Brain research
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The psychobiological personality model of Cloninger distinguishes four heritable temperament traits (harm avoidance (HA), novelty seeking (NS), reward dependence (RD) and persistence (P)) and three character traits (self-directedness (SD), cooperativeness (CO) and self-transcendence (ST)) which develop during lifetime. Prior research already showed that individual differences in temperament are reflected in structural variances in specific brain areas. ⋯ The character traits correlated with GMV and WMV in the frontal, temporal and limbic regions involved in the corresponding cognitive tasks: self-reflection for SD, mentalizing and empathizing with others for CO and religious belief for ST. This study shows that individual variations in brain morphology can be related to the temperament and character dimensions, and lends support to the hypothesis of a neurobiological basis of personality traits.
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The effects of a sensorimotor task on ipsilateral primary motor cortex (ipsi-M1) excitability mediated via the transcallosal pathway, including the changes in short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF), were examined in ten right-handed subjects. Transcranial magnetic stimulation (TMS) was delivered to evoke a motor evoked potential (MEP) from the first dorsal interosseous (FDI). The test-TMS intensity was adjusted to around 120% of the resting motor threshold (rMT). ⋯ The MEPs evoked during the FM task were markedly increased compared with those evoked during the pFM task, and these effects were not dependent on the electromyographic activity of the FDI performing these tasks. SICI was significantly decreased during the FM task, indicating disinhibition of the ipsi-M1, and these effects were also noted when the subjects used their non-dominant hand. The present findings suggest that the differences between the effects of the FM and pFM tasks on ipsi-M1 excitability were caused by their property.
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This study examined the neuroprotective effects of magnesium-sulfate (MgSO(4)) on the cerebral blood flow (CBF) and extracellular glutamate concentration in an eleven vessel occlusion (11VO) rat model. Twenty-one male Sprague-Dawley rats (250-350g) were used for the 11VO ischemic model, which was induced by a 10-min transient occlusion. The animals were divided into 3 groups, including ischemic-induced animals (ischemia group), ischemic-induced and MgSO(4) treated animals (MgSO(4) group), and sham animals for comparison. ⋯ A significantly lower level of glutamate release was observed in the MgSO(4) group than in the ischemia group during the ischemic and reperfusion episode. Our staining results revealed a significant decrease in neuronal cell death in the hippocampus in the MgSO(4) group compared to the ischemia group. These results suggest that MgSO(4) is responsible for the protection of neuronal cells by suppressing the release of extracellular glutamate under ischemic conditions and the CBF response during the initial reperfusion period.
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Spinal cord injury (SCI) pain in humans is difficult to treat, and the lack of valid methods to measure behavior comparable to the complex human pain experience preclinically represents an important obstacle to finding better treatments for this type of central pain. The place escape/avoidance paradigm (PEAP) relies on the active choice of an animal between its natural preference for a dark environment or pain relief, and it has been suggested to measure the affective-motivational component of pain. We have modified the method to a T10 spinal cord contusion model (SCC) of at-level central neuropathic pain in Sprague-Dawley rats. ⋯ Third, we demonstrated a decrease in escape/avoidance behavior in response to treatment with the analgesic drug pregabalin. Thus, the PEAP may be applicable as a surrogate correlate of human pain. In conclusion, the primary finding in this study was a sensitivity to change in escape/avoidance behavior induced by pharmacological modulation with analgesics, supporting the use of the PEAP as a central outcome measure in preclinical SCI pain research.
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Reactive oxygen species and their detrimental effects on the brain after transient ischemia have been implicated in the pathogenesis of the ischemic injury. The Kelch-like ECH-associated protein 1 (Keap1)-nuclear factor erythroid 2-related factor 2 (Nrf2) system is currently recognized as the major cellular defense mechanism under oxidative stress, but the involvement of the Keap1-Nrf2 system in the ischemic brain injuries has not been fully investigated to date. In the present study, we investigated temporal changes of Keap1, Nrf2, and their downstream antioxidative proteins in post-ischemic mice brains with respect to spacial differences between the peri-infarct regions and the regions destined to infarct. ⋯ In the same peri-infarct region, downstream antioxidative proteins such as thioredoxin, glutathione, and heme oxygenase-1 showed significant increases at later time-points of 24-72 h of reperfusion after tMCAO. In the regions destined to infarct, a similar trend of expression changes to those in the peri-infarct regions was observed in Keap1, Nrf2, and 3 downstream antioxidative proteins with much less reactions. The changes found in this study suggest that the induced antioxidative stress proteins after cerebral ischemia may play an important endogenous neuroprotective response under oxidative stress after ischemic stroke.