Neuroscience letters
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Neuroscience letters · Feb 2010
Tapentadol, but not morphine, selectively inhibits disease-related thermal hyperalgesia in a mouse model of diabetic neuropathic pain.
Neuropathic pain in diabetic patients is a common distressing symptom and remains a challenge for analgesic treatment. Selective inhibition of pathological pain sensation without modification of normal sensory function is a primary aim of analgesic treatment in chronic neuropathic pain. Tapentadol is a novel analgesic with two modes of action, mu-opioid receptor (MOR) agonism and noradrenaline (NA) reuptake inhibition. ⋯ In contrast, 3.16 mg/kg morphine, the dose that resulted in full anti-hyperalgesic efficacy under diabetic conditions, produced significant anti-nociception in non-diabetic controls. Selective inhibition of disease-related hyperalgesia by tapentadol suggests a possible advantage in the treatment of chronic neuropathic pain when compared with classical opioids, such as morphine. It is hypothesized that this superior efficacy profile of tapentadol is due to simultaneous activation of MOR and inhibition of NA reuptake.
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Neuroscience letters · Feb 2010
Imipramine enhances cell proliferation and decreases neurodegeneration in the hippocampus after transient global cerebral ischemia in rats.
This study was aimed to determine whether imipramine chronic treatment promotes neurogenesis in the dentate gyrus (DG) and interferes with neuronal death in the CA1 subfield of the hippocampus after transient global cerebral ischemia (TGCI) in rats. After TGCI, animals were treated with imipramine (20mg/kg, i.p.) or saline during 14 days. 5-Bromo-2'-deoxyuridine-5'-monophosphate (BrdU) was injected 24h after the last imipramine or saline injection to label proliferating cells. In order to confirm the effect of TGCI on neuronal death and cell proliferation, a group of animals was sacrificed 7 days after TGCI. ⋯ Chronic imipramine treatment increased cell proliferation in the SGZ of DG and reduced the neurodegeneration in the CA1 of the hippocampus 14 days after TGCI. Immunohistochemistry for DCX detected an increased number of newly generated neurons in the hippocampal DG 14 days after TGCI, which was not affected by imipramine treatment. Further studies are needed to evaluate whether imipramine treatment for longer time would be able to promote survival of newly generated neurons as well as to improve functional recovery after TGCI.
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Neuroscience letters · Jan 2010
Perspective taking modulates event-related potentials to perceived pain.
Recent event-related brain potential (ERP) study disentangled an early automatic component and a late top-down controlled component of neural activities to perceived pain of others. This study assessed the hypothesis that perspective taking modulates the top-down controlled component but not the automatic component of empathy for pain by recording ERPs from 24 subjects who performed pain judgments of pictures of hands in painful or non-painful situations from either self-perspective or other-perspective. ⋯ Neural response to perceived pain over the central-parietal area was significantly reduced at 370-420 ms when performing the pain judgment task from other-perspective compared to self-perspective. The results suggest that shifting between self-perspectives and other-perspectives modulates the late controlled component but not the early automatic component of neural responses to perceived pain.
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Neuroscience letters · Jan 2010
Gamma-secretase inhibitor (GSI1) attenuates morphological cerebral vasospasm in 24h after experimental subarachnoid hemorrhage in rats.
Notch signaling plays an important role in the arteriogenesis. We hypothesized that the Notch inhibitor--gamma-secretase inhibitor (GSI1) exerted its effects on the vasospasm via regulation of NF-kappaB and MMP-9. In this study, 160 male Sprague-Dawley (SD) rats were randomly assigned into four groups: Sham, subarachnoid hemorrhage (SAH), SAH treated with dimethyl sulfoxide (DMSO) and SAH treated with GSI1. ⋯ Severe morphological vasospasm in the basilar artery was observed in SAH and DMSO treated rats. GSI1 significantly effected on neurological deficits, but not on mortality; significantly reduced morphological vasospasm, blood-brain barrier permeability, brain water content; significantly decreased the protein level of Notch1, NF-kappaB p50 and MMP-9, as well as the DNA-binding activity of NF-kappaB (EMSA) and the activity of MMP-9 (Zymography). These findings suggest that GSI1 plays a critical role in the attenuation of acute cerebral vasospasm, which may provide a novel therapeutic target for cerebral vasospasm after SAH insult.
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Neuroscience letters · Jan 2010
Insufficient sleep impairs driving performance and cognitive function.
Cumulative sleep deprivation may increase the risk of psychiatric disorders, other disorders, and accidents. We examined the effect of insufficient sleep on cognitive function, driving performance, and cerebral blood flow in 19 healthy adults (mean age 29.2 years). All participants were in bed for 8h (sufficient sleep), and for <4h (insufficient sleep). ⋯ The brake reaction time in a harsh-braking test was significantly longer after insufficient sleep than after sufficient sleep (546.2+/-23.0 vs. 478.0+/-51.2 ms, P<0.05). Whereas there were no significant correlations between decrease in oxyHb and the changes of cognitive function or driving performance between insufficient sleep and sufficient sleep. One night of insufficient sleep affects daytime cognitive function and driving performance and this was accompanied by the changes of cortical oxygenation response.