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.

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.

Segregated neural circuits that effect particular domain-specific behaviors can be differentiated from neuroanatomical structures implicated in many different aspects of behavior. The basal ganglionic components of circuits regulating nonlinguistic motor behavior, speech, and syntax all function in a similar manner. Hence, it is unlikely that special properties and evolutionary mechanisms are associated with the neural bases of human language.

The conclusion that language is not really innate or modular is based on several fallacies. I show that the target article confuses communicative skills with linguistic abilities, and that its discussion of brain/language relations is replete with factual errors. I also criticize its attempt to contrast biological and linguistic principles. Finally, I argue that no case is made for the “alternative” approach proposed here.

Both autonomy and local specificity are compatible with observed interconnectivity at the cell level when considering two different levels: cell assemblies and brain systems. Early syntactic structuring processes in particular are likely to representan autonomous module in the language/brain system.

Müller attempts to downplay cases of dissociation between language and cognition as evidence against the modularity of language. We review cases of associations between verbal and nonverbal abilities as further evidence against the notion of language as an autonomous subsystem. We also point out a discrepancy between his proposal of homologies between nonhuman primates' communication and human language and recent proposals on the evolution of language.

Müller misconstrues autonomy to mean strict locality of brain function, something quite different from the functional autonomy that linguists claim. Similarly, he misperceives the interaction of learned and innate components hypothesized in current generative models. Evidence from sign languages, Creole languages, and neurological studies of rare forms of aphasia also argues against his conclusions.

I enlarge on the theme that the brain mechanisms required for languageand other aspects of the human mind evolved through selective changes in the regulatory genes governing growth. Extension of the period of postnatal growth increases the role of the environment in structuring the brain, and spatiotemporal programming (heterochrony) ofgrowth might explain hierarchical representation, hemispheric specialization, and perhaps sex differences.

Müller's goal of bringing neuroscience to bear on controversies in linguistics is laudable. However, some of his specific proposals about innateness and autonomy are misguided. Recent studies on the neurobiology of regular and irregular inflectional morphology indicate that these two linguistic processes are subserved by anatomically and physiologically distinct neural subsystems, whose functional organization is likely to be under direct genetic control rather than assembled by strictly epigenetic factors.

Neurobiological models of language need a level of analysis that can account for the typical range of language phenomena. Because linguistically motivated models have been successful in explaining numerous language properties, it is premature to dismiss them as biologically irrelevant. Models attempting to unify neurobiology and linguistics need to be sensitive to both sources of evidence.

We agree with Müller's epigenetic view of evolution and ontogeny and applaud his multilevel perspective. With him, we stress the importance in ontogeny of progressive specialisation rather than prewired structures. However, we argue that he slips from “speech” to “language” and that, in seeking homologies, these two levels need to be kept separate in the analysis of evolution and ontogeny.

Because Müiller fails to distinguish between two senses of the term “autonomy,” there is a danger that his results will be misinterpreted by both linguists and neuroscientists. Although he may very well have been successful in refuting one sense of autonomy, he may actually have helped to provide an explanation for the correctness of autonomy in its other sense.

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. (shrink)