Brain research
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Human adolescents often consume alcohol in a binge-like manner at a time when changes are occurring within specific brain structures, such as the medial prefrontal cortex (mPFC) and the basolateral nucleus of the amygdala (BLN). In particular, the number of neurons and glia is changing in both of these areas in the rat between adolescence and adulthood (Markham et al., 2007; Rubinow and Juraska, 2009). The current study investigated the effects of ethanol exposure during adolescence on the number of neurons and glia in the adult mPFC and BLN in Long-Evans male and female rats. ⋯ In the adult mPFC, ethanol administration during adolescence resulted in a decreased number of glia in males, but not females, and had no effect on the number of neurons. Adolescent ethanol exposure had no effects on glia or neuron number in the BLN. These results suggest that glia cells in the prefrontal cortex are particularly sensitive to binge-like exposure to ethanol during adolescence in male rats only, potentially due to a decrease in proliferation in males or protective mechanisms in females.
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The objective of this study was to observe the pathophysiological time window of performing minimally invasive procedures for the intracerebral hematoma evacuation. Thirty-six rabbits were randomly placed in either a normal control group (NC group, 6 rabbits), a model control group (MC group, 6 rabbits) or a minimally invasive group (MI group, 24 rabbits). A model of intracerebral hemorrhage (ICH) was established in the MC and MI groups. ⋯ Performing minimally invasive procedures for evacuation of ICH in 6h showed the most remarkable decrease of the glutamate level, BBB permeability and BWC, followed by a significant difference observed at 12h within the MI subgroups. Performing minimally invasive procedures in early stages after ICH for the hematoma evacuation could decrease the perihematomal glutamate level, BBB permeability and BWC significantly. The pathophysiological time window of minimally invasive procedures for hematoma evacuation might be 6-12h after hemorrhage.
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Previous studies have demonstrated that fractalkine, a newly discovered chemokine, is implicated in spinal cord neuron-to-microglia activation signaling as well as mediation of neuropathic and inflammatory pain via its sole receptor CX3CR1, which is specifically expressed on microglia. However, whether it is involved in bone cancer pain (BCP) and the underlying mechanisms have not been elucidated. ⋯ Furthermore, we demonstrated that blockade of CX3CR1 suppressed the activation of microglia and the expression of p38 mitogen-activated protein kinase (MAPK) in the spinal cord in BCP rats. These results suggest a new mechanism of BCP, in which the microglia CX3CR1/p38 signaling cascade potentially plays an important role in facilitating pain processing in BCP rats.
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Administration of sevoflurane at the onset of reperfusion has been confirmed to provide a cerebral protection. However, little is known about the mechanism. In this study, we tested the hypothesis that sevoflurane postconditioning induces neuroprotection through the up-regulation hypoxia inducible factor-1α (HIF-1α) and heme oxygenase-1 (HO-1) involving phosphatidylinositol-3-kinase (PI3K)/Akt pathway. ⋯ Compared with the control group, sevoflurane postconditiong significantly ameliorated neuronal injury, up-regulated mRNA and protein levels of HIF-1α and HO-1, inhibited the activity of caspase-3, and decreased the number of TUNEL-positive cells and infarct sizes. However, the selective PI3K inhibitor, wortmannin not only partly eliminated the neuroprotection of sevoflurane as shown by reducing infarct size and apoptotic neuronal cells, but also reversed the elevation of HIF-1α, HO-1 and p-Akt expression in the ischemic penumbra induced by sevoflurane. Therefore, our data demonstrate that the cerebral protection from sevoflurane postconditioning is partly mediated by PI3K/Akt pathway via the up-regulation of HIF-1α and HO-1.
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Motor cortex stimulation (MCS) is a promising clinical procedure to help alleviate chronic pain. Animal models demonstrated that MCS is effective in lessening nocifensive behaviors. The present study explored the effects of MCS on cortical somatosensory evoked potentials (SEPs) recorded at the primary somatosensory cortex (SI) of the rat. ⋯ Application of naloxone completely prevented the inhibitory effect of MCS on ipsilateral SEPs. These results demonstrate that MCS blocked the transmission of somatosensory information to the primary somatosensory cortex, and this interference was mediated by the endogenous opioid system. This inhibitory effect on sensory transmission induced by MCS may reflect its antinociceptive effect.