Neuroscience
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We study the transition in the functional networks that characterize the human brains' conscious-state to an unconscious subliminal state of perception by using k-core percolation. We find that the most inner core (i.e., the most connected kernel) of the conscious-state functional network corresponds to areas which remain functionally active when the brain transitions from the conscious-state to the subliminal-state. ⋯ Thus, the inner core and most robust component of the conscious brain corresponds to the unconscious subliminal state. This finding imposes constraints to theoretical models of consciousness, in that the location of the core of the functional brain network is in the unconscious part of the brain rather than in the conscious state as previously thought.
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Perceptual selection can be guided by the contents of working memory (WM). Neuroimaging and neuropsychological data point to a role of a fronto-parietal and fronto-thalamic networks in WM guidance. Here we assessed the effect of transcranial direct current stimulation of the left dorsal frontal cortex (lDFC) in a combined WM/attention paradigm. ⋯ Notably, across two experiments we found that lDFC-tDCS modulated WM guidance of visual selection in the context of high processing loads in WM. No effects of tDCS were observed in WM accuracy. These findings suggest that the role of the left dorsal frontal cortex in WM guidance is associated with selective attentional control rather than mnemonic processing.
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Silent angina is a critical phenomenon in the clinic and is more commonly associated with women patients suffering from myocardial ischemia. Its underlying cause remains mysterious in medicine. With our recent discovery of female-specific Ah-type baroreceptor neurons (BRNs), we hypothesize that cardiac analgesia is due to the direct activation of Ah-type BRNs by elevated levels of circulating serotonin (5-HT) myocardial infarction (MI) patients. ⋯ Although the tail-flick reflex and mean arterial pressure were dramatically reduced in female MI rats with elevated serum 5-HT, intrapericardial capsaicin-evoked muscular discharges were significantly inhibited in comparing with those of males, which were mimicked by microinjection of 5-HT or SR57227A into the nodose. Ah-type BRNs displayed robust inward currents at lower concentrations of 5-HT than the C-type or the A-type, with significantly increased expression and cellular distribution of 5-HT3AR but not 5-HT3BR compared to the A- and C-types. Activation of 5-HT3AR in Ah-type BRNs by 5-HT contributes significantly to cardiac analgesia, which may suggest the pathogenic condition that silent angina occurs mainly in female patients.
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Physical exercise is now generally considered as a strategy to maintain cognitive abilities and to prevent age-related cognitive decline. In the present study, Wistar rats were subjected to moderate intensity treadmill exercise for 6 months prior to sacrifice at 12-, 24- and 32-month of age. This chronic physical intervention was tested on motility in the Open field (OF). ⋯ Massive ChAT fiber aberrations in all investigated areas which developed in senescence were clearly attenuated by exercise. The results suggest that moderate intensity chronic exercise in the rat is especially beneficial in advanced age. In conclusion, chronic exercise attenuates the age-related decline in cognitive and motor behaviors as well as age-related cholinergic fiber reduction, reduces malformations of cholinergic forebrain innervation.
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Astrocytes regulate extracellular glutamate homeostasis in the central nervous system through the Na+-dependent glutamate transporters glutamate transporter-1 (GLT-1) and glutamate aspartate transporter (GLAST). Impaired astrocyte glutamate uptake could contribute to the development of epilepsy but the regulation of glutamate transporters in epilepsy is not well understood. In this study, we investigate the expression of GLT-1 and GLAST in the mouse intrahippocampal kainic acid (IHKA) model of temporal lobe epilepsy (TLE). ⋯ GLAST immunoreactivity was increased in specific layers at 1 and 3 days post-IHKA in the ipsilateral hippocampus. GLAST synaptosomal protein levels were significantly elevated at 30 days compared to 7 days post-IHKA in the ipsilateral hippocampus. Our findings suggest that astrocytic glutamate transporter dysregulation could contribute to the development of epilepsy.