Brain research
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Exercise can increase neurogenesis and affect gene expression in the brains of adult rats. Little is known about how exercise intensity affects neurogenesis and associated gene expression in juvenile rats. ⋯ The low-, but not the high-, intensity exercise paradigm resulted in significantly increased expression of BDNF, NMDAR1, and Flk-1 mRNA. Gene expression levels in the low-intensity exercise group were greater than the high-intensity group for these four molecules.
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The present study examined the hypothesis that cerebral ischemic tolerance induced by hyperbaric oxygen preconditioning (HBO-PC) is associated with an increase of antioxidant enzyme activity. Male Sprague-Dawley rats (250-280 g, n=74) were divided into sham, middle cerebral artery occlusion (MCAO) for 90 min, and MCAO plus HBO-PC groups. HBO-PC was conducted four times by given 100% oxygen at 2.5 atmosphere absolute (ATA), for 1 h at every 12 h interval for 2 days. ⋯ Malondialdehyde (MDA) content, activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) sampled from the hippocampus, ischemic penumbra or core of cortex were measured. HBO-PC decreased mortality rate, improved neurological recovery, lessened neuronal injury, reduced the level of MDA and increased the antioxidant activity of CAT and SOD. These observations demonstrated that an upregulation of the antioxidant enzyme activity by HBO preconditioning plays an important role in the generation of tolerance against brain ischemia-reperfusion injury.
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The present study was undertaken to investigate whether celecoxib could regulate the tetrodotoxin-resistant (TTX-R) sodium channel current in rat dorsal root ganglia (DRG) and whether prostaglandin E2 (PGE2) and calcitonin gene-related protein (CGRP) were involved in celecoxib's analgesia during acute incisional pain. Seventy-five rats were randomly allocated into three groups. Group A was the control group receiving a placebo (sugar pill) 1 h before and 12 h after surgery (right hind paw incisional pain). ⋯ The results showed both of a decrease in mechanical withdrawal thresholds and an increase of TTX-R sodium channel current density in DRG neurons in group B were significantly lower than those of group A at 24 h and 48 h after the operation (P<0.05). The increase in PGE2 and CGRP concentrations at incisional paw tissue and DRG neurons in group B were lower than those of groups A at 24 h and 48 h after the operation (P<0.05). This study indicates that: 1) celecoxib can inhibit TTX-R sodium channel current density in rat DRG neurons; 2) PGE2 and CGRP participate in celecoxib's analgesic effect on acute incisional pain.
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Peripheral nerve injury in animals can cause neuropathic pain often expressed in the form of hyperalgesia and allodynia. Spinal nerve ligation, in which the fifth and sixth lumbar (L5 and L6) or only the L5 spinal nerve is ligated and cut, is a model commonly used to produce neuropathic pain. The purpose of the present study was to test whether there is any anatomical evidence to support the suggestion that terminating unmyelinated (C) fibres of injured and adjacent uninjured nerves interact at the level of the spinal dorsal horn. ⋯ This suggests that neurons located in regions of overlap receive input from both L4 (intact) and L5 (injured) afferents. Consequently, spinal neurons located in regions of terminal overlap may show augmented responses to activation of the intact L4 nerve due to neuronal sensitisation resulting from injury to the adjacent L5 nerve. This may in part provide an anatomical basis for hyperalgesic reaction to injury.
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SCS is used to improve peripheral circulation in selected patients with ischemia of the extremities. However the mechanisms are not fully understood. The present study investigated whether blockade of ERK and AKT activation modulated SCS-induced vasodilation. ⋯ These data suggest that ERK and AKT pathways are involved in SCS-induced vasodilation.