13 results on '"Dawson, R"'
Search Results
2. Regional distribution of the muscarinic cholinoceptor and acetylcholinesterase in guinea pig brain
- Author
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Dawson, R. M. and Jarrott, B.
- Published
- 1980
- Full Text
- View/download PDF
3. Regional differences in glutaminase activation by phosphate and calcium in rat brain: Impairment in aged rats and implications for regional glutaminase isozymes
- Author
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Wallace, D. R., primary and Dawson, R., additional
- Published
- 1993
- Full Text
- View/download PDF
4. Effect of age and monosodium-L-glutamate (MSG) treatment on neurotransmitter content in brain regions from male fischer-344 rats
- Author
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Wallace, D. R., primary and Dawson, R., additional
- Published
- 1990
- Full Text
- View/download PDF
5. The stimulation of the brain alkaline phospholipase A1 attacking phosphatidylethanolamine by various salts and metal chelators
- Author
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Dawson, R. M. C., Irvine, R. F., Hemington, N., and Hirasawa, K.
- Abstract
Rat brain contains a soluble, high molecular weight phospholipase A
1 of alkaline pH optimum which shows a preference for phosphatidylethanolamine as substrate. There is evidence that the same enzyme exists in liver and kidney. At low osmotic concentrations of buffer the enzyme is markedly stimulated by CaCl2 . However, MgCl2 and MnCi2 are equally as effective although at concentrations above 2 mM the activation falls away with MnCl2 . The phospholipase A1 is stimulated by divalent metal ion chelators (EDTA, EGTA, CDTA) and by sodium phosphate and sodium sulphate. The activity is inhibited by hexanol, benzyl alcohol, diethylether and detergents. Although the activity can be inhibited by saturated and unsaturated fatty acids, no evidence could be obtained that the activators function by counteracting the inhibitory action of fatty acids liberated at the interface of the substrate and incubation medium. It is suggested that to achieve good enzymic hydrolysis a certain type of organised hydrated phosphatidylethanolamine structure is required in which the negative zeta potential has been reduced by metallic cations in the incubation medium.- Published
- 1982
- Full Text
- View/download PDF
6. Building biosynthetic schools: reviewing compartmentation of CNS taurine synthesis.
- Author
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Dominy J, Eller S, and Dawson R Jr
- Subjects
- Animals, Carboxy-Lyases metabolism, Central Nervous System cytology, Central Nervous System enzymology, Humans, Cell Compartmentation, Central Nervous System metabolism, Taurine biosynthesis
- Abstract
Taurine is one of the mammalian brain's most abundant and indispensable amino acids. Considerable strides have been made in understanding taurine biosynthesis within the brain, but many disputed issues nonetheless remain. Heading the list is the cellular origin of biosynthetically derived taurine: glial or neuronal? This article reviews the competing theories surrounding cellular compartmentation of taurine biosynthesis in the brain. It concludes that while in vitro systems clearly show astrocytes to be fully capable of taurine synthesis and neurons to be limited to synthesizing taurine from hypotaurine, there is insufficient evidence to attribute these processes to any one cell type in vivo. Instead, there is a growing body of evidence that suggests brain taurine biosynthesis is occurring via a more cooperative metabolic interaction between astrocytes and neurons.
- Published
- 2004
- Full Text
- View/download PDF
7. Endogenous excitatory amino acid release from brain slices and astrocyte cultures evoked by trimethyltin and other neurotoxic agents.
- Author
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Dawson R Jr, Patterson TA, and Eppler B
- Subjects
- Animals, Aspartic Acid metabolism, Astrocytes drug effects, Brain drug effects, Brain growth & development, Cells, Cultured, Cerebral Cortex metabolism, Glutamic Acid metabolism, Glutamine metabolism, In Vitro Techniques, Male, Ouabain pharmacology, Potassium Chloride pharmacology, Rats, Rats, Inbred F344, Rats, Sprague-Dawley, Sodium Glutamate pharmacology, Taurine metabolism, Veratrine pharmacology, gamma-Aminobutyric Acid metabolism, Aging metabolism, Astrocytes metabolism, Brain metabolism, Excitatory Amino Acids metabolism, Neurotoxins pharmacology, Trimethyltin Compounds pharmacology
- Abstract
Trimethyltin (TMT) is a toxic alkyltin compound that is known to produce neuronal necrosis in the CNS. The present study examined the effects of TMT on the release of excitatory amino acids (EAA) from cortical slices prepared from adult and aged (24 months old) rats. The calcium dependence of TMT-induced EAA efflux was evaluated and compared to other neurotoxic agents. The actions of TMT were also evaluated in an astrocyte culture model to assess glial contributions to TMT-induced EAA efflux. TMT (10-1000 microM) evoked a dose-related increase in GLU and ASP efflux during a 30 min incubation period and this efflux was sustained or slightly higher during a 15 min recovery period. TMT-stimulated GLU efflux was not altered in aged rats. TMT-induced GLU efflux was significantly reduced by removing extracellular calcium and including 10 microM EGTA in the incubation media. Calcium channel blockers (nifedipine, verapamil, flunarizine, amiloride, neomycin) and MK-801 did not significantly attenuate TMT-induced GLU efflux. Diltiazem (25 microM) produced modest but inconsistent reductions in TMT-induced GLU efflux from brain slices, and significantly inhibited the leakage of lactate dehydrogenase (LDH) from TMT-treated astrocyte cultures. TMT did not increase GLU efflux from glial cultures during a 30 min incubation period, but did significantly elevate GLU efflux during the 15 min recovery period. TMT evoked the release of EAA by both calcium dependent and independent mechanisms in brain slices. TMT at high concentrations also produced a delayed increase in glial GLU efflux. These studies suggest that excitotoxic mechanisms may contribute to TMT-induced neurotoxicity.
- Published
- 1995
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8. Glutamate efflux from rat brain slices and cultures: a comparison of the depolarizing agents potassium, 4-aminopyridine, and veratrine.
- Author
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Patterson TA, Kim EK, Meldrum MJ, and Dawson R Jr
- Subjects
- Amino Acids analysis, Amino Acids metabolism, Animals, Astrocytes drug effects, Astrocytes metabolism, Brain drug effects, Brain metabolism, Cells, Cultured, Cerebellum physiology, Chromatography, High Pressure Liquid, Corpus Striatum physiology, Frontal Lobe physiology, Hippocampus physiology, In Vitro Techniques, Male, Organ Specificity, Parietal Lobe physiology, Rats, Rats, Sprague-Dawley, Temporal Lobe physiology, 4-Aminopyridine pharmacology, Astrocytes physiology, Brain physiology, Glutamic Acid metabolism, Membrane Potentials drug effects, Potassium Chloride pharmacology, Veratrine pharmacology
- Abstract
The major excitatory amino acid neurotransmitter in the mammalian brain is glutamate (GLU). GLU release from nerve terminals is both calcium-dependent and -independent, yet these mechanisms of release are not fully understood. Potassium, 4-aminopyridine (4-AP) and veratrine are commonly used depolarizing agents that were studied for their ability to stimulate GLU efflux from brain slices. These agents produced significant regional variations in GLU efflux from rat brain slices. Potassium was the most potent of the three secretogogues tested. 4-AP produced a significant GLU efflux only in the cerebellum. Veratrine produced consistent stimulation of GLU efflux from all brain regions tested. Potassium was the only depolarizing agent tested that stimulated GLU release from primary astroglial cultures of rat cerebral cortex. All three agents also demonstrated an ability to inhibit GLU reuptake in brain slice preparations. This data suggest that both GLU release and uptake are modulated in a regionally selective manner, and that commonly used depolarizing agents affect not only calcium-dependent neuronal release, but also uptake and glial responses.
- Published
- 1995
- Full Text
- View/download PDF
9. Regulation of phosphate-activated glutaminase (PAG) by glutamate analogues.
- Author
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Dawson R Jr and Wallace DR
- Subjects
- Animals, Dizocilpine Maleate pharmacology, Feedback, Male, Rats, Rats, Inbred F344, Rats, Sprague-Dawley, Glutamates pharmacology, Glutaminase drug effects, Receptors, Glutamate drug effects
- Abstract
The ability of structural analogues of glutamate (GLU) to modulate phosphate activated glutaminase (PAG) was assessed in the present series of studies. A number of GLU receptor agonists and antagonists were tested for their ability to inhibit synaptosomal PAG activity. PAG activity was determined by measuring GLU formation from 0.5 mM glutamine (GLN) in the presence of 10 mM phosphate. GLU analogues at 5-10 mM were found to significantly inhibit PAG activity. It was determined that PAG inhibition occurred regardless of whether the GLU analogues were receptor agonists or antagonists, however, PAG inhibition was influenced by analogue chain length, isomeric form and substituent substitution. The glutamate uptake blockers, dihydrokainic acid and DL-threo-beta-hydroxyaspartic acid were relatively weak inhibitors of PAG (< 25% inhibition) as were the receptor agonists, ibotenic acid and (+-)cis-2,3-piperidine-dicarboxylic acid. Other GLU analogues produced inhibition of PAG in the range of 40-70%. PAG inhibition by GLU analogues did not appear to differ substantially among the brain regions evaluated (cortex, striatum and hippocampus). The endogenous amino acids, glycine, taurine and N-acetylaspartic acid, also significantly inhibited PAG activity in the 5-10 mM range. The noncompetitive NMDA antagonists, (+)MK801 and ketamine, at a concentration of 5 mM, significantly stimulated PAG activity 1.5-2 fold over control values. The activation of PAG by (+)MK801 was dose-related, stereoselective and appeared to result from a synergistic interaction with phosphate to enhance substrate (GLN) binding to PAG.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1993
- Full Text
- View/download PDF
10. Ammonia regulation of phosphate-activated glutaminase displays regional variation and impairment in the brain of aged rats.
- Author
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Wallace DR and Dawson R Jr
- Subjects
- Aging metabolism, Amino Acids analysis, Animals, Brain enzymology, Chromatography, High Pressure Liquid, Glutamates metabolism, Glutamic Acid, In Vitro Techniques, Male, Potassium pharmacology, Rats, Rats, Inbred F344, Rats, Sprague-Dawley, Aging drug effects, Ammonia pharmacology, Brain drug effects, Glutaminase drug effects
- Abstract
The regulation of PAG by ammonia in whole brain (Sprague-Dawley) and regional (Fischer-344) synaptosomal preparations from adult and aged animals was assessed. Whole brain synaptosomal preparations from both age groups displayed a significant decrease in PAG activity with increasing ammonium chloride concentrations, however, the aged rats exhibited a significant attenuation in ammonia-induced PAG inhibition. PAG activity measured in synaptosomes prepared from the striatum (STR), temporal cortex (TCX) and hippocampus (HIPP) was also inhibited by ammonium chloride. The STR showed the greatest degree of ammonia-induced PAG inhibition (55%) followed by the HIPP (30-35%) and the TCX (25-30%). This reduction in PAG activity was significantly attenuated in STR from aged rats at ammonium chloride concentrations greater than 50 microM and in the TCX, PAG activity was significantly attenuated in the aged rats at ammonia concentrations of 0.5 and 1.0 mM. Ammonia regulation of PAG activity in the HIPP appeared to be unaffected by age. Ammonium chloride concentrations up to 5 mM had no effect on GLU release from cortical slices, although GLN efflux was significantly enhanced. These findings suggest that isozymes of PAG may exist in different brain regions based on their differential sensitivity to ammonia. The attenuation of ammonia-induced PAG inhibition seen in aged rats may have deleterious effects in the aged brain.
- Published
- 1992
- Full Text
- View/download PDF
11. [3H]D-aspartic acid release in brain slices of adult and aged Fischer 344 rates.
- Author
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Meldrum MJ, Glenton P, and Dawson R Jr
- Subjects
- Animals, Brain drug effects, Calcium Channels physiology, Electric Stimulation, Hippocampus drug effects, Hippocampus metabolism, Kainic Acid pharmacology, Male, Peptides, Cyclic pharmacology, Rats, Rats, Inbred F344, Temporal Lobe drug effects, Temporal Lobe metabolism, omega-Conotoxin GVIA, Aging physiology, Aspartic Acid metabolism, Brain metabolism
- Abstract
Alterations in glutamate content and uptake have been reported to occur in aged animals. The present studies used [3H]D-Aspartic acid [( 3H]-D-ASP) release as a marker for glutamate neurotransmission. Frequency dependent [3H]-D-ASP release was measured in adult (8 month) and aged (28-30 month) Fischer 344 rats. Relatively high stimulation frequencies (greater than 10 Hz) were required to induce [3H]-D-ASP release in both adult and aged F344 rats in temporal cortex and hippocampus. In both brain areas aged animals showed significantly more [3H]-D-ASP release than adult animals. Kainic acid 1 mM failed to induce the release of [3H]-D-ASP in either temporal cortex or hippocampus. Omega conotoxin GVIA (5 x 10(-9) M) a N and L type voltage sensitive calcium channel antagonist failed to inhibit [3H]-D-ASP stimulated release. These results demonstrate an increase in [3H]-D-ASP release in aged compared to adult F344 rats. The data also suggest a novel calcium channel may be involved in [3H]-D-ASP release.
- Published
- 1992
- Full Text
- View/download PDF
12. Monoamine and amino acid content in brain regions of Brattleboro rats.
- Author
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Dawson R Jr, Wallace DR, and King MJ
- Subjects
- 3,4-Dihydroxyphenylacetic Acid metabolism, Animals, Dopamine metabolism, Glutamates metabolism, Glutamic Acid, Glutamine metabolism, Hydroxyindoleacetic Acid metabolism, Norepinephrine metabolism, Rats, Rats, Brattleboro, Serotonin metabolism, Spinal Cord metabolism, Taurine metabolism, Tissue Distribution, Amino Acids metabolism, Biogenic Monoamines metabolism, Brain metabolism
- Abstract
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.
- Published
- 1990
- Full Text
- View/download PDF
13. Different long-term effects of bilateral and unilateral nucleus basalis lesions on rat cerebral cortical neurotransmitter content.
- Author
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Arendash GW, Millard WJ, Dawson R Jr, Dunn AJ, and Meyer EM
- Subjects
- Animals, Cerebral Cortex physiology, Cholinergic Fibers physiology, Ibotenic Acid, Male, Neural Pathways metabolism, Rats, Rats, Inbred Strains, Time Factors, Acetylcholine metabolism, Basal Ganglia physiology, Biogenic Monoamines metabolism, Cerebral Cortex metabolism, Neuropeptide Y metabolism, Somatostatin metabolism
- Abstract
Young adult rats received either unilateral or bilateral ibotenic acid infusions in their nucleus basalis, destroying most of the cholinesterase-staining neurons in that region. Cerebral cortex levels of choline acetyltransferase, somatostatin, neuropeptide Y, and monoamines were then assayed 2.5 and 10 months after bilateral lesions, or, 2.5, 10, and 14 months after unilateral lesions. Entorhinal and cerebral cortex levels of several amino acid transmitters were also measured. As expected, choline acetyltransferase activity was decreased in the frontal cortex ipsilateral to the ibotenic acid infusion in unilaterally or bilaterally lesioned animals. Parietal cortex concentrations of somatostatin and neuropeptide Y were altered by lesioning in a complicated, time-dependent manner. Thus, while unilateral lesions transiently decreased or had no effect on these neuropeptide levels, bilateral lesions elevated the level of each neuropeptide by over 100% at 10 months. Other cortical transmitter systems investigated appeared to be less affected by nucleus basalis-lesions. Unilateral lesions had no effect on prefrontal cortex norepinephrine, serotonin, or dopamine content at 14 months post-lesioning. These different neurochemical effects of unilateral and bilateral nucleus basalis lesions may be important for developing a model for the trans-synaptic effects of cortical cholinergic deafferentation.
- Published
- 1989
- Full Text
- View/download PDF
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