Electrophysiological spatiotemporal dynamics during implicit visual threat processing.

Numerous studies have found evidence for corticolimbic theta band electroencephalographic (EEG) oscillations in the neural processing of visual stimuli perceived as threatening. However, varying temporal and topographical patterns have emerged, possibly due to varying arousal levels of the stimuli. In addition, recent studies suggest neural oscillations in delta, theta, alpha, and beta-band frequencies play a functional role in information processing in the brain. This study implemented a data-driven PCA based analysis investigating the spatiotemporal dynamics of electroencephalographic delta, theta, alpha, and beta-band frequencies during an implicit visual threat processing task. While controlling for the arousal dimension (the intensity of emotional activation), we found several spatial and temporal differences for threatening compared to nonthreatening visual images. We detected an early posterior increase in theta power followed by a later frontal increase in theta power, greatest for the threatening condition. There was also a consistent left lateralized beta desynchronization for the threatening condition. Our results provide support for a dynamic corticolimbic network, with theta and beta band activity indexing processes pivotal in visual threat processing.

A review of rodent models of type 2 diabetic skeletal fragility.

Evidence indicating that adult type 2 diabetes (T2D) is associated with increased fracture risk continues to mount. Unlike osteoporosis, diabetic fractures are associated with obesity and normal to high bone mineral density, two factors that are typically associated with reduced fracture risk. Animal models will likely play a critical role in efforts to identify the underlying mechanisms of skeletal fragility in T2D and to develop preventative treatments. In this review we critically examine the ability of current rodent models of T2D to mimic the skeletal characteristics of human T2D. We report that although there are numerous rodent models of T2D, few have undergone thorough assessments of bone metabolism and strength. Further, we find that many of the available rodent models of T2D have limitations for studies of skeletal fragility in T2D because the onset of diabetes is often prior to skeletal maturation and bone mass is low, in contrast to what is seen in adult humans. There is an urgent need to characterize the skeletal phenotype of existing models of T2D, and to develop new models that more closely mimic the skeletal effects seen in adult-onset T2D in humans.