No abstract available.
Animals ; Brain* ; Excitatory Amino Acids* ; N-Methylaspartate* ; Rats* ; Receptors, Glutamate* ; Receptors, N-Methyl-D-Aspartate*

Excitatory Amino Acids ; secretion ; Humans ; Neurotransmitter Agents ; secretion ; Pain, Postoperative ; etiology ; metabolism ; prevention & control

BACKGROUNDS: The importance of toxic extracellular levels of excitatory amino acids, as well as of high extracellular levels of inhibitory amino acids, is considered to be related with the pathophysiology of neuronal cell loss during cerebral ischemia. METHODS: The extracellular concentration of glutamate, glycine, and taurine in the hippocampus were determined during and after transient global ischemia in the New Zealand white rabbit. Because the cerebroprotective effects of profound hypothermia are well known and clinically widely used,we used the hypothermia group as an experimental group compared with normothermic control group in the experimental protocol. To derive a quantitative descriptor reflecting the magnitude of amino acid neurotransmitter changes with ischemia, we defined the 'taurine index' as: [glutamate]x[glycine]/[taurine]. RESULTS: Ischemia led to large increases in both excitatory (glutamate and glycine) and inhibitory amino acids(taurine) in the normothermic group. Taurine index was increased during ischemia and after reperfusion and had a close relationship with the severity of ischemia-induced neuronal damage. CONCLUSIONS: The taurine index appears to be a reliable biochemical marker to determine the severity of ischemic injury.
Amino Acids ; Biomarkers ; Brain Ischemia ; Excitatory Amino Acids ; Glutamic Acid ; Glycine ; Hippocampus ; Hypothermia ; Ischemia ; Neurons ; Neurotransmitter Agents ; New Zealand ; Reperfusion ; Subject Headings ; Taurine*

During operations, neurosurgeons usually perform multiple temporary occlusions of parental artery, possibly resulting in the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this study, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model to compare between single occlusion and repeated transient occlusions within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. From real time monitoring of glutamate release in 11 VO model, the change of extracellular glutamate level in repeated transient occlusion group was smaller than that of single occlusion group, and the onset time of glutamate release in the second ischemic episode of repeated occlusion group was delayed compared to the first ischemic episode which was similar to that of single 10 min ischemic episode. These results suggested that repeated transient occlusion induces less glutamate release from neuronal cell than single occlusion, and the delayed onset time of glutamate release is attributed to endogeneous protective mechanism of ischemic tolerance.
Arteries ; Biosensing Techniques ; Brain Ischemia ; Excitatory Amino Acids ; Glutamic Acid ; Glycosaminoglycans ; Humans ; Ischemia ; Laser-Doppler Flowmetry ; Neurons ; Parents

Animals ; Brain ; metabolism ; Codonopsis ; Excitatory Amino Acids ; metabolism ; Female ; Hypoxia ; metabolism ; Male ; Mice ; Mice, Inbred Strains ; Selenium ; pharmacology

Periventricular white matter damage is one of the characteristics of brain damage in preterm infants, and it is the most important type of encephalopathy. The pathological changes including the white matter of coagulation necrosis, oligodendrocyte damage, myelin damage, axonal injury and reactive gliosis and microglia infiltration in necrotic areas. All of these lesions are closely related to the nervous system sequelae in later-neonatal period. The pathogenesis of periventricular leukomalacia in premature infants are mainly cause by its immature brain vascular, and precursor oligodendrocytes of the attack of hypoxia, ischemia, infection, oxygen free radicals, inflammatory cytokines, increasing glutamate, and other high-risk factors. In this paper, an overview of progress in the study of the pathogenesis of periventricular white matter damage in premature infants through literature review to provide a theoretical support for clinical prevention, diagnosis and treatment.
Apoptosis ; Cerebrovascular Circulation ; Cytokines ; physiology ; Excitatory Amino Acids ; toxicity ; Humans ; Infant, Newborn ; Infant, Premature ; Leukomalacia, Periventricular ; classification ; etiology ; Risk Factors

Magnesium ion is known to selectively block the N-methyl-D-aspartate (NMDA)-induced responses and to have anticonvulsive action, neuroprotective effect and antinociceptive action in the behavioral test. In this study, we investigated the effect of Mg2+ on the responses of dorsal horn neurons to cutaneous thermal stimulation and graded electrical stimulation of afferent nerves as well as to excitatory amino acids and also elucidated whether the actions of Ca2+ and Mg2+ are additive or antagonistic. Mg2+ suppressed the thermal and C-fiber responses of wide dynamic range (WDR) cell without any effect on the A-fiber responses. When Mg2+ was directly applied onto the spinal cord, its inhibitory effect was dependent on the concentration of Mg2+ and duration of application. The NMDA- and kainate-induced responses of WDR cell were suppressed by Mg2+, the NMDA-induced responses being inhibited more strongly. Ca2+ also inhibited the NMDA-induced responses current-dependently. Both inhibitory actions of Mg2+ and Ca2+ were additive, while Mg2+ suppressed the EGTA-induced augmentation of WDR cell responses to NMDA and C-fiber stimulation. Magnesium had dual effects on the spontaneous activities of WDR cell. These experimental findings suggest that Mg2+ is implicated in the modulation of pain in the rat spinal cord by inhibiting the responses of WDR cell to noxious stimuli more strongly than innocuous stimuli.
Animals ; Electric Stimulation ; Excitatory Amino Acids ; Magnesium* ; N-Methylaspartate ; Neuroprotective Agents ; Posterior Horn Cells* ; Rats* ; Spinal Cord

OBJECTIVETo study the changes of excitatory amino acids (EAAs) and intracellular calcium ([Ca2+]i), and the protective effect of EAAs receptor antagonists in the tissues of rabbit lumbar spinal cord after 40-minues ischemia and 4-hours reperfusion.

METHODSThirty healthy rabbits were divided into six groups: sham-operation, 40-minues ischemia, 4-hour reperfusion, ketamine and MgSO4 treatment, ketamine treatment, and saline treatment groups. The contents of EAAs (glutamate and aspartate) and [Ca2+]i were measured.

RESULTSThe contents of glutamate and aspartate were decreased to 15.18 micromol/g+/-2.33 micromol/g and 9.99 micromol/g+/-0.69 micromol/g, respectively; 13.75 micromol/g+/-2.58 micromol/g and 6.49 micromol/g+/-1.39 micromol/g after reperfusion. In the ischemia group, the [Ca2+]i was elevated to 221.2 microg/g+/-4.27 microg/g, and elevated further to 298.3 microg/g+/-9.26 microg/g after reperfusion, being significantly higher than that of ischemia and control groups. Ketamine could obviously increase the level of glutamate and aspartate and decrease the level of [Ca2+]i during the ischemia and reperfusion injury.

CONCLUSIONSThe excitotoxicity of EAAs and the overload of calcium induced by EAAs play a harmful role in ischemia and reperfusion injury. Ketamine has an effective inhibitory effect.

Animals ; Calcium ; analysis ; Excitatory Amino Acids ; blood ; Female ; Ischemia ; blood ; Male ; Rabbits ; Random Allocation ; Receptors, Amino Acid ; antagonists & inhibitors ; Reperfusion Injury ; blood ; Spinal Cord ; blood supply

Recent researches on ALS pathogenesis are focusing on abnormal immunological factors, excitotoxic substances, neurotrophic factors, and oxidative stress. It is well known that glutamate and aspartate are major putative excitatory neurotransmitters and possess excitotoxic properties that lead to neuronal death. In this study the authors checked the plasma level of amino acids in ALS and control groups and tried to understand any association between excitotoxic amino acids and sporadic ALS. The concentration of amino acids was measured by the HPLC method in the fasting plasma of fifteen ALS and nine control subjects. When we evaluated 19 amino acids or their metabolites, none showed significant difference between ALS and control groups. The mean concentrations of glutamic acid in ALS and control groups were 42.3+26.7 mmol/L and 57.4+17.0 mmol/L respectively, which showed no significant difference (p>O. 05). It was not possible to compare the level of aspartic acid in ALS and control groups as the levels were very low in individuals of both groups. In conclusion, authors could not note any significant correlations between sporadic ALS and excitotoxic substances, such as glutamate and aspartate. However, further studies m the excitotoxic levels in cerebrospinal fluid, spinal cord and brain, could be helpful to understand the overexcitation character of motor neuron by excitatory amino acids.
Amino Acids* ; Amyotrophic Lateral Sclerosis* ; Aspartic Acid ; Brain ; Cerebrospinal Fluid ; Chromatography, High Pressure Liquid ; Excitatory Amino Acids ; Fasting ; Glutamic Acid ; Immunologic Factors ; Motor Neurons ; Nerve Growth Factors ; Neurons ; Neurotransmitter Agents ; Oxidative Stress ; Plasma ; Spinal Cord

The author has examined the effect of cortical spreading depression(CSD) on the changes in extracellular concetration of aspartate and glutamate in the neocortex of anesthetized rats using microdialysis and high performance liquid chromatography(HPLC). The rats were prepared by halothane anesthesia and artificial ventilation. Rats were placed in a stereotaxic frame, and craniotomies were performed over the frontal and parietal cortexes on one side. The CSD was elicited by local application of KCI-soaked small pellets to the frontal cortex. The CSD was monitored by the changes of direct current(DC) potential in the parietal cortex. The microdialysis probe was implanted in the anterior part of the parietal cortex. Amino acids were analyzed by HPLC and fluorescence detection. Baseline concentration of the aspartate was 34.9+/-15.9nM and that of glutamate was 189.8+/-29.1nM(mean standard deviation). The perfusate for analysis was obtained 30 minutes after the beginning of the 300mM KCl induced CSD. Aspartate was found to increase to 146+/-55% baseline, glutamate up to 173+/-30% baseline(mean standard deviation). The increment of glutamate was statistically significant(p<0.05). Then 2M KCI-doaked pellets were applied for more frequent CSD amd the samples were collected. Aspartate increased up to 258+/-97% baseline, glutamate up to 174+/-57% baseline(mean standard deviation), The increment of glutamate and aspartate accompanying 2M KCI induced CSD were also statistically significant(p<0.05). These data suggest that the excitatory amino acids were released during the CSD and this may explain the various aspects of CSD that could contribute to the secondary neuronal damage in the compromised nerve cell.
Amino Acids ; Anesthesia ; Animals ; Aspartic Acid* ; Cerebral Cortex* ; Chromatography, High Pressure Liquid ; Cortical Spreading Depression* ; Craniotomy ; Excitatory Amino Acids ; Fluorescence ; Glutamic Acid* ; Halothane ; Microdialysis ; Neocortex ; Neurons ; Rabeprazole ; Rats* ; Ventilation