We argue that formal analogical reasoning is not a uniquely human trait but is found in chimpanzees, if not in monkeys. We also contest the claim that the relational matching-to-sample task is not exemplary of analogical behavior, and we provide evidence that symbolic-like treatment of relational information can be found in nonhuman species, a point in contention with the relational reinterpretation hypothesis.

Our results on hippocampal long-term potentiation are considered in the context of Xia et al.'s hypothesis. Whereas the target article proposes presynaptic PKC involvement in adenylyl cyclase activation by phosphorylation of nenromodulin, we suggest an additional postsynaptic role involving RC3/nenrogranin. Finally, we examine the possibility that the adenylyl cyclase mutant mouse may display normal learning with a selective impairment of memory.

The following questions are discussed: (1) Who determines the nature of “control variables”? (2) Is the “positional monopoly” healthy? (3) Does a descending command alter reflex threshold alone without eoncomitantly altering stiffness? (4) How does the CNS deal with history-dependent effects? (5) Should we abandon the idea that the CNS controls classical Newtonian variables such as muscle length?

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.

It has been suggested that type I adenylyl cyclase may play a unique role in long-term potentiation, due to both unique regulatory properties as well as a specialized distribution within the mammalian brain. This would allow an integration of the signals wrought by increased intracellular calcium with those conveyed into the cellular milieu via increased cAMP. These results are discussed in the context of changes in cellular structure, because of changing interactions between G proteins and cytoskeletal components, which might be expected to accompany chronic synaptic activation.