrenia reflect a failure of this mechanism.

Most phobias are focussed on a small number of fear-inducing stimuli (e.g., snakes, spiders). A review of the evidence supporting biological and cognitive explanations of this uneven distribution of phobias suggests that the readiness with which such stimuli become associated with aversive outcomes arises from biases in the processing of information about threatening stimuli rather than from phylogenetically based associative predispositions or “biological preparedness.” This cognitive bias, consisting of a heightened expectation of aversive outcomes following fear-relevant stimuli, generates and maintains robust learned associations between them. Some of the features of such stimuli which determine this expectancy bias are estimates of how dangerous they are, the semiotic similarity between them and their aversive outcomes, and the degree of prior fear they elicit. Ontogenetic and cultural factors influence these features of fear-relevant stimuli and are hence important in determining expectancy bias. The available evidence does not exclude the possibility that both expectancy biases and specific evolved predispositions coexist, but the former can explain a number of important findings that the latter cannot.

This commentary acknowledges the importance of Davey's biocognitive approach to the uneven distribution of fears on the basis of its contribution to a human model for understanding fear. An integrated heredity-environment and developmental transactional approach based on field/system theory is recommended in place of the mechanistic heredity × environment interactionism that Davey uses to explain behavioral ontogeny.

A major problem in developing an effective gene therapy for the nervous system lies in understanding the principles that maintain or turn off the expression of genes following their transfer into the CNS.

A number of proteins homologous to recoverin have been identified in the brains of the several vertebrate species. The brainderived members originally contain four EF-hand domains, but NH2- terminal domain is aberrant. Many of these proteins inhibited light-induced rhodopsin phosphorylation at high [Ca2+], suggesting that the brain-derived members may act as a Ca2+-sensitive modulator of receptor phosphorylation, as recoverin does.

It is accepted that “primary awareness” may emerge from the integration of two classes of information. It is unclear, however, why this cannot take place within the comparator rather than in conjunction with feedback to the perceptual systems. The model has plausibility in relation to the continuity of conscious experience in the normal waking state and may be extended to encompass certain aspects of the “sense of self” which are frequently disrupted in psychotic patients.

Perspective and reflection (whether involving conceptual or nonconceptual content) have each been considered in some way basic to phenomenal consciousness. Each has possible evolutionary value, though neither seems sufficient for consciousness. Consider an account of consciousness in terms of the combination of perspective and reflection, its relationship to the problem of other minds, and its capacity to inherit evolutionary explanation from its components.

Grafting embryonic brain tissue into the brain of patients with visual field loss due to cerebral lesions may become a method to restore visual function. This method is not without risk, however, and will only be considered in cases of complete blindness after bilateral occipital lesions, when other, risk-free neuropsychological methods fail.

Genetic abnormalities of three factors related to the photoreceptor mechanism have been reported in both animal models and humans. Apoptotic mechanism has also been suggested as a final common pathway of photoreceptor cell death. Our findings of increased level of glutamate in photoreceptor cells in rds mice suggest that amino acid might mediate between these two pathological mechanisms.

This commentary focuses upon two issues raised by Davey's target article: (1) whether there are certain core features of stimuli we learn to fear, rather than specific types of objects or situations, which implies some element of innateness; and (2) whether expectancy biases serve to maintain rather than generate anxiety.

This commentary reviews data supporting circuitry reconstruction, replacement neurotransmitters, and trophic action as mechanisms whereby transplants promote recovery of function. Issue is taken with the thesis of Sinden et al. that adequate data exist to indicate that reconstruction of hippocampal circuitry damaged by hypoxia with CA1 transplants is a confirmed mechanism whereby these transplants produce recovery. Sinden et al.'s and Stein & Glasier's proposal that there is definitive evidence showing that all transplants produce trophic effects is also questioned.

Site-specific phenotypic effects of the 73 known alleles in the rhodopsin gene that cause retinal degeneration are difficult to interpret because most alleles are documented in only one case or one family, which means variation in effects could actually arise from interactions with other loci. However, sample sizes necessary to detect epistatic interaction may place an answer to this question beyond our grasp.

Behavioral research suggests that rule-governed behavior should be less sensitive to environmental changes and thus more resistant to extinction (disconfirmation) than contingency-governed behavior. The opposite is implied in Davey's discussion of ontogenetic and phylogenetic contributions to fear development. The generality of the behavioral findings and their apparent inconsistency with the present article should be further explored with more sensitive research paradigms.

Gray takes an information-processing paradigm as his departure point, invoking a comparator as part of the system. He concludes that consciousness is to be found “in” the comparator but is unable to point to how the comparison takes place. Thus, the comparator turns out not to be an entity arising out of brain research per se, but out of the logic of the paradigm. In this way, Gray both reinvents dualism and remains trapped in the language game of his own model – ending up dealing with the unknowable.