Brain research
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The objective of this study was to determine the relation between the chronic consumption of a high-fat diet (HFD) and antioxidants on long-term potentiation (LTP) in dentate gyrus (DG) of the adult rat hippocampus in vivo. Forty adult male Wistar rats were randomly assigned into five groups (N=6-8): control group consumed an ordinary diet; HFD group received HFD only; ANO group received HFD plus antioxidants; RHFD group received a restricted HFD (30% less fat than the HFD group); and RANO group received restricted HFD plus antioxidants. ⋯ The results showed that HFD decreased EPSP slope and PS amplitude with respect to the control group, whereas antioxidants increased these parameters compared to the control group. It was suggested that chronic HFD consumption can impair hippocampal LTP in the granular cells of the DG, and antioxidant supplementation reverses the impairment of synaptic plasticity induced in DG.
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Adult neurogenesis can be influenced by a variety of factors. Stress is one of the most potent inhibitors of hippocampal neurogenesis. Stress effects on adult hippocampal neurogenesis are affected differently by environmental factors, including social interaction. ⋯ Finally, to evaluate whether sexual experience alters adult hippocampal function, we tested learning and memory in a recognition memory task. The results demonstrated that sexual activity increased the expression of brain-derived neurotrophic factor, tyrosine kinase B, and cAMP response element-binding factor. Furthermore, the results supported the view that sexual interaction could be helpful for buffering adult hippocampal neurogenesis and recognition memory function against the suppressive actions of chronic stress.
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Earlier research has demonstrated that hyperbaric oxygen (HBO2) can produce an antinociceptive effect in models of acute pain. Recent studies have revealed that HBO2 can produce pain relief in animal models of chronic pain as well. The purpose of the present investigation was to ascertain whether HBO2 treatment might suppress allodynia in rats with neuropathic pain and whether this effect might be blocked by the opioid antagonist naltrexone (NTX). ⋯ These NTX-infused, HBO2-treated rats exhibited an allodynic response comparable to that exhibited by rats receiving nerve crush only. Analysis of the AUC data showed that HBO2 significantly reduced the nerve crush-induced allodynia; this anti-allodynic effect of HBO2 was reversed by NTX. These results implicate opioid receptors in the pain relief induced by HBO2.
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In this study we investigated the functional connectivity in 23 Mild TBI (mTBI) patients with and without memory complaints using resting state fMRI in the sub-acute stage of injury as well as a group of control participants. Results indicate that mTBI patients with memory complaints performed significantly worse than patients without memory complaints on tests assessing memory from the Automated Neuropsychological Assessment Metrics (ANAM). Altered functional connectivity was observed between the three groups between the default mode network (DMN) and the nodes of the task positive network (TPN). ⋯ Furthermore, an increased functional connectivity between the TPN and SN appears to be associated with reduced performance on memory assessments. Overall the results suggest that a disruption in the segregation of the DMN and the TPN at rest may be mediated through both a direct pathway of increased FC between various nodes of the TPN and DMN, and through an indirect pathway that links the TPN and DMN through nodes of the SN. This disruption between networks may cause a detrimental impact on memory functioning following mTBI, supporting the Default Mode Interference Hypothesis in the context of mTBI related memory deficits.
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Motor symptoms of Parkinson's disease are commonly treated using l-DOPA although long-term treatment usually causes debilitating motor side effects including dyskinesias. A putative source of dyskinesia is abnormally high levels of phosphorylated extracellular-regulated kinase (pERK) within the striatum. In animal models, the serotonin 1A receptor agonist ±8-OH-DPAT reduces dyskinesia, suggesting it may exhibit efficacy through the pERK pathway. ⋯ Neither compound alone affected motor cortex pERK. Surprisingly, in the ventromedial striatum, ±8-OH-DPAT potentiated l-DOPA-induced pERK; in the motor cortex, ±8-OH-DPAT potentiated pERK with l-DOPA or SKF81297. Our results support previous work that the striatal pERK pathway is dysregulated after dopamine depletion, but call into question the utility of pERK as a biomarker of dyskinesia expression.