Neuroscience
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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.
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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.
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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.
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Some evidence has shown an increased number of activated microglial cells in patients with schizophrenia. It is hypothesized that activated microglia may contribute to the pathogenesis of schizophrenia. We injected saline or Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) into the ventral hippocampus in adult Sprague-Dawley rats via micro-pump; at the same time, the rats were intragastrically administrated with saline or minocycline once a day for 14 consecutive days. ⋯ Minocycline was able to ameliorate deficits of social interaction and PPI but not hyperlocomotion. Minocycline was also able to inhibit the microglial activation. In conclusion, intrahippocampal administration of GM-CSF in adult rats may serve as a potential schizophrenia animal model, which may be related with the microglia hypothesis of schizophrenia.
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Electrical stimulation of the vagus nerve attenuates tumor necrosis factor (TNF) synthesis by macrophages and reduces the systemic inflammatory response. Current evidence suggests that the α7 nicotinic acetylcholine receptor present in the celiac/superior mesenteric ganglia is a key component in vagus nerve signaling to the spleen; however, there is currently no direct anatomical evidence that the α7 receptor is present in the murine celiac/superior mesenteric ganglia. ⋯ Double-labeling for α7 and tyrosine hydroxylase shows that α7 receptor protein is present on noradrenergic neurons within the ganglia and prejunctionally on noradrenergic nerve fibers within the spleen. The α7 receptor in the ganglia provides a possible location for the action of α7-selective agonists, while prejunctional α7 receptor expressed on splenic nerves may induce an increase in norepinephrine release in a positive feedback system enhanced by lymphocyte-derived acetylcholine.