DATA SYNTHESIS: The effects of rehabilitation training are related with the expressions of endogenous cerebral protective factor fos immediate early gene, calcitonin gene-related peptide, heat shock protein, glial fibrillary acidic protein, growth associated protein 43, N-methyl-D-aspartate receptor, nitricoxide synthase, proliferating cell nuclear antigen, S-100 albumen, nidogen, brain-derived neurotrophic factor and tubulin.
During cerebral ischemia,N-methyl-D-aspartate receptor(NMDA-R),especially NR2B subunit,changes its struc- ture and function via tyrosine or serine/threonine phosphorylation,and activates the downstream signal pathways to induce excitatory neurotoxicity and cell apoptosis.
N-Methyl-D-Aspartate(NMDA) ,a special nervous mediator, is reported to have close relationship with overflow of ca2+ , which in turn increase the production of free radicals, worsen brain edema,eventurally cause the death of neurons.
Results cDNA microarray analysis showed that the mRNA expression of PSD-93, which correlated with the function of N-methyl-D-aspartate receptors (NMDARs)-nitric oxide (NO) signal transduction pathway, was significantly higher in epilepsy patients than those in the control group. The results of RT-PCR were consistent with the cDNA microarray data.
To define the role of MAPK-dependent transcription in the amnesic property of anesthetics, we conducted a series of studies to examine the effect of a prototype intravenous anesthetic propofol on the MAPK response to N-methyl-D- aspartate receptor (NMDAR) stimulation in hippocampal neurons.
The N-methyl-D-aspartate receptor (NMDAR) plays a pivotal role in the process of glutamate-induced excitotoxicity associated with many neurological disorders including stroke, epilepsy, traumatic brain injury and some neurodegenerative diseases, et al.
Background: The N-methyl-D-aspartate receptor (NMDAR) plays a pivotal role in the process of glutamate-induced excitotoxicity associated with many neurological disorders including stroke, epilepsy, traumatic brain injury and some neurodegenerative diseases.
ve: Using the rat complex partial seizure model induced by kainate, we evaluated the distribution and density of N-methyl-D-aspartate receptor type I (NMDAR1) in the vulnerable brain areas including hippocampus and dentate gyrus, and aimed to find out the antiepileptic mechanisms of vagus nerve stimulation (VNS).
During cerebral ischemia,N-methyl-D-aspartate receptor(NMDA-R),especially NR2B subunit,changes its struc- ture and function via tyrosine or serine/threonine phosphorylation,and activates the downstream signal pathways to induce excitatory neurotoxicity and cell apoptosis.
N-Methyl-D-Aspartate(NMDA) ,a special nervous mediator, is reported to have close relationship with overflow of ca2+ , which in turn increase the production of free radicals, worsen brain edema,eventurally cause the death of neurons.
Results cDNA microarray analysis showed that the mRNA expression of PSD-93, which correlated with the function of N-methyl-D-aspartate receptors (NMDARs)-nitric oxide (NO) signal transduction pathway, was significantly higher in epilepsy patients than those in the control group. The results of RT-PCR were consistent with the cDNA microarray data.
To define the role of MAPK-dependent transcription in the amnesic property of anesthetics, we conducted a series of studies to examine the effect of a prototype intravenous anesthetic propofol on the MAPK response to N-methyl-D- aspartate receptor (NMDAR) stimulation in hippocampal neurons.
The effects of intracerebroventricular (icv) agonists and antagonists of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors on the general anesthesia of propofol were studied.
Activation of rat cerebellum granule cells by N-methyl-D-aspartate (NMDA, 10-4-10-3 M) results in progressive increase in reactive oxygen species (ROS) and suppression of the ouabain-sensitive part of Na/K-ATPase activity.
Objective: To study the effect of glycine site/NMDA (N-methyl-D-aspartate) receptor antagonist MRZ2/576 on the conditioned place preference (CPP) and locomotor activity induced by morphine in mice.
Background and purpose A low-affinity, use-dependent N-Methyl-D-Aspartate (NMDA) antagonist AR-R15896AR has neuroprotective properties in animal models of ischaemic stroke.
Rats after cerebral ischemia and reperfusion were treated with MK-801.It was found that MK-80l could block the combination of the excitatory amino acids with N-methyl-D-aspartate receptors and protect the respiratory capacity of the brain mitochondria.These findings suggest that the administration of MK-801 is able to improve the cerebral mitochondrial respiratory capacity.
Using in situ hybridization method, alteration of the mRNA concentration of both the preprocholecystokin(PCCK) and preproenkephalin(PPE) after rat brain injury and the mechenism of this trauma inducing change in neuropeptide neuropeptide gene expression were analysed. The results showed that 48h after in jury of the rat brain,the concentration of mRNA coding for PPE,and PCCK was increased significantly in ipsilateral side specially in the cortical area,hippocampus.The ketamine, a N-meth...
AIM:To study the changes of hippocampal quinolinic acid (QA) concentrations during acute and chronic seizures induced by ip injection of kainic acid (KA, 12 mg kg-1) in rats. METHODS:The extraction and measurement of QA in the hippocampus were performed using a gas chromatography-mass spectrometry method. RESULTS:When acute seizures were fully established 3 h after KA injection, no significant changes of hippocampal QA were found. During,chronic seizures observed on d 30 after KA inj...