Neuroreport
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Case Reports
Deep brain stimulation of the anterior cingulate cortex: targeting the affective component of chronic pain.
Deep brain stimulation (DBS) has shown promise for relieving nociceptive and neuropathic symptoms of refractory chronic pain. We assessed the efficacy of a new target for the affective component of pain, the anterior cingulate cortex (ACC). A 49-year-old man with neuropathic pain underwent bilateral ACC DBS. ⋯ Stimulating the ACC at 130 Hz, 330 µs and 3 V facilitated neuropathic pain relief. The DBS remained efficacious during the 2-year follow-up period. Affective ACC DBS can relieve chronic neuropathic pain refractory to pharmacotherapy and restore quality of life.
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Our assumption that blood pressure (BP) in supratentorial hypertensive intracerebral hemorrhage patients does not differ significantly according to the hemispheric laterality has never been verified before. This study was carried out to explore the possibility of hemispheric BP differences and whether this might influence the outcomes. A review of the charts/radiographic images of 281 patients with putaminal/thalamic hemorrhages diagnosed within 6 h of symptom onset was performed. ⋯ Multivariate regression analysis showed that patients with SBPs of at least 220 mmHg were 2.9 times more likely to harbor left-sided hemorrhages. There were no significant intergroup differences in responsiveness to a continuous intravenous nicardipine infusion or 30-day mortality rates. Although the differences in BPs are unlikely to have influenced outcomes, future trials involving supratentorial hypertensive intracerebral hemorrhages may benefit from considering hemispheric differences in BP and other demographic variables.
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In this study, we examined the anti-inflammatory mechanism by which gabapentin attenuates morphine tolerance in rats. Gabapentin enhanced the antinociceptive effect of morphine and attenuated chronic morphine tolerance when administered intrathecally with morphine in naive rats. ⋯ In addition, the effects of gabapentin were reversed by coadministration of the anti-IL-10 antibody. Our findings indicate that enhancement of the antinociceptive effect of morphine by gabapentin may occur through upregulation of the anti-inflammatory cytokine IL-10 and inhibition of proinflammatory cytokines in the rat spinal cord.
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Re-exposure to morphine-associated environments elicits morphine-seeking behavior after a long period of withdrawal in rats with a history of morphine dependence. Adaptations in glutamate receptor 1 (GluR1) phosphorylation in limbic brain regions have been shown to occur during withdrawal from addictive drugs, such as cocaine, methamphetamine, and heroin. However, whether similar adaptations exist after spontaneous withdrawal from repeated morphine intake has not been studied. ⋯ Phosphorylation of GluR1 at Ser845, but not Ser831, increases in the nucleus accumbens and central amygdala from 1 to 10 days of withdrawal, and there were no changes in GluR1 phosphorylation at Ser845 or Ser831 in the hippocampal CA1 subregion from 1 to 10 days of withdrawal. Significant positive correlations between numbers of drug-seeking responses and GluR1 phosphorylation at Ser845 in the nucleus accumbens were found in individual animals. These results suggest that time-dependent and region-specific changes in phosphorylation of GluR1 at Ser845, but not Ser831, are involved in the drug-seeking behavior elicited by re-exposure to the morphine-associated context.
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Transient global ischemia induces selective hippocampal pyramidal neuronal death. Under conditions of severe ischemic hypoxia, hypoxia-inducible factor-1α (HIF-1α) induces apoptosis. Exendin-4 (Ex-4), the glucagon-like peptide-1 receptor (GLP-1R) agonist, provides neuroprotection against brain damage after cerebral ischemia. ⋯ These in-vivo results were confirmed in vitro in SH-SY5Y cells and primary cortical neurons treated with 100 nM of Ex-4 under hypoxic conditions (0.1%>O2). We found that Ex-4 decreased the HIF-1α expression in the SH-SY5Y cell line and primary cortical neurons under hypoxic conditions, and this effect was reversed by cotreatment with exendin (9-39), a GLP-1R antagonist. These results suggest that HIF-1α may be involved in the neuroprotective effect of Ex-4 in the hypoxia-damaged brain.