Neuroscience
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The perception of tool-object pairs involves understanding their action-relationships (affordances). Here, we sought to evaluate how an observer visually encodes tool-object affordances. Eye-movements were recorded as right-handed participants freely viewed static, right-handed, egocentric tool-object images across three contexts: correct (e.g. hammer-nail), incorrect (e.g. hammer-paper), spatial/ambiguous (e.g. hammer-wood), and three grasp-types: no hand, functional grasp-posture (grasp hammer-handle), non-functional/manipulative grasp-posture (grasp hammer-head). ⋯ Unlike the functional grasp-posture, the manipulative grasp-posture caused the greatest disruption in the object-oriented priming effect, ostensibly as it does not afford tool-object action due to its non-functional interaction with the operant tool-end that actually engages with the object (e.g., hammer-head to nail). The enhanced attention towards the manipulative grasp-posture may serve to encode grasp-intent. Results here shed new light on how an observer gathers action-information when evaluating static tool-object scenes and reveal how contextual and grasp-specific affordances directly modulate visuospatial attention.
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The effects of sensory loss on central processing in various sensory systems have already been described. The olfactory system holds the special ability to be activated by a sensorimotor act, without the presentation of an odor. In this study, we investigated brain changes related to chronic peripheral smell loss. ⋯ The areas involved were not different from those that emerged in healthy controls. However, functional connectivity appears to be different between the two groups, with a decrease in functional connectivity in the brain in patients with chronic peripheral sensory loss. We can further conclude that the loss of the sense of smell may induce far-reaching effects in the whole brain, which lead to compensatory mechanisms from other sensory systems due to the close interconnectivity of the olfactory system with other functional networks.
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Defining the markers corresponding to a high risk of developing depression in humans would have major clinical significance; however, few studies have been conducted since they are not only complex but also require homogeneous groups. This study compared congenital learned helpless (cLH) rats, selectively bred for high stress sensitivity and learned helplessness (LH) behavior, to congenital non-learned helpless (cNLH) rats that were bred for resistance to uncontrollable stress. Naïve cLH rats show some depression-like behavior but full LH behavior need additional stress, making this model ideal for studying vulnerability to depression. ⋯ These reductions corresponded primarily to reduced inter-hemispheric connectivity. The main reduction however was in the sensory system. It is argued that reduced connectivity and inter-hemispheric connectivity of the sensory system reflects an internal convergence state which may precede other depressive symptomatology and therefore could be used as markers for vulnerability to the development of depression.
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The 5-HT6 receptor (5-HT6R) is almost exclusively expressed in the brain and has emerged as a promising target for cognitive disorders, including Alzheimer's disease. In the present study, we have determined the cell types on which the 5-HT6R is expressed by colocalizing 5-HT6R mRNA with that of a range of neuronal and interneuronal markers in the rat brain. Here, we show that 5-HT6R mRNA was expressed at high levels in medium spiny neurons in caudate putamen and in nucleus accumbens, as well as in the olfactory tubercle. ⋯ Serotonergic, dopaminergic or cholinergic neurons did not express 5-HT6R mRNA. These data indicate that the 5-HT6R is located on GABAergic and glutamatergic principal neurons, and on a subset of interneurons mainly belonging to the 5-HT3aR subgroup suggesting that the 5-HT6R is positioned to regulate the balance between excitatory and inhibitory signaling in the brain. These data provide new insights into the mechanisms of 5-HT6R signaling.
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The hypocretin/orexin system regulates, among other things, sleep and energy homeostasis. The system is likely regulated by both homeostatic and circadian mechanisms. Little is known about local differences in the regulation of hypocretin activity. ⋯ This study further demonstrates that the hypocretin-1 peptide level in the frontal brain peaks during dark as does prepro-hypocretin mRNA in the hypothalamus. However, in midbrain and brainstem tissue caudal to the hypothalamus, there was less circadian fluctuation and a tendency for higher levels during the light phase. These data suggest that regulation of the hypocretin system differs between brain areas.