The highly ordered neuronal projections from the retina to the tectum mesencephali (optic tectum) in several vertebrate groups have been intensively studied. Several hypotheses so far have been proposed, suggesting mechanisms to explain the topographical and biochemical specificity of the retinotectal projections during ontogeny. In the present paper we compare the main hypotheses of retinotectal development with respect to the nature of specificity envisaged, the activity-dependence versus inheritance criterium and the strategy of argument, in casu the descriptive versus interferential type (...) of argument. Matching of the current developmental hypotheses and mechanisms for elimination or persistance of contralateral, respectively ipsilateral connections, is attempted with respect to the known neuroanatomical connectivity data in the amphibian optic tectum and with respect to the symmetry relations between ipsilateral and contralateral connection patterns described in amphibians and other vertebrate groups. Local mechanisms influencing the survival potential of synaptic contacts between retinal afferents and tectal neurons are probably essential for generating global symmetry patterns. Finally, a global topological approach is discussed with respect to its applicability in the amphibian retinotectal projection system. Basic assumptions of topological modeling appear to rely on anatomical and functional properties of the visual system like left-right symmetry, dichotomy, (absence of) convergence and segregation of fibers and neurons into columnar information units. It is concluded however, that more neuroanatomical, physiological and ultrastructural data are needed to establish a formalized operation model of the amphibian retinotectal system. (shrink)

Experiential factors such as long-term deliberate practice are powerful and necessary conditions for outstanding achievement. Nevertheless, to be able to reject the role of biology based individual differences (including genetic ones) in the manifestation of talent requires designs that expose heterogeneous samples to so-called testing-the-limits conditions, allowing asymptotic levels of performance to be analyzed comparatively. When such research has been conducted, as in the field of lifespan cognition, individual differences, including biology based ones, come to the fore and demonstrate that (...) the orchestration of excellence requires joint attention to genetic–biological and experiential factors. (shrink)

There is an argument that has recently been deployed in favor of thinking that the mind is mostly (or even exclusively) composed of cognitive modules; an argument that draws from some ideas and concepts of evolutionary and of developmental biology. In a nutshell, the argument concludes that a mind that is massively composed of cognitive mechanisms that are cognitively modular (henceforth, c-modular) is more evolvable than a mind that is not c-modular (or that is scarcely c-modular), since a cognitive mechanism (...) that is c-modular is likely to be biologically modular (henceforth, b-modular), and b-modular characters are more evolvable (e.g., Sperber 2002, Carruthers 2005). In evolutionary biology, the evolvability of a character in an organism is understood as the “organism’s capacity to facilitate the generation of non-lethal selectable phenotypic variation from random mutation” with respect to that character. Here I will argue that the notion of cognitive modularity needed to make this argument plausible will have to be understood in terms of the biological notion of variational independence; that is, it will have to be understood in such a way that a cognitive feature is c-modular only if few or no other morphological changes (cognitive and not) are significantly correlated with variations of that feature arising in members of the relevant population. I will also argue that all –except for (possibly) one—of the connotations contained in a cluster of notions of cognitive modularity widely accepted in some of the mainstream currents of thought in classical cognitive science, are simply irrelevant to the argument. In order to argue for this, I will have to examine the question as to whether there are any strong theoretical connections between (1) those connotations and (2) notions of modularity accepted in biology, specially in evolutionary and in developmental biology, that are thought to be most relevant to arguments to the effect that biological modularity enhances evolvability. (shrink)

This article began as a review of a conference, organized by Gerhard Schlosser, entitled “Modularity in Development and Evolution.” The conference was held at, and sponsored by, the Hanse Wissenschaftskolleg in Delmenhorst, Germany in May, 2000. The article subsequently metamorphosed into a literature and concept review as well as an analysis of the differences in current perspectives on modularity. Consequently, I refer to general aspects of the conference but do not review particular presentations. I divide modules into three kinds: structural, (...) developmental, and physiological. Every module fulfills none, one, or multiple functional roles. Two further orthogonal distinctions are important in this context: module-kinds versus module-variants-of-a-kind and reproducer versus nonreproducer modules. I review criteria for individuation of modules and mechanisms for the phylogenetic origin of modularity. I discuss conceptual and methodological differences between developmental and evolutionary biologists, in particular the difference between integration and competition perspectives on individualization and modular behavior. The variety in views regarding modularity presents challenges that require resolution in order to attain a comprehensive, rather than a piecemeal and fragmentary, evolutionary developmental biology. (shrink)

August Weismann is famous for having argued against the inheritance of acquired characters. However, an analysis of his work indicates that Weismann always held that changes in external conditions, acting during development, were the necessary causes of variation in the hereditary material. For much of his career he held that acquired germ-plasm variation was inherited. An irony, which is in tension with much of the standard twentieth-century history of biology, thus exists – Weismann was not a Weismannian. I distinguish three (...) claims regarding the germ-plasm: (1) its continuity, (2) its morphological sequestration, and (3) its variational sequestration. With respect to changes in Weismann’s views on the cause of variation, I divide his career into four stages. For each stage I analyze his beliefs on the relative importance of changes in external conditions and sexual reproduction as causes of variation in the hereditary material. Weismann believed, and Weismannism denies, that variation, heredity, and development were deeply intertwined processes. This article is part of a larger project comparing commitments regarding variation during the latter half of the nineteenth century. (shrink)