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101.
Incubations of rat striatal slices have been used to assay MPP+ neurotoxicity. MPP+, at concentrations of 1 mM or higher, caused a marked increase in hydroxyl radicals, measured as malondialdehyde (MDA) accumulation,
but not in nitric oxide production. At these doses, MPP+ showed an effect on dopamine terminals, causing a massive dopamine decrease, and on non-neuronal glial cells, where a marked
reduction in glutamine synthetase activity was detected. At lower concentrations (25 μM), the toxic effect on dopaminergic
endings was maintained without increasing malondialdehyde concentrations or inhibiting glutamine synthetase activity. The
effect on glutamine synthetase was prevented by the addition to the medium of 0.5% dimethyl sulfoxide, a hydroxyl-radical
scavenger, but this did not protect the effect of dopamine depletion. We propose that non-selective effects of MPP+, at doses of 1 mM or higher, are mediated by extracellular overproduction of hydroxyl radicals. The main factor responsible
for this overproduction would not be the released dopamine but rather the MPP+ itself, through non selective inhibition of the mitochondrial respiratory chain or through a redox cycling that can trigger
oxygen radical production. 相似文献
102.
N-methyl-D-aspartate (NMDA) inhibits carbachol-stimulated phosphoinositide breakdown in rat brain cortical slices but not in isolated membranes (1). To gain insight into the mechanisms, we examined the effects of NMDA on carbachol-stimulated [3H]inositol phosphate and intermediates of phosphatidylinositol cycle accumulation in rat cortical slices. The inhibition is primarily on the synthesis of inositol phospholipids subsequent to activation of muscarinic cholinergic receptors. In the absence of lithium, NMDA inhibited carbachol-stimulated [32P]PtdIns but not [32P]PtdOH synthesis. Carbachol-stimulated CDP-DAG formation required trace amount of Ca2+ and the response was inhibited by NMDA at low but not high extracellular Ca2+ concentrations. The inhibition due to NMDA was only seen at millimolar extracellular Mg2+. The inhibition of carbachol-stimulated CDP-DAG formation was not affected by adding tetrodotoxin or cobalt chloride suggesting the inhibitory effect was not due to releasing of neurotransmitters. The inhibitory effects of NMDA could be abolished by MK-801, the specific NMDA receptor associated channel antagonist. When cortical slices were preincubated with ligands and lithium to allow the build up of CDP-DAG, carbachol stimulated the incorporation of [3H]Ins into [3H]PtdIns. However, this response was not inhibited by NMDA. These results suggest that CDP-DAG synthesis is the primary site of regulation by NMDA. Because CDP-DAG cytidyltransferase requires Mg2+ as cofactor and is sensitive to Ca2+ it is possible that NMDA inhibits ligand-stimulated PtdIns breakdown by blocking the replenish of agonist-sensitive PtdIns pool through changes of divalent cation homeostasis. 相似文献
103.
Neurochemical Research - We examined the involvement of voltage-activated Ca2+ channels (VACCs) on K+(50 mM)-evoked [3H]dopamine ([3H]DA) release from superfused rat striatal slices. Neither... 相似文献
104.
[3H]Norepinephrine ([3H]NE) efflux from preloaded rat hippocampal slices was increased in a dose-dependent manner by excitatory amino acids, with the following order of potencies: N-methyl-D-aspartate (NMDA) greater than kainic acid (KA) greater than L-glutamate greater than or equal to D,L-homocysteate greater than L-aspartate greater than quinolinic acid greater than quisqualic acid. The effect of the excitatory amino acids was blocked by physiological concentrations of Mg2+, with the exception of KA. D,L-2-Amino-7-phosphonoheptanoic acid dose-dependently inhibited the NMDA effect (ID50 = 69 microM), whereas at 1 mM it was ineffective versus KA. The release of [3H]-NE induced by quinolinic acid was blocked by 0.1 mM D,L-2-amino-7-phosphonohepatanoic acid. gamma-D-Glutamylglycine dose-dependently inhibited the KA effect with an ID50 of 1.15 mM. Tetrodotoxin (2 microM) reduced by 40 and 20% the NMDA and KA effects, respectively. The data indicate that [3H]NE release from hippocampal slices can be used as a biochemical marker for pharmacological investigations of excitatory amino acid receptors and their putative agonists and antagonists. 相似文献
105.
Opposite Effects of δ and μ Opioid Receptor Agonists on the In Vitro Release of Substance P-Like Material from the Rat Spinal Cord 总被引:5,自引:2,他引:3
Annie Mauborgne Olivier Lutz Jean-Claude Legrand Michel Hamon Frangois Cesselin 《Journal of neurochemistry》1987,48(2):529-537
Superfusion of slices from the dorsal half of the lumbar enlargement of rat spinal cord with Krebs-Henseleit medium supplemented with 30 microM bacitracin allowed the collection of substance P-like immunoreactive material (SPLI), which was released at a rate of approximately 10 pg/4 min. Tissue depolarization by an excess of K+ (30-60 mM) or veratridine (50 microM) induced a marked increase in SPLI outflow, provided that Ca2+ was present in the superfusing fluid. K+- or veratridine-induced SPLI overflow could be modulated in opposite directions by mu and delta opioid receptor agonists. Thus, the two preferential mu agonists Tyr-D-Ala-Gly-MePhe-Gly-ol (DAGO; 10 microM) and Tyr-D-Ala-Gly-MePhe-Met(O)5-OH (FK-33824; 0.1 microM) enhanced SPLI overflow from depolarized tissues, whereas the selective delta agonists Tyr-D-Thr-Gly-Phe-Leu-Thr (deltakephalin; 3 microM) and [2-D-penicillamine, 5-D-penicillamine]enkephalin (50 microM) reduced it. The effect of DAGO was antagonized by a low concentration (1 microM) of naloxone but not by the selective delta antagonist ICI-154129 (50 microM). In contrast, the latter drug prevented the inhibitory influence of delta agonists on K+-induced SPLI release. Complementary experiments with morphine (10 microM) and [2-D-alanine, 5-D-leucine]enkephalinamide (3 microM), in combination with 1 microM naloxone or 50 microM ICI-154129 for the selective blockade of mu or delta receptors, respectively, confirmed that the stimulation of mu receptors increased, whereas the stimulation of delta receptors reduced, SPLI overflow. The results suggest that, at the spinal level, and antinociceptive action of delta but not mu agonists might involve a presynaptic inhibition of substance P-containing primary afferent fibers. 相似文献
106.
Philippe Vayer Brigitte Charlier Paul Mandel Michel Maitre 《Journal of neurochemistry》1987,49(4):1022-1024
The effects of some anticonvulsant drugs have been investigated on gamma-hydroxybutyrate release from rat hippocampal and striatal slices. Sodium valproate and ethosuximide inhibited the depolarization-evoked release of gamma-hydroxybutyrate induced by 40 mM K+. The IC50 values for these two drugs are in the concentration range of valproate and ethosuximide that exists in rat brain after administration of anticonvulsant doses to the animals. Trimethadione and pentobarbital are without significant effects. It can be concluded that the inhibition of gamma-hydroxybutyrate release, particularly that observed for hippocampus, might explain the protective effect of valproate and ethosuximide on gamma-hydroxybutyrate-induced seizures and perhaps on other kinds of epileptoid phenomenon. 相似文献
107.
Cyclic GMP Formation and Inositol Phosphate Accumulation Do Not Share Common Origins in Rat Brain Slices 总被引:3,自引:3,他引:0
David A. Kendall 《Journal of neurochemistry》1986,47(5):1483-1489
Cyclic GMP formation and inositol phospholipid hydrolysis were studied in rat brain slices to determine if the two processes have common origins. Muscarinic cholinergic stimulation enhanced [3H]inositol phosphate ([ 3H]IP) accumulation from slices prelabelled with [3H]inositol but did not affect cyclic GMP formation in the cortex, striatum, or cerebellum. An elevated level of extracellular K+ stimulated accumulation of both cyclic GMP and [3H]IP in cortex slices. The former, but not the latter, was reduced by lipoxygenase and phospholipase A2 inhibition. Calcium channel activation enhanced and blockade reduced K+-stimulated [3H]IP formation without affecting the cyclic GMP level, and there were differences in the Ca2+ requirements for the two responses. Thus, there is no support for the concept that guanylate cyclase activation inevitably accompanies inositol phospholipid breakdown, and the evidence presented demonstrates that K+ stimulation promotes cyclic GMP and [3H]IP accumulation by different transducing pathways. 相似文献
108.
Abstract: Adult rat cerebral cortex slices when incubated in media of increasing K+ concentrations, from 3 to 20 mM ("physiological" conditions), exhibited an increase of Ki + and a decrease of Nai + and Cli - . This phenomenon appeared at 30 days postnatally, which is fairly late during development. Over 20 mM-K+ ("pathological" conditions) an intense water uptake was observed together with an increase of Nai + and Cli - . This was observed in both adult and young animals. The results are discussed in relation to the well known properties of glial (Na+ ,K+ )-ATPase and carbonic anhydrase. 相似文献
109.
Thymidine Transport in the Central Nervous System 总被引:10,自引:9,他引:1
Reynold Spector 《Journal of neurochemistry》1980,35(5):1092-1098
110.
Solubility of plant invertases 总被引:1,自引:0,他引:1
Solubilization of acid invertase associated with cell wall preparations from aged slices of Jerusalem artichoke tuber tissue was achieved at high ionic 相似文献