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In a previous paper, I argued that neuroscience and psychology could in principle undermine libertarian free will by providing support for a subset of what I called “statements of local determination.” I also argued that Libet-style experiments have not so far supported statements of that sort. In a commentary to the paper, Adina Roskies and Eddy Nahmias accept the claim about Libet-style experiments, but reject the claim about the possibilities of neuroscience. Here, I explain why I still disagree with their conclusion, despite being sympathetic to a lot of what they say in support of it. [ABSTRACT FROM PUBLISHER]

This paper considers the way mathematical and computational models are used in network neuroscience to deliver mechanistic explanations. Two case studies are considered: Recent work on klinotaxis by Caenorhabditis elegans, and a long-standing research effort on the network basis of schizophrenia in humans. These case studies illustrate the various ways in which network, simulation, and dynamical models contribute to the aim of representing and understanding network mechanisms in the brain, and thus, of delivering mechanistic explanations. After outlining this mechanistic construal of network neuroscience, two concerns are addressed. In response to the concern that functional network models are nonexplanatory, it is argued that functional network models are in fact explanatory mechanism sketches. In response to the concern that models which emphasize a network’s organization over its composition do not explain mechanistically, it is argued that this emphasis is both appropriate and consistent with the principles of mechanistic explanation. What emerges is an improved understanding of the ways in which mathematical and computational models are deployed in network neuroscience, as well as an improved conception of mechanistic explanation in general. [ABSTRACT FROM AUTHOR]

People have disagreed on the significance of Libet-style experiments for discussions about free will. In what specifically concerns free will in a libertarian sense, some argue that Libet-style experiments pose a threat to its existence by providing support to the claim that decisions are determined by unconscious brain events. Others disagree by claiming that determinism, in a sense that conflicts with libertarian free will, cannot be established by sciences other than fundamental physics. This paper rejects both positions. First, it is argued that neuroscience and psychology could in principle provide support for milder deterministic claims that would also conflict with libertarian free will. Second, it is argued that Libet-style experiments—due to some of their peculiar features, ones that need not be shared by neuroscience as a whole—currently do not (but possibly could) support such less demanding deterministic claims. The general result is that neuroscience and psychology could in principle undermine libertarian free will, but that Libet-style experiments have not done that so far. [ABSTRACT FROM AUTHOR]

David Buller and Valerie Hardcastle have argued that various discoveries about the genetics and nature of brain development show that most “central” psychological mechanisms cannot be adaptations because the nature of the contribution from the environment on which they are based shows they are not heritable. Some philosophers and scientists have argued that a strong role for the environment is compatible with high heritability as long as the environment is highly stable down lineages. In this paper I support this view by arguing that the discoveries Buller and Hardcastle refer to either do not show as strong a role for the environment as they suggest, or these discoveries show that the brain's developmental process depends in many cases on input from the environment that is highly stable across generations. [ABSTRACT FROM AUTHOR]

Several influential psychologists have attempted to estimate to what extent human happiness levels are directly controlled by genes by comparing the happiness levels of identical twins raised apart. If we discover that the happiness levels of identical twins raised apart tend to be closer than the happiness levels of fraternal twins raised apart, this is taken as evidence that average happiness levels are largely controlled by genes. However, if it turns out that identical twins' happiness levels tend to be substantially different, as different as fraternal twins raised apart, it has been argued that this implies that the environment largely determines happiness levels. I contend that this interpretation of the data rests on a set of questionable, closely related assumptions: a) that pairs of identical twins raised apart are raised in substantially different environments; b) that genetically identical twins aren't identical in other pertinent ways; and c) that average levels of affect that are correlated with certain sets of genes in the environments the twin studies were conducted in will be correlated with those genes in other relevant environments because those genes govern average affect levels. In this paper, I will show that these assumptions are false and explain how to properly go about investigating the contingent causal links between genes and happiness. In the end, I argue that there is no good evidence that our genes delimit our hedonic potential and that the fact that this misinterpretation of the data has been widely disseminated is potentially harmful to human well-being. [ABSTRACT FROM PUBLISHER]

In response to points raised by our critics in this book symposium, we offer some clarifications about how to understand the role of science in assessing the multiple realization thesis. We also consider the connection between functionalism and multiple realization in the contexts of both psychological and biological sciences. [ABSTRACT FROM AUTHOR]

Contrastive neuroimaging is often taken to provide evidence about the localization of cognitive functions. After canvassing some problems with this approach, I offer an alternative: neuroimaging gives evidence about regions of the brain that beardifference-makingrelationships to psychological processes of interest. I distinguish between the specificity and what I call the systematicity of a difference-making relationship, and I show how at least some neuroimaging experiments can give evidence for systematic difference-making. [ABSTRACT FROM PUBLISHER]

Marcelo Fischborn discusses the significance of neuroscience for debates about free will. Although he concedes that, to date, Libet-style experiments have failed to threaten “libertarian free will” (free will that requires indeterminism), he argues that, in principle, neuroscience and psychology could do so by supporting local determinism. We argue that, in principle, Libet-style experiments cannot succeed in disproving or even establishing serious doubt about libertarian free will. First, we contend that “local determination”, as Fischborn outlines it, is not a coherent concept. Moreover, determinism is unlikely to be established by neuroscience in any form that should trouble compatibilists or libertarians—that is, anyone who thinks we might have free will. We conclude that, in principle, neuroscience will not be able undermine libertarian free will and explain why these conclusions support a coherent compatibilist notion of causal sourcehood. [ABSTRACT FROM PUBLISHER]