Neuroscience letters
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Neuroscience letters · Nov 2005
Regulation of calcitonin gene-related peptide and TRPV1 in a rat model of osteoarthritis.
Pain in osteoarthritis (OA) remains an intractable problem in a majority of patients, with many of the commonly prescribed analgesics providing insufficient relief and considerable side effects. However, the structural or mechanistic cause of OA pain is still unknown. Animal models to address this issue have only recently been established, with much of the research to date focused on tissue pathology rather than pain. ⋯ Expression of calcitonin gene-related peptide (CGRP) and the vanilloid receptor TRPV1 was quantified in these backlabelled cells and was enriched in the knee afferents in all animals studied, compared to the expression in neurons across the whole dorsal root ganglia (DRG). Analysis of the backlabelled population in the osteoarthritis model and controls showed an increase in both CGRP and TRPV1 expression in the iodoacetate model compared with control animals. Therefore, there is a potential role for CGRP and TRPV1 in the manifestation of pain behaviour accompanied by OA changes in the knee in the iodoacetate induced model.
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Neuroscience letters · Nov 2005
Fenofibrate, a peroxisome proliferator-activated receptor alpha agonist, exerts neuroprotective effects in traumatic brain injury.
Peroxisome proliferator-activated receptor alpha (PPARalpha) has been demonstrated to reduce inflammation in various inflammatory diseases. As traumatic brain injury (TBI) caused a neuroinflammatory response, we examined the effect of fenofibrate, a PPARalpha agonist, on the post-traumatic consequences caused by lateral fluid percussion of brain in rats. The effects of fenofibrate (50 and 100mg/kg) were evaluated on the consequences of TBI in the early phase (6 and 24h) and the late phase (7 days) after TBI. ⋯ The present data represents the first demonstration that fenofibrate, a PPARalpha agonist, exerts neuroprotective effects in TBI. The activation of receptor PPARalpha could be beneficial by counteracting the deleterious inflammatory response following TBI. This suggests that PPARalpha activation could be a new and promising therapeutic strategy for the treatment of brain trauma.
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Neuroscience letters · Nov 2005
Early T1- and T2-weighted MRI signatures of transient and permanent middle cerebral artery occlusion in a murine stroke model studied at 9.4T.
Early reperfusion following stroke results in reduced tissue injury. Paradoxically, restoration of blood flow under certain conditions may also cause delayed neuronal damage (reperfusion injury). The interrelationship of changes in T1, T2 and diffusion weighted images of tissue water were studied in mouse models of permanent and transient focal cerebral ischemia. ⋯ In contrast to permanent MCAO, there were increases in T2 (P<0.001) in the infarct area present in the reperfusion phase within 90 min of transient MCAO. There was considerable infarct growth at 24h (P<0.001). This study demonstrates that following either type of occlusion there are early increases in T1 suggesting an elevated water content in the stroke lesion, while only following transient MCAO are there early increases in T2, indicative of early vasogenic oedema with breakdown of the blood-brain barrier.
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Neuroscience letters · Oct 2005
Volatile anesthetics disrupt frontal-posterior recurrent information transfer at gamma frequencies in rat.
We seek to understand neural correlates of anesthetic-induced unconsciousness. We hypothesize that cortical integration of sensory information may underlie conscious perception and may be disrupted by anesthetics. A critical role in frontal-posterior interactions has been proposed, and gamma (20-60 Hz) oscillations have also been assigned an essential role in consciousness. ⋯ Transfer entropy was calculated from 1-s wavelet-transformed ERPs. We found that (1) feedforward transfer entropy (FF-TE) and feedback transfer entropy (FB-TE) were balanced in conscious-sedated state; (2) anesthetics at concentrations producing unconsciousness augmented both FF-TE and FB-TE at 30 Hz but reduced them at 50 Hz; (3) reduction at 50 Hz was more pronounced for FB-TE, especially between frontal and posterior regions; (4) at high concentrations, both FF-TE and FB-TE at all frequencies were at or below conscious-sedated baseline. Our findings suggest that inhalational anesthetics preferentially impair frontal-posterior FB information transfer at high gamma frequencies consistent with the postulated role of frontal-posterior interactions in consciousness.
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Neuroscience letters · Oct 2005
Isoflurane preconditioning protects motor neurons from spinal cord ischemia: its dose-response effects and activation of mitochondrial adenosine triphosphate-dependent potassium channel.
We examined in a rabbit model of transient spinal cord ischemia (SCI) whether isoflurane (Iso) preconditioning induces ischemic tolerance to SCI in a dose-response manner, and whether this effect is dependent on mitochondrial adenosine triphosphate-dependent potassium (K(ATP)) channel. Eighty-six rabbits were randomly assigned to 10 groups: Control group (n=8) received no pretreatment. Ischemic preconditioning (IPC) group (n=8) received 5 min of IPC 30 min before SCI. ⋯ Iso 3 group showed a better neurologic outcome and more VMNCs than Iso 1 group (p<0.05). And, the Iso 1, Iso 2 and Iso 3 groups showed a better neurologic outcome and higher VMNC numbers than the corresponding Iso 1HD, Iso 2HD and Iso 3HD groups (p<0.05). This study demonstrates that Iso preconditioning protects the spinal cord against neuronal damage due to SCI in a dose-response manner via the activation of mitochondrial K(ATP) channels.