Brain research
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Cyclosporin A (CsA) has been demonstrated to be neuroprotective in ischemic and traumatic brain injuries by inhibiting mitochondrial permeability transition pore (mPTP) opening, thereby maintaining mitochondrial homeostasis and inhibiting pro-apoptotic protein release. The effects of CsA on early brain injury (EBI) after subarachnoid hemorrhage (SAH), however, have not been investigated. This study was designed to explore the effects of CsA on apoptotic signaling pathways and EBI after experimental SAH using four equal groups (n=36) of adult male SD rats, including the sham group, SAH+vehicle group, SAH+CsA2 group, and SAH+CsA10 group. ⋯ Treatment with high dose (10mg/kg) CsA markedly decreased expressions of Cytochrome C, AIF, and cleaved caspase-3, and inhibited apoptosis pathways. Administration of CsA following SAH significantly ameliorated EBI, including cortical apoptosis, brain edema, blood-brain barrier (BBB) impairment, and neurobehavioral deficits. These findings suggest that early administration of CsA may ameliorate EBI and provide neuroprotection in the SAH model through potential mechanisms that include blockage of mPTP opening and inhibition of apoptotic cell death pathways.
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To assess developmental characteristics of nociceptive responses induced by bee venom (BV) injection in neonatal rats, we exposed pups to intra-plantar injection of various BV concentrations given at different time points between postnatal day 1 and day 28 (P1-P28). Persistent spontaneous nociception (PSN) as well as thermal and mechanical nociceptive response was compared before and after a BV injection. There were distinct age-related changes in the baseline paw withdrawal thermal latency (PWTL) and paw withdrawal mechanical threshold (PWMT) when examined on P1, P4, P7, P14, P21, and P28. ⋯ Neonatal rats receiving intra-plantar BV injection showed a time-dependent change in nociceptive responses, including (1) a dose-related increase in PSN from P1 to P28; (2) a non-specific decrease (indistinguishable between saline and BV injection) in PWTL and PWMT up to P14 and P21, respectively; and (3) a specific decrease (in response to BV injection only) in PWTL and PWMT after P14 and P21, respectively. These findings indicate that characteristic changes in the baseline and BV-induced nociceptive response are both time-dependent and modality-specific in neonatal rats. The data reveal a critical postnatal period during which nociceptive stimulation could have a significant influence on nociceptive behavior in adult rats and suggest that preclinical models of neonatal nociception should be evaluated according to different postnatal time points.
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Previous neuroimaging studies have shown that implicit and explicit processing of self-relevant (schematic) material elicit activity in many of the same brain regions. Electrophysiological studies on the neural processing of explicit self-relevant cues have generally supported the view that P300 is an index of attention to self-relevant stimuli; however, there has been no study to date investigating the temporal course of implicit self-relevant processing. The current study seeks to investigate the time course involved in implicit self-processing by comparing processing of self-relevant with non-self-relevant words while subjects are making a judgment about color of the words in an implicit attention task. ⋯ Results showed that latency of P2 component, which indexes the time required for perceptual analysis, was more prolonged in processing self-relevant words compared to processing non-self-relevant words. Our results suggested that the judgment of the color of the word interfered with automatic processing of self-relevant information and resulted in less efficient processing of self-relevant word. Together with previous ERP studies examining processing of explicit self-relevant cues, these findings suggest that the explicit and the implicit processing of self-relevant information would not elicit the same ERP components.
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Previous studies showed the role of basolateral amygdala (BLA) in cannabinoid-induced antinociception. Furthermore, the nucleus accumbens (NAc) plays an important role in mediating the suppression of pain in animal models. The present study extended the role of dopamine receptors within the NAc in antinociceptive effect of cannabinoid receptor agonist, WIN55,212-2, microinjected into the BLA following the tail-flick and formalin tests in rats. ⋯ Our findings showed that intra-accumbal SCH-233909 dose-dependently prevented antinociception induced by intra-BLA administration of WIN55,212-2 (15 μg/rat) in time set intervals in formalin, but not tail-flick test. Besides, administration of sulpiride in the NAc could affect WIN-induced analgesia in both models of pain. In conclusion, it seems that D2 receptors located in the NAc, in part, mediate the antinociceptive responses of cannabinoid within the BLA, while D1 receptors only are involved in modulation of persistent inflammatory model of pain.
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Friedreich's ataxia (FRDA) is the most common form of hereditary ataxia. In addition to proximal spinal cord and brain stem atrophy, mild to moderate atrophy of the cerebellum has been reported in advanced FRDA. The aim of this study was to examine dysfunction in motor-related areas involved in the execution of finger tapping tasks in individuals with FRDA, and to investigate functional re-organization of cortico-cerebellar, cortico-striatal and parieto-frontal loops as a result of the cerebellar pathology. ⋯ Although the pattern of the BOLD signal from the putamen was different during the self-paced regular finger tapping task to the other tasks in controls, in individuals with FRDA there was no distinction of the signal between the tasks suggesting that primary cerebellar pathology may cause secondary basal ganglia dysregulation. While individuals with FRDA tapped at a slightly lower rate (0.59Hz) compared with controls (0.74Hz) they showed significantly decreased activity of the SMA and the inferior parietal lobule, which may suggest disruption to the fronto-parietal connections. These findings suggest that the motor impairments in individuals with FRDA result from dysfunction extending beyond the spinal cord and cerebellum to include sub-cortical and cortical brain regions.