Behavioural brain research
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Co-infusion of ultra-low dose naloxone and morphine attenuates morphine tolerance through the prevention of mu opioid receptor-Gs protein coupling. We previously demonstrated that chronic intrathecal infusion of morphine leads to tolerance and spinal neuroinflammation. The aim of present study was to examine the possible mechanisms by which ultra-low dose naloxone modulates spinal neuroinflammation, particularly the role of anti-inflammatory cytokine interleukin 10 (IL-10). ⋯ The increase of IL-10 protein and mRNA were 1.5- and 3-fold, respectively, compared to that in morphine-infused rat spinal cords. A combination of daily rrIL-10 (1 microg) injection with morphine infusion produced, in a less potent, preservative antinociception and inhibited pro-inflammatory cytokine production compared to ultra-low dose naloxone co-infusion, and the effect of ultra-low dose naloxone co-infusion was inhibited by daily intrathecal anti-rat IL-10 antibody injection. These results demonstrate that IL-10 contributes to the attenuation of pro-inflammatory cytokine expression caused by ultra-low dose naloxone/morphine co-infusion and thus the attenuation of morphine tolerance.
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In humans, fluctuating hormone levels throughout the menstrual cycle are believed to regulate many cyclical sexual behaviors and motivational processes. However, there is a dearth of research investigating the neural correlates of this phenomenon. We used functional magnetic resonance imaging to identify brain regions involved in sexual arousal's regulatory process. ⋯ Tripled two-group differences analysis revealed that significant activation in the comparison was observed in non-ovulatory phases of the menstrual cycle in parts of the right inferior frontal gyrus, right lateral occipital cortex, and left postcentral gyrus, as well as in the bilateral superior parietal lobule. Thus, our results indicate that brain activity differs in the ovulatory phase of the menstrual cycle compared to during other menstrual phases. This finding provides neurological evidence for the ovulatory cycle's modulation of the processing of the sexual arousal in female human brain.
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More intelligent persons (high IQ) typically present a higher cortical activity during tasks requiring the encoding of visuo-spatial information, namely higher alpha (about 10 Hz) event-related desynchronization (ERD; Doppelmayr et al., 2005). The opposite is true ("neural efficiency") during the retrieval of the encoded information, as revealed by both lower alpha ERD and/or lower theta (about 5 Hz) event-related synchronization (ERS; Grabner et al., 2004). To reconcile these contrasting results, here we evaluated the working hypothesis that more intelligent male subjects are characterized by a high cortical activity during the encoding phase. ⋯ This was not true for parietal counterpart of these EEG rhythms. These results reconcile previous contrasting evidence confirming that more intelligent persons do not ever show event-related cortical responses compatible with "neural efficiency" hypothesis. Rather, their cortical activity would depend on flexible and task-adapting features of frontal activation.
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Whereas acute stress often results in analgesia, chronic stress can trigger hyperalgesia/allodynia. This influence of long-term stress on nociception is relevant to numerous painful pathologies, such as fibromyalgia (FM), characterized by diffuse muscular pain (hyperalgesia) and/or tenderness (allodynia). Hence, there is a need for pre-clinical models integrating a chronic-stress dimension to the study of pain. ⋯ This stress also resulted in mechanical allodynia in the von Frey filaments model (60% decrease in threshold during week 2-5). However, such a stress regimen had no influence in the Randall-Selitto test of mechanical hyperalgesia, and in the tail immersion models of cold (4 degrees C) or hot (48 degrees C) thermal hyperalgesia, as well as cold (15 degrees C) allodynia. This model of prolonged/intermittent restraint stress may be useful in investigating the mechanisms linking stress and pain, and provide an assay to assess the potential therapeutic efficacy of drugs targeted against painful pathologies with a strong stress component, including but not restricted to FM.
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Depression and anxiety tend to be the most prevalent conditions among the multitude of neurobehavioural disorders which cause distress in the survivors of traumatic brain injury (TBI). The objective of the present investigation was to examine depression-like and anxiety-like behaviour of rats following diffuse TBI. Impact accelerated TBI was induced in anaesthetised rats by a modified weight drop method. ⋯ Chronic escitalopram (10 and 20 mg/kg) treatment significantly attenuated the TBI associated behavioural deficits. In conclusion, the aforesaid behavioural anomalies observed in TBI rats are analogous to comorbid anxiety and depression in humans. These findings substantiate the TBI rats as a candidate model of comorbid anxiety and depression.