There is considerable evidence that the hippocampal system contributes both to (1) the temporary maintenance of memories and to (2) the processing of a particular type of memory representation. The findings on amnesia suggest that these two distinguishing features of hippocampal memory processing are orthogonal. Together with anatomical and physiological data, the neuropsychological findings support a model of cortico-hippocampal interactions in which the temporal and representational properties of hippocampal memory processing are mediated separately. We propose that neocortical association areas maintain (...) shortterm memories for specific items and events prior to hippocampal processing as well as providing the final repositories of long-term memory. The parahippocampal region supports intermediate-term storage of individual items, and the hippocampal formation itself mediates an organization of memories according to relevant relationships among items. Hippocampal-cortical interactions produce (i) strong and persistent memories for events, including their constituent elements and the relationships among them, and (ii) a capacity to express memories flexibly across a wide range of circumstances. (shrink)

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.

The study of signed languages has inspired scientific' speculation regarding foundations of human language. Relationships between the acquisition of sign language in apes and man are discounted on logical grounds. Evidence from the differential hreakdown of sign language and manual pantomime places limits on the degree of overlap between language and nonlanguage motor systems. Evidence from functional magnetic resonance imaging reveals neural areas of convergence and divergence underlying signed and spoken languages.

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 argues that general cognitive skills and linguistic skills are not necessarily independent. However, cross-linguistic evidence from an inherited specific language disorder affecting productive rules suggests significant degrees of modularity, innateness, and universality of language. Confident claims about the overall nature of such a complex system still await more interdisciplinary research.

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.

Müller argues that double dissociations do not imply underlying modularity of the cognitive system, citing neural networks as examples of fully distributed systems that can give rise to double dissociations. We challenge this claim, noting that suchdouble dissociations typically do not “scale-up,” and that even some singledissociations can be difficult to account for in a distributed system.

It is argued that Llewellyn's hypothesis about the lack of rapid eye movement (REM)-sleep dreaming leading to loss of personal identity and deficits in episodic memory, affectivity, and prospection is insufficiently grounded because it does not integrate data from neurodevelopmental studies and makes reference to an outdated definition of episodic memory.

The model proposed by Redish et al. considers vulnerabilities within decision systems based on expectancy-value assumptions. Further understanding of processes leading to addiction can be gained by considering other inputs to decision-making, particularly affective associations with behaviors. This consideration suggests additional decision-making vulnerabilities that might explain addictive behaviors.

Human agents draw a variety of inferences effortlessly, spontaneously, and with remarkable efficiency – as though these inferences were a reflexive response of their cognitive apparatus. Furthermore, these inferences are drawn with reference to a large body of background knowledge. This remarkable human ability seems paradoxical given the complexity of reasoning reported by researchers in artificial intelligence. It also poses a challenge for cognitive science and computational neuroscience: How can a system of simple and slow neuronlike elements represent a large (...) body of systemic knowledge and perform a range of inferences with such speed? We describe a computational model that takes a step toward addressing the cognitive science challenge and resolving the artificial intelligence paradox. We show how a connectionist network can encode millions of facts and rules involving n-ary predicates and variables and perform a class of inferences in a few hundred milliseconds. Efficient reasoning requires the rapid representation and propagation of dynamic bindings. Our model (which we refer to as SHRUTI) achieves this by representing (1) dynamic bindings as the synchronous firing of appropriate nodes, (2) rules as interconnection patterns that direct the propagation of rhythmic activity, and (3) long-term facts as temporal pattern-matching subnetworks. The model is consistent with recent neurophysiological evidence that synchronous activity occurs in the brain and may play a representational role in neural information processing. The model also makes specific psychologically significant predictions about the nature of reflexive reasoning. It identifies constraints on the form of rules that may participate in such reasoning and relates the capacity of the working memory underlying reflexive reasoning to biological parameters such as the lowest frequency at which nodes can sustain synchronous oscillations and the coarseness of synchronization. (shrink)

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.

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.

Sherman presents a slightly revised definition of empathy, in which empathy is the cognitive ability to place oneself in the world of another, imagining all of the realities, feelings, and circumstances of that person in the context of their world.

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.