Evidence is presented from a polyglot savant to suggest that double dissociations between linguistic and nonverbal abilities are more important than Müller's target article implies. It is also argued that the special nature of syntax makes its assimilation to other aspects of language or to nonhuman communication systems radically implausible.

Achievement test differences between boys and girls and between young men and young women, mostly favoring males, extend far beyond mathematics. Such pervasive differences, illustrated here, may require an explanatory theory broader than Geary's.

Latash & Anson propose that so-called abnormal movements may be stable and adaptive coordination and control solutions to task goals in action. Their interpretation of this established viewpoint is confused throughout in the persistent crossing of frames of reference, both in the description of movement and action and the proposed theory for motor control.

Several target articles in this BBS special issue address the topic of cerebellar and olivary functions, especially as they pertain to motor earning. Another important topic is the neural interaction between the limbic system and the cerebellum during associative learning. In this commentary we present some of our data on olivo-cerebellar and limbic-cerebellar interactions during eyeblink conditioning. [HOUK et al.; SIMPSON et al.; THACH]

Contrary to Müller's claims, and in support of modular theories, genetic factors play a substantial and significant role in language. The finding that some children with specific language impairment (SLI) have nonlinguistic impairments may reflect improper diagnosis of SLI or impairments that are secondary to linguistic impairments. Thus, such findings do not argue against the modularity thesis. The lexical/functional distinction appears to be innate and specifically linguistic and could be instantiated in either symbolic or connectionist systems.

Latash & Anson's discussion of movements of “atypical” populations is potentially topical but unhelpful. Abnormal movements can be distinguished from any compensatory adjustments in Parkinson's, Huntington's, and Alzheimer's diseases and schizophrenia. To suggest otherwise may do “atypical” populations and their caregivers a disservice. It would be more meaningful to discuss the relative modularity and separability of cognitive and motor processes.

Studies comparing movement-related cortical potentials, post-excitatory inhibition after transcranial magnetic brain stimulation, and PET findings in normal controls and patients with cerebellar degeneration demonstrate plasticity of cerebro-cerebellar interactions and hereby support Thach's theory that the cerebellum has the ability to play a role in building behavioral context-response linkages and to build up appropriate responses from simpler constitutive elements, [THACH]

I have provided evidence that Geary's model does not explain male dominance in spatial abilities by sexual selection. The current literature concerning the relations of nonverbal IQ to testosterone, hand preference, and right- and left-hand skill, as well as the organizing effects of testosterone on cerebral lateralization during the perinatal period, does not support Geary's arguments.

Latash & Anson are commended for pointing out that investigators of atypical motor performance have too often failed to recognize the adaptive nature of many atypical movement characteristics. However, the authors' assumption that atypical motor patterns can be considered “normal” and, by implication, that it is futile to attempt to teach different patterns to patients that may be more functional, is criticized.

The central problem in Geary's theory is how differences are conceptualized. Recent research has shown that between-sex differences on certain tasks are a consequence of averaging within sex differences. A mixture distribution models between-sex differences on several tasks well and does not appear congenial to a sexual-selection perspective.

One can disagree with Müller that it is neurobiologically questionable to suppose that human language is innate, specialized, and species-specific, yet agree that the precise brain mechanisms controlling language in any individual will be influenced by epigenesis and genetic variability, and that the interplay between inherited and acquired aspects of linguistic capacity deserves to be investigated.

Two major themes have emerged in the commentaries elicited by the target articles that concern cerebellar long-term depression (LTD) (CRÉPEL, VINCENT, and LINDEN). First, is a lively debate concerning the potential role of a nitric oxide/cGMP cascade in cerebellar LTD induction. Second is a much broader issue relating to the interchange of information between cerebellar physiologists concerned with mechanisms at a cellular and synaptic level and those working at the level of systems physiology, behavior, or modeling. What contributions can cellular physiologists make to the study of motor learning? Cellular physiologists can provide testable hypotheses to help determine if these synaptic phenomena do underlie particular behaviors (e.g., if cerebellar LTD underlies vestibulo-ocular reflex [VOR] adaptation or eyeblink conditioning, then blockade of cerebellar LTD via, say, mGluRl inhibition, should interfere with these forms of motor learning). In addition, we can provide descriptive parametric information about basal synaptic function and use-dependent synaptic modifications that can constrain the range of models proposed to underlie a given behavior (e.g., are the timing constraints on LTD induction consistent with VOR adaptation or eyeblink conditioning?).

Chomskyian claims of a genetically hard-wired and cognitively autonomous “universal grammar” are being promoted by generative linguistics as facts about language to the present day. The related doctrine of an evolutionary discontinuity in language emergence, however, is based on misconceptions about the notions of homology and preadaptation. The obvious lack of equivalence between symbolic communicative capacities in existing nonhuman primates and human language does not preclude common roots. Normal and disordered language development is strongly influenced by the genome, but there is no evidence for the existence of specific genes underlying “universal grammar.” In the mature brain, stages of language processing can be distinguished and “first-pass” syntactic analyses appear to precede semantic decoding. However, this partial seriality – as well as behavioral and clinical dissociations between lexical and functional categories – can be best described, not in terms of serially activated and discrete modules, but in terms of classes of cell assemblies that differ in their distributional properties. Whereas cell assemblies involved in semantic interpretation (“content word” assemblies) are widely distributed and are generally less vulnerable to focal lesion, those involved in structural decoding (functor assemblies) are primarily distributed within the left perisylvian cortices and are selectively vulnerable to left perisylvian lesion. These distributional differences are explained in terms of the perceptuomotor components involved in the acquisition of relevant representations. The emerging “motivated” or “toposemantic” brain regional specificity can only be accommodated with “soft” and maturational versions of modularity. The failure to reproduce double dissociations in current connectionist models is due to overly simple neuroscientific assumptions, notably that of overall equipotentiality. Linguistic models should not be expected to be “implemented” in the brain, but need to be constrained by neuroscientific evidence on how biological brains function.

From the perspective of evolutionary theory, we believe it makes more sense to view the sex differences in spatial cognition as being an evolutionary by-product of selection for optimal rates of fetal development. Geary does not convince us that his proposed selective factors operated with “sufficient precision, economy, and efficiency.” Moreover, the archaeological evidence does not support his proposed evolutionary scenario.

The target article on cellular mechanisms of long-term depression appears to have been well received by most authors of the relevant commentaries. This may be due to the fact that this review aimed to give a general account of the topic, rather than just describe previous work of the present author. The present response accordingly only raises questions of major interest for future research.

Observations are made on Latash & Anson's theme that changed motor patterns should not be viewed as pathological. Normality in motor control might be characterised in terms of qualitative differences in control mechanisms rather than differences in movement patterns. Understanding of the concepts implicit in instructions to subjects should be confirmed. Principles of energy expenditure in atypical movements are outlined. If restoration of normality is not adopted as a criterion for therapeutic intervention, what might be proposed as an alternative?

Several commentators argue that there remains a gap between cerebellar long-term depression (LTD) studied in vitro and cerebellar functions such as motor learning. Recent developments in a gene-targeting technique for producing mutant mice defective in particular gene products has opened a new era for the study of synaptic plasticity and learning. There are three mutants in which cerebellar LTD are clearly deficient in vitro. Two of these mice show clear impairment in the conditioned eyeblink response, a paradigm known to involve the cerebellum. In contrast, one mutant with apparently normal cerebellar LTD showed no impairment in the conditioned eyeblink response. These new lines of evidence support the view that cerebellar LTD is a cellular basis for discrete motor learning.

Epstein et al. fail to show that L2 learners have full access to UG because they do not explain the relationship between UG and functional categories (FCs). Nor do they provide an explanation of why learners with (supposed) full knowledge of FCs fail to use them in a native-like way.

The assumption that adaptive changes in motor patterns are optimal is questioned. Instances are cited where alteration of the adaptive motor patterns may be warranted. Other issues discussed are: (1) the relationship between central nervous system (CNS) priorities and the individual's priorities, (2) the use of cognitive bypass strategies by impaired individuals, and (3) conceiving CNS priorities as coordinative rules.

Sexual selection provides an adequate partial explanation for the difference in means between the distributions, but fails to explain the difference in variance, that is, the overrepresentation of both boys with outstanding mathematical reasoning ability (OMRA) and boys with mental retardation. Other genetic factors are probably at work. While spatial ability is correlated with OMRA, so are other cognitive abilities. OMRA is not reducible to spatial ability; hence selection for navigational skill is unlikely to be the only mechanism by which males have gained an advantage in OMRA.