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91.
Childhood absence epilepsy (CAE) is a well-defined generalized epilepsy syndrome clinically characterized by frequent absence seizures. The aim of this study was to assess the activity of GABA transaminase (GABA-T) and the kinetic parameters of GABA uptake in platelets from patients with CAE. We studied 13 patients with CAE and eight sex- and age-matched controls. The mean activity of GABA-T was lower in patients with CAE than in controls (1.22+/-0.05 vs. 1.75+/-0.10 micromol/min/kg protein). The capacity of GABA uptake into the platelets was higher in patients using valproate (0.66+/-0.09 micromol/min/kg protein), but not in those using ethosuximide (0.34+/-0.05 micromol/min/kg protein), when compared to controls (0.26+/-0.06 micromol/min/kg protein). The affinity of the transporters was not altered. The observed peripheral alterations may indicate impaired function of brain GABAergic systems in children with absence epilepsy. 相似文献
92.
beta-N-Oxalylamino-L-alanine (BOAA) is a dicarboxylic diamino acid present in Lathyrus sativus (chickling pea). Excessive oral intake of this legume in remote areas of the world causes humans and animals to develop a type of spastic paraparesis known as lathyrism. BOAA is one of several neuroactive glutamate analogs reported to stimulate excitatory receptors and, in high concentrations, cause neuronal vacuolation and necrosis. The present study investigates the action of BOAA in vitro on CNS high-affinity transport systems for glutamate, gamma-aminobutyric acid (GABA), aspartate, glycine, and choline and in the activity of glutamate decarboxylase (GAD), the rate-limiting enzyme in the decarboxylation of glutamate to GABA. Crude synaptosomal fractions (P2) from rat brain and spinal cord were used for all studies. [3H]Aspartate transport in brain and spinal cord synaptosomes was reduced as a function of BOAA concentration, with reductions to 40 and 30% of control values, respectively, after 15-min preincubation with 1 mM BOAA. Under similar conditions, transport of [3H]glutamate was reduced to 74% (brain) and 60% (spinal cord) of control values. High-affinity transport of [3H]GABA, [3H]glycine, and [3H]choline, and the enzyme activity of GAD, were unaffected by 1 mM BOAA. While these data are consistent with the excitotoxic (convulsant) activity of BOAA, their relationship to the pathogenesis of lathyrism is unknown. 相似文献
93.
Amino Acid Neurotransmitters in the CNS: Properties of Diaminobutyric Acid Transport 总被引:4,自引:3,他引:1
Uptake of L-2,4-diaminobutyric acid (DABA), a positively charged analogue of gamma-aminobutyric acid (GABA), by a synaptosomal fraction isolated from rat brain occurred with a Km of 54 +/- 12 microM and a Vmax of 1.3 +/- 0.2 nmol/min/mg protein. The transport of DABA was inhibited competitively by GABA whereas that of GABA was affected in the same manner by addition of DABA. The maximal accumulation of DABA ([DABA]i/[DABA]c) was observed to increase as the second power of the transmembrane electrical potential ([K+]i/[K+]e) and the first power of the sodium ion concentration gradient. These findings indicate that DABA is transported on the GABA carrier with a net charge of +2, where one charge is provided by the cotransported Na+ and the second is contributed by the amino acid itself. Since uptake of GABA, an electroneutral molecule, is accompanied by transfer of two sodium ions, the results obtained with DABA suggest that one of the sodium binding sites on the GABA transporter is in proximity to the amino acid binding site. 相似文献
94.
Involvement of nine classical neurotransmitters in the abnormal sessile behavior of the rotiferBrachionus plicatilis was investigated. Only norepinephrine (NE), dopamine (DA) and octopamine (OA) induced sessility. NE and DA behaved as a full, OA as a partial agonist; NE was more potent than DA. Catecholamines may be involved as neurotransmitters in the pedal gland secretory mechanism. 相似文献
95.
96.
Cytosolic-free calcium and neurotransmitter release with decreased availability of glucose or oxygen
Gary E. Gibson Thomas Manger Lourdes Toral-Barza Gary Freeman 《Neurochemical research》1989,14(5):437-443
Exposing brain slices to reduced oxygen tensions or impairing their ability to utilize oxygen with KCN decreases acetylcholine (ACh) but increases dopamine (DA) and glutamate in the medium at the end of a release incubation. To determine if these changes are due to alterations in the presynaptic terminals, release from isolated nerve endings (i.e. synaptosomes) was determined during histotoxic hypoxia (KCN). KCN reduced potassium-stimulated synaptosomal ACh release and increased dopamine and glutamate release. Since several lines of evidence suggest that altered calcium homeostasis underlies these changes in release, the effects of reducing medium calcium concentrations from 2.3 to 0.1-mM were determined. In low calcium medium, KCN still increased dopamine and glutamate release, but had no effect on ACh release. Hypoxia increased cytosolic-free calcium in both the normal and low calcium medium, although the elevation was less in the low calcium medium. Thus, the effects of histotoxic hypoxia on cytosolic free calcium concentration paralleled those on glutamate and dopamine release. Reducing the glucose concentration of the medium also increased cytosolic-free calcium. The data are consistent with the hypothesis that hypoxia and hypoglycemia increase cytosolic-free calcium, which stimulates the release of dopamine and glutamate, whose excessive release may lead to subsequent cellular damage postsynaptically.Abbreviations (cps)
counts per second
- (FAM)
fura-2 acetoxymethylester
- (ACh)
acetylcholine
- (Cai)
cytosolic free calcium concentration
- (DMSO)
dimethylsulphoxide
- (DA)
dopamine
- (TES)
N-tris[hydroxymethyl]methyl-2-aminoethanesulfonic acid
- (Rmin)
the ratio of the fluorescence of fura at 510 nm after excitation at 340 nm to that after excitation at 380 nm in the absence of calcium
- (Rmax)
or to that in the presence of saturating calcium
- (SNK)
Student-Newman-Keuls 相似文献
97.
98.
Calcium-activated potassium (KCa) channels are highly modulated by a large spectrum of metabolites. Neurotransmitters, hormones, lipids, and nucleotides are capable of activating and/or inhibiting KCa channels. Studies from the last few years have shown that metabolites modulate the activity of KCa channels via: (1) a change in the affinity of the channel for Ca2+ (K1/2 is modified), (2) a parallel shift in the voltage axis of the acitvation curves, or (3) a change in the slope (effective valence) of the voltage dependence curve. The shift of the voltage dependence curve can be a direct consequence of the change in the affinity for Ca2+. Recently, the mechanistic steps involved in the modulation of KCa channels are being uncovered. Some interactions may be direct on KCa channels and others may be mediated via G-proteins, second messengers, or phosphorylation. The information given in this review highlights the possibility that KCa channels can be activated or inhibited by metabolites without a change in the intracellular Ca2+ concentration. 相似文献
99.
Monoamine and amino acid content were measured in brain regions from 12 week old male, homozygous Brattleboro (DI,n=12) and Long-Evans control (LE,n=12) rats. Norepinephrine (NE) content was significantly elevated (16–25%) in the spinal cord, pons-medulla and anterior hypothalamus of DI rats when compared to LE controls. NE content of the neurointermediate lobe of pituitary in DI rats was almost twice that of LE controls. Serotonin content was also significantly elevated in the spinal cord, pons-medulla, anterior hypothalamus and forebrain of DI rats relative to the LE controls. Taurine content in DI rats was increased (31–42%) above that of LE rats in the anterior hypothalamus, striatum and forebrain. Glutamine content was also greater in DI rats than LE in the spinal cord, pons-medulla, anterior hypothalamus, striatum, hippocampus and forebrain. The changes in monoamine and amino acid content were discussed in relation to the cardiovascular and osmoregulatory deficits that are present in DI rats due to arginine vasopressin (AVP) deficiency. The possible role of AVP in modulating NE turnover was also discussed. The increase in brain TAU content in DI rats may be a physiological response to hypernatremia. 相似文献
100.
We have investigated the possible role of plasma membrane oxidoreductases in the Ca2+ export mechanisms in rat brain synaptic membranes. Ca2+ efflux in nerve terminals is controlled both by a high-affinity/low capacity Mg-dependent ATP-stimulated Ca2+ pump and by a low affinity/high capacity ATP-independent Na+-Ca2+ exchanger. Both Ca2+ efflux mechanisms were strongly inhibited by pyridine nucleotides, in the order NADP>NAD>NADPH>NADH with IC50 values of ca. 10 mM for NADP and ca. 3 mM for the other agents in the case of the ATP-driven Ca2+ pump and with IC50 values between 8 and 10 mM for the Na+-Ca2+ exchanger. Oxidizing agents such as DCIP and ferricyanide inhibited the ATP-driven Ca2+ efflux mechanism but not the Na+-Ca2+ exchanger. In addition, full activation of plasma membrane oxidoreductases requires both an acceptor and an electron donor; therefore the combined effects of both substrates added together were also studied. When plasma membrane oxidoreductases of the synaptic plasma membrane were activated in the presence of both NADH (or NADPH) and DCIP or ferricyanide, the inhibition of the ATP-driven Ca2+ pump was optimal; by contrast, the pyridine nucleotide-mediated inhibition of the Na+-Ca2+ exchanger was partially released when both substrates of the plasma membrane oxidoreductases were present together. Furthermore, the activation of plasma membrane oxidoreductases also strongly inhibited intracellular protein phosphorylation in intact synaptosomes, mediated by eithercAMP-dependent protein kinase, Ca2+ calmodulin-dependent protein kinases, or protein kinase C.Abbreviations Hepes
4-(2-hydroxyethyl)-1-piperazine ethanesulfonic acid
- SDS
sodium dodecyl sulfate
- EGTA
ethylenglycol-bis(-aminoethylether)-N,N,N,N-tetraacetic acid
- DCIP
dichlorophenol-indophenol 相似文献