Neuroscience
-
Restrained eaters (REs) characterized by less efficient response inhibition are at risk for future onset of binge eating and bulimic pathology. Previous imaging studies investigating REs have been based on task-related functional magnetic resonance imaging (fMRI) and little is known about resting-state neural activity underlying restrained eating. To illuminate this issue, we investigated resting-state fMRI differences between REs (n=22) and unrestrained eaters (UREs) (n=30) using regional homogeneity (ReHo) analysis, which measures the temporal synchronization of spontaneous fluctuations. ⋯ Compared with UREs, REs showed more ReHo in brain regions associated with food reward (i.e., orbitofrontal cortex (OFC), dorsal-lateral prefrontal cortex (dlPFC)), attention (i.e., lingual gyrus, cuneus, inferior parietal lobule) and somatosensory functioning (i.e., paracentral lobule, anterior insula). In addition, ReHo values for the left dlPFC and left anterior insula, respectively, were negatively and positively correlated with SSRT among REs but not UREs. In concert with previous studies, these results suggest altered local synchronization may help to explain why dieting to maintain or lose weight often fails or increases risk for binge eating among REs.
-
The aim of present study was to elucidate the role of Interleukin-10 (IL-10) in the neuroprotection of hyperbaric oxygen (HBO) against traumatic brain injury (TBI) in mice. The TBI in mice was induced by controlled cortical impact (CCI). HBO was given for 1h at 2.0 absolute atmosphere (ATA) in 100% O2. ⋯ IL-10 deficiency aggravated TBI-induced damage in the brain and abrogated the beneficial effects of HBO on neuroinflammation, apoptosis, and edema after TBI. IL-10 deficiency itself had no significant effect on brain water content and neurological status. In conclusion, IL-10 played an important role in the neuroprotection of HBO therapy against TBI in mice.
-
Correlated electrophysiological and behavioral experiments in the snail Helix lucorum were conducted to investigate the contribution of nitric oxide (NO) to synaptic plasticity during withdrawal reflex and aversive context memory development. Time, stimulation frequency and number of tetani/electrical shocks were determined in vitro and in vivo. In isolated brain preparations, nerve tetanization accompanied by bath application of serotonin induced long-term facilitation (LTF) of the excitatory postsynaptic potential (EPSP) in withdrawal interneurons. ⋯ Testing on the second day after training demonstrated that the sham-injected group maintained selective aversive context memory, whereas the L-NNA-injected snails were not different between the two contexts. Together these results demonstrated that inhibition of NO synthesis prevents memory formation and influences synaptic plasticity in the withdrawal interneurons that underlie the behavioral changes. This suggests that NO influences the behavior via regulation of synaptic plasticity.
-
The suprachiasmatic nucleus (SCN) is typically considered our autonomous clock synchronizing behavior with physiological parameters such as blood pressure (BP), just transmitting time independent of physiology. Yet several studies show that the SCN is involved in the etiology of hypertension. Here, we demonstrate that the SCN is incorporated in a neuronal feedback circuit arising from the nucleus tractus solitarius (NTS), modulating cardiovascular reactivity. ⋯ Examining this possibility we observed that elevation of BP, induced by α1-agonist infusion, was more than twice the magnitude in SCN-lesioned animals as compared to in controls, indicating indeed an active involvement of the SCN in short-term BP regulation. We propose that the SCN receives BP information directly from the NTS enabling it to react to hemodynamic perturbations, suggesting the SCN to be part of a homeostatic circuit adapting BP response. We discuss how these findings could explain why lifestyle conditions violating signals of the biological clock may, in the long-term, result in cardiovascular disease.
-
We investigated the effect of taurine on inflammatory cytokine expression, on astrocyte activity and cerebral edema and functional outcomes, following traumatic brain injury (TBI) in rats. 72 rats were randomly divided into sham, TBI and Taurine groups. Rats subjected to moderate lateral fluid percussion injury were injected intravenously with taurine (200mg/kg) or saline immediately after injury or daily for 7days. Functional outcome was evaluated using Modified Neurological Severity Score (mNSS). ⋯ Compared with the TBI group, taurine significantly suppressed growth-related oncogene (GRO/KC) and interleukin (IL)-1β levels while elevating the levels of regulated on activation, normal T cell expressed and secreted (RANTES) at 1day. And taurine markedly decreased the level of 17 cytokine: eotaxin, Granulocyte colony-stimulating factor (G-CSF), Granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-gamma (IFN-γ), IL-1α, IL-1β, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-13, IL-17, leptin, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), vascular endothelial growth factor (VEGF), and only increased the level of MIP-1α in a week. The results suggest that taurine effectively mitigates the severity of brain damage in TBI by attenuating the increase of astrocyte activity and edema as well as pro-inflammatory cytokines.