First, Wang et al. (2013) examined connectivity in an anesthetized

animal selleck kinase inhibitor in the absence of behavior and so studies are needed to show how these spatially precise patterns of functional connectivity are altered across goal states, attentional states, and levels of arousal. Second, there were no interventional measures of interactivity, which leaves open the possibility that correlations were driven by common sources. Electrical and optogenetic stimulation are a growing trend for causal mapping (e.g., Keller et al., 2011). Finally, Wang et al. (2013) restricted their field of view to a subset of peri-Rolandic regions. Future work should investigate how these precise patterns selleck products of somatotopic BOLD connectivity relate to motor and prefrontal cortical dynamics, and how they change in the wider neural context (McIntosh, 1999). In summary, Wang et al. (2013) have precisely examined the relationship

between anatomical connectivity, BOLD signal correlations, and neuronal spiking correlations within primate somatosensory cortex. Their work presents a coherent picture of the interareal connectivity and dynamics at the fine scale of topographically mapped body surface representations, enriching our understanding of functional connectivity and its anatomical underpinning. “
“The architectural complexity and cellular diversity of the mammalian brain represent major challenges to the pursuit of etiological factors that underlie human degenerative brain disorders. A further impediment particular to the analysis of degenerative brain diseases is their PtdIns(3,4)P2 protracted time course. And although animal models have greatly informed current views on

these disorders, they have often failed to recapitulate key aspects of the diseases. Thus, reductionist in vitro approaches using human cells, such as the analysis of patient-derived neurons generated using iPSC, have been met with particular excitement (Abeliovich and Doege, 2009, Takahashi and Yamanaka, 2006 and Yamanaka, 2007). More recent advances offer a variety of additional tools, such as for the genetic correction of disease-associated mutations in patient-derived cultures. Even with such advances, cell-based approaches to study human neurodegenerative diseases are limited by the inherent genetic diversity of the human population, as well as technical variation among accessible human tissue samples. Recent studies using human reprogramming-based cell models of neuronal disorders have brought a number of mechanistic topics to the fore, including the significance of non-neuronal or non-cell-autonomous factors in disease, the relevance of epigenetic mechanisms, and the potential of cell-based drug discovery approaches.