Neuroscience letters
-
Neuroscience letters · May 2012
Neonatal electroencephalography shows low sensitivity to anesthesia.
This study examined EEG under clinical anesthesia in neonates and infants, to clarify how growth affects EEG during anesthesia. Subjects comprised 62 neonates and infants. Patients were divided into four groups according to age: Group 1 (neonates), <1 month; Group 2, 1-2 months; Group 3, 3-5 months; and Group 4, 6 months to 2 years. ⋯ Conversely, these processed EEG parameters in Group 1 showed little anesthesia-dependent change under sevoflurane concentrations between 0.5% and 2% (SEF90: 7.3 (1.2) Hz vs. 7.7 (2.1) Hz; BSR: 0.51 (0.20) vs. 0.62 (0.29); RBR: -1.00 (0.17) vs. -1.03 (0.27); ApEn: 0.32 (0.18) vs. 0.25 (0.14), respectively). The unique EEG features of neonates during anesthesia rapidly change to the usual anesthesia-dependent patterns seen in older children, with a boundary of 3-5 months old. In infants younger than 6 months old, neural network regulation reflected in EEG by anesthesia is weak.
-
Neuroscience letters · May 2012
Involvement of spinal monocyte chemoattractant protein-1 (MCP-1) in cancer-induced bone pain in rats.
In this study, we examined the involvement of chemokine monocyte chemoattractant protein-1 (MCP-1) in the spinal cord of a rat model of cancer-induced bone pain (CIBP). In this model, CIBP was established by an intramedullary injection of Walker 256 cells into the tibia of rats. ⋯ Likewise, an intrathecal injection of exogenous recombinant MCP-1 induced a striking mechanical allodynia in naïve rats. These results suggest that increases in spinal MCP-1 and CCR2 expression are involved in the development of mechanical allodynia associated with bone cancer rats.
-
Neuroscience letters · May 2012
Mutation analysis of LRRK2, SCNA, UCHL1, HtrA2 and GIGYF2 genes in Chinese patients with autosomal dorminant Parkinson's disease.
Autosomal dorminant Parkinson's disease (ADPD) has been associated with mutations in the SCNA, LRRK2, UCHL1, HtrA2 and GIGYF2 genes. We studied the prevalence of variants in all five genes in 12 Chinese unrelated families with ADPD and 4 families with both essential tremor (ET) and Parkinson's disease (PD) phenotypes using direct sequencing analysis. ⋯ However, no pathogenic mutations in the five genes were found in these families. Our result indicated that SCNA, LRRK2, UCHL1, HtrA2 and GIGYF2 genes' mutations might not be a main reason for Chinese ADPD.
-
Neuroscience letters · May 2012
TREK1 activation mediates spinal cord ischemic tolerance induced by isoflurane preconditioning in rats.
The aim of this study is to examine the role of one of the two-pore (2P) domain K(+) channels, TREK (TWIK-related K(+) channels, TREK)-1, mediated neuroprotection on spinal cord afforded by isoflurane preconditioning. In Experiment 1, male Sprague-Dawley rats were randomly assigned to control (Con) group, an isoflurane preconditioning (Iso) group, and sham group. Twenty-four hours after the last pretreatment, spinal cord ischemia was induced in Con and Iso groups. ⋯ Amiloride pretreatment abolished the protective effects of Iso preconditioning. These finding indicate that isoflurane preconditioning had a neuroprotective effect against spinal cord ischemia reperfusion injury. These effects may be mediated through the TREK1 pathway.
-
Neuroscience letters · Apr 2012
Evaluation of the effects of treatment with sAPPα on functional and histological outcome following controlled cortical impact injury in mice.
Treatment with sAPPα, the product of non-amyloidogenic processing of the amyloid precursor protein (APP) has been shown to be protective following diffuse traumatic brain injury (TBI), by improving motor outcome and reducing axonal injury. However the effects of treatment with sAPPα following a focal TBI have yet to be determined. ⋯ However the effect of treatment with sAPPα was not as dramatic as that seen previously following a diffuse injury. Nonetheless, these improvements in functional outcome were acompanied by a small but significant improvement in the amount of cortical and hippocampal at 7 days post-injury, and provide further support for the efficacy of sAPPα as a potential neuroprotective agent following TBI.