Neuroscience
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Inhalation of carbon dioxide (CO2) is frequently employed as a biological challenge to evoke intense fear and anxiety. In individuals with panic disorder, CO2 reliably evokes panic attacks. Sensitivity to CO2 is highly heterogeneous among individuals, and although a genetic component is implicated, underlying mechanisms are not clear. ⋯ Conversely, DβH-positive cell counts within the LC were significantly higher in CO2-sensitive strains. Collectively, our data provide evidence for strain dependent, differential CO2-sensitivity and potential differences in monoaminergic systems regulating panic and anxiety. Comparative studies between CO2-vulnerable and resistant strains may facilitate the mechanistic understanding of differential CO2-sensitivity in the development of panic and anxiety disorders.
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Imaging studies have described hemodynamic activity during fear conditioning protocols with stimulus trains in which a visual conditioned stimulus (CS+) is paired with an aversive unconditioned stimulus (US, painful laser pulse) while another visual stimulus is unpaired (CS-). We now test the hypothesis that CS Event Related Spectral Perturbations (ERSPs) are related to ratings of CS Expectancy (likelihood of pairing with the US), Valence (unpleasantness) and Salience (ability to capture attention). ERSP windows in EEG were defined by both time after the CS and frequency, and showed increased oscillatory power (Event Related Synchronization, ERS) in the Delta/Theta Windows (0-8Hz) and the Gamma Window (30-55Hz). ⋯ The CS Valence and Salience were greater for CS+ than CS-, and were correlated with each other and with the ERD at overlapping channels, particularly in the Alpha Window. Expectancy and CS Skin Conductance Response were greater for CS+ than CS- and were correlated with ERSP at fewer channels than Valence or Salience. These results suggest that Alpha ERSP activity during fear conditioning reflects Valence and Salience of the CSs more than conditioning per se.
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Previous work (Brown et al., 2003a,b) has shown that limb position drifts when individuals make repetitive movements in the absence of visual feedback. The purpose of this study was to examine whether limb position drift might reflect a misalignment in visual and proprioceptive maps by examining the nature of information used to specify new movements from a drifted limb position. In a virtual reality (VR) environment, participants made continuous movements with their dominant right hand between two targets positioned 15cm apart, paced by a 0.625-Hz metronome. ⋯ For new movement specification, accurate proprioceptive information about the drifted limb position was used, even though it was apparently not available for detecting drift in the first place. Movement distance varied directly with the extent of limb drift, although the differentiation of visual and proprioceptive control of distance could not be analyzed, as our control conditions were not significantly different for this measure. We suggest that movement drift, in the absence of visual feedback during cyclic repetitive movements, reflects a misalignment between largely accurate visual and proprioceptive maps, rather than a weighted fusion of the two modalities.
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Working memory (WM) refers to the holding and manipulation of information during cognitive tasks. Its underlying neural mechanisms have been explored through both functional magnetic resonance imaging (fMRI) and electroencephalography (EEG). Trial-by-trial coupling of simultaneously collected EEG and fMRI signals has become an important and promising approach to study the spatio-temporal dynamics of such cognitive processes. ⋯ Additionally, the activation of single-trial P3 amplitudes was detected in multiple brain regions, including the insula, the cuneus, the lingual gyrus (LG), and the middle occipital gyrus (MOG). Moreover, we found significant correlations between P3 features and behavioral performance. These findings suggest that the single-trial integration of simultaneous EEG and fMRI signals may provide new insights into classical cognitive functions.
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World-wide, two degenerative retinal diseases, glaucoma and age-related macular degeneration, are estimated to affect more than 12% of individuals over the age of 40 (Tham et al., 2014; Wong et al., 2014). Current therapies can slow progression, but cannot restore lost neurons or vision. Thus, there is increasing interest in developing strategies for therapeutic retinal regeneration. ⋯ In the mammalian retina, there is no de novo neurogenesis in adults and only very limited injury-induced regeneration has been induced using exogenous growth factors. The study by (Webster et al., 2017) (Evidence of BrdU Positive Retinal Neurons after Application of an Alpha7 Nicotinic Acetylcholine Receptor Agonist, this issue) is the first to show robust, retinal neurogenesis in an adult, mammalian retina in the absence of overt injury and provides evidence that the source of the new neurons is likely to be the Müller glia. This exciting finding has the potential to be a game-changer in the field of retinal regeneration.