Neuroscience letters
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Neuroscience letters · Aug 2007
Measure of the electroencephalographic effects of sevoflurane using recurrence dynamics.
This paper proposes a novel method to interpret the effect of anesthetic agents (sevoflurane) on the neural activity, by using recurrence quantification analysis of EEG data. First, we reduce the artefacts in the scalp EEG using a novel filter that combines wavelet transforms and empirical mode decomposition. ⋯ Finally, a pharmacokinetic and pharmacodynamic (PKPD) model is built to describe the relationship between the concentration of sevoflurane and the processed EEG measure ('determinism' of the recurrence plot). A test sample of nine patients shows the recurrence in EEG data may track the effect of the sevoflurane on the brain.
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Neuroscience letters · Aug 2007
A new model of severe neurogenic pulmonary edema in spinal cord injured rat.
We describe a new model of neurogenic pulmonary edema in spinal cord injured Wistar male rats. The pulmonary edema was elicited by an epidural thoracic balloon compression spinal cord lesion, performed under a low concentration of isoflurane (1.5 or 2%) in air. Anesthesia with 1.5% isoflurane promoted very severe interstitial and intraalveolar neurogenic pulmonary edema with a significantly increased thickness of the alveolar walls and massive pulmonary hemorrhage. ⋯ Anesthesia with 2% isoflurane promoted severe interstitial and intraalveolar neurogenic pulmonary edema with less thickening of the alveolar walls and pulmonary hemorrhage. For evoking severe neurogenic pulmonary edema in spinal cord injured rats, 2% isoflurane anesthesia would be more suitable. However, if very severe neurogenic pulmonary edema needs to be evoked, spinal cord injury under 1.5% isoflurane anesthesia could be used, but one-third of the animals will be lost.
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Neuroscience letters · Jul 2007
Expression of oligodendrocyte myelin glycoprotein and its receptor NgR after the injury of rat central nervous system.
Oligodendrocyte myelin glycoprotein (OMgp) is one kind of myelin-derived inhibitor, which strongly inhibits axonal regeneration through binding to its receptor NgR after the injury to the adult central nervous system (CNS). However, expression of OMgp and NgR after the adult spinal cord injury (SCI) remains unclear. Study on these problems will help to understand more comprehensively about the functions of these proteins in CNS during regeneration. ⋯ We also found that the expression of OMgp is not limited in oligodendrocytes and its receptor NgR is not limited in neurons. They both can be expressed by these two kinds of cells. The roles of these factors in CNS regeneration require further study.
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Neuroscience letters · Jun 2007
Intracellular delivery of Neuroglobin using HIV-1 TAT protein transduction domain fails to protect against oxygen and glucose deprivation.
Neuroglobin (Ngb) is a heme protein that is primarily localised in the retina and the brain. Its physiological role is largely unknown. It has been reported that its overexpression protects neurons from hypoxia in vitro and in vivo, suggesting that the rapid modulation of the Ngb level in the nerve cells may be a promising stroke treatment strategy. ⋯ In both cell types, however, the treatment with the TAT-Ngb fusion protein did not show any effect on cell viability. This discrepancy to earlier reports might be due to the experimental model for oxygen glucose deprivation we employed. Alternatively, intracellular delivery of Ngb by the TAT/CPP might not have beneficial effects in the treatment of ischemic pathology.
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Neuroscience letters · Jun 2007
Differential regulation of glutamate receptors in trigeminal ganglia following masseter inflammation.
The present study examined whether N-methyl-D-aspartate receptor (NMDAR), 5-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunits and group I metabotropic glutamate receptors (mGluRs) are constitutively expressed in trigeminal ganglia (TG) using Western blot analysis in male Sprague-Dawley rats. We then investigated whether experimental induction of masseter inflammation influences glutamate receptor expressions by comparing the protein levels from naïve rats to those from complete Freund's adjuvant (CFA) inflamed rats. Our results showed that NMDAR1 (NR1), NMDAR2A (NR2A), NMDAR2B (NR2B), AMPAR1 (GluR1) and AMPAR2 (GluR2) subunits, and group I metabotropic glutamate receptor, mGluR5, are constitutively expressed in TG. ⋯ The level of mGluR5 protein was significantly up-regulated in TG 3 days after CFA-induced masseter inflammation. There were no inflammation-induced changes in any of the proteins we analyzed in the contralateral, non-inflamed TG. These results suggested that muscle inflammation differentially modulates glutamate receptor subunits at the primary afferent level in male rats and that these inflammation-induced transcriptional changes may contribute to functionally different aspects of craniofacial muscle pain.