The synthetic position adopted by Müller is weakened by a large number of overinterpretations and misrepresentations, together with a caricatured view of innateness and modularity.

Müller provides a valuable synthesis of neurobiological evidence on the epigenetic development of neural structures involved in language acquisition. The pluripotentiality of developing neural tissue crucially constrains linguistic/cognitive theorizing about supposedly innate neural mechanisms and contributes significantly to our understanding of experience–dependent processes involved in language acquisition. Without this understanding, any proposed explanation of language acquisition is suspect.

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.

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.

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.

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.

Müller's target article aims to summarize approaches to the question of how language elements (phonemes, morphemes, etc.) and rules are laid down in the brain. However, it suffers from being too vague about basic assumptions and empirical predictions of neurobiological models, and the empirical evidence available to test the models is not appropriately evaluated. (1) In a neuroscientific model of language, different cortical localizations of words can only be based on biological principles. These need to be made explicit. (2) Evidence for and against word class differences could be evaluated more rigorously. (3) All (and only) humans are able to learn languages with complex syntactic structures; it is, therefore, not appropriate to deny innateness and universality of syntactic principles. The real question appears to be the following: Which neurobiological principles are the linguistic principles based on?

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.

The belief that syntax is an innate, autonomous, species-specific module is highly questionable. Syntax demonstrates the mosaic nature of evolutionary change, in that it made use of (and led to the enhancement of) numerous preexisting neurocognitive features. It is best understood as an emergent characteristic of the explosion of semantic complexity that occurred during hominid evolution.

Müller's review of the neuroscientific evidence undermines nativist claims for autonomous syntax and the argument from the poverty of the stimulus. Generativists will appeal to data from language acquisition, but here too there is growing evidence against the nativist position. Epigenetic naturalism, the developmental alternative to nativism, can be extended to epigenetic socionaturalism, acknowledging the importance of sociocultural processes in language and cognitive development.

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.

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.

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.

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.

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.

To what extent, if any, does Universal Grammar (UG) constrain second language (L2) acquisition? This is not only an empirical question, but one which is currently investigable. In this context, L2 acquisition is emerging as an important new domain of psycholinguistic research. Three logical possibilities have been articulated regarding the role of UG in L2 acquisition: The first is the “no access” hypothesis that claims that no aspect of UG is available to the L2 learner. The second is the “partial access” hypothesis that claims that only LI instantiated principles and LI instantiated parameter-values of UG are available to the learner. The third, called the “full access” hypothesis, asserts that UG in its entirety constrains L2 acquisition.

In this paper we argue that there is no compelling evidence to support either of the first two hypotheses. Moreover, we provide evidence concerning functional categories in L2 acquisition consistent with the claim that UG is fully available to the L2 learner (see also Flynn 1987; Li 1993; Martohardjono 1992; Schwartz & Sprouse 1991; Thomas 1991; White 1989). In addition, we will attempt to clarify some of currently unclear theoretical issues that arise with respect to positing UG as an explanatory theory of L2 acquisition. We will also investigate in some detail certain crucial methodological questions involved in experimentally testing the role of UG in L2 acquisition and finally, we will present a set of experimental results of our own supporting the “Full Access” hypothesis.

Although the Full-access hypothesis accounts for a range of empirical generalizations of L2A, it underrepresents the role of language transfer in the construction of the L2 grammar. We suggest the possibility that linguistic principles which constrain the L2 grammar are available both directly from UG and via the L1, a logical hypothesis which Epstein et al. do not consider.

This target article's handling of theory and data and the range of evidence surveyed for its main contention fall short of normal BBS standards. However, the contention itself is reasonable and can be supported if one rejects the “knowledge” metaphor for linguistic competence and accepts that “syntactic principles” are no more than the way the brain does language.

The Epstein, Flynn, and Martohardjorno full access hypothesis could be enhanced by inclusion of criteria for falsification.

While child language development theory must explain invariant “success,” foreign language learning theory must explain variation and lack of success. The fundamental difference hypothesis (FDH) outlines such a theory. Epstein et al. ignore the explanatory burden, mischaracterize the FDH, and underestimate the resources of human cognition. The field of second language acquisition is not divided into camps by views on “access” to UG.