Fluorometric microbore amino acid analyzer: The construction of an inexpensive, highly sensitive instrument using o-phthalaldehyde as a detection agent

Lee, How-Ming; Forde, M.Diane; Lee, Mei C.; Bucher, Doris

doi:10.1016/0003-2697(79)90585-2

Cited by 34 publications

(7 citation statements)

References 9 publications

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“…The amino acid analyzer had a limit of detection of 1-3 pmol/sample. Amino acids from the deproteinated samples were detected fluorometrically as the o-phthalaldehyde derivatives (Lee et al, 1979;Leach et al, 1986).…”

Section: Methodsmentioning

confidence: 99%

Vicious Cycle Involving Na⁺Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation

1996

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The mechanisms by which neurons die after cerebral ischemia and related conditions in vivo are unclear, but they are thought to involve voltage-dependent Na ϩ channels, glutamate receptors, and nitric oxide (NO) formation because selective inhibition of each provides neuroprotection. It is not known precisely what their roles are, nor whether they interact within a single cascade or in parallel pathways. These questions were investigated using an in vitro primary cell culture model in which striatal neurons undergo a gradual and delayed neurodegeneration after a brief (5 min) challenge with the glutamate receptor agonist NMDA. Unexpectedly, NO was generated continuously by the cultures for up to 16 hr after the NMDA exposure. Neuronal death followed the same general time course except that its start was delayed by ϳ4 hr. Application of the NO synthase inhibitor nitroarginine after, but not during, the NMDA exposure inhibited NO formation and protected against delayed neuronal death. Blockade of NMDA receptors or of voltage-sensitive Na ϩ channels [with tetrodotoxin (TTX)] during the postexposure period also inhibited both NO formation and cell death. The NMDA exposure resulted in a selective accumulation of glutamate in the culture medium during the period preceding cell death. This glutamate release could be inhibited by NMDA antagonism or by TTX, but not by nitroarginine. These data suggest that Na ϩ channels, glutamate receptors, and NO operate interdependently and sequentially to cause neurodegeneration. At the core of the mechanism is a vicious cycle in which NMDA receptor stimulation causes activation of TTX-sensitive Na ϩ channels, leading to glutamate release and further NMDA receptor stimulation. The output of the cycle is an enduring production of NO from neuronal sources, and this is responsible for delayed neuronal death. The same neurons, however, could be induced to undergo more rapid NMDA receptor-dependent death that required neither TTX-sensitive Na ϩ channels nor NO.

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Section: Methodsmentioning

confidence: 99%

Vicious Cycle Involving Na⁺Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation

1996

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“…California, USA), as described by Lee et al (1979), using standard ion-exchange column chromatographic separation techniques and fluorimetric detection of amino acids after reaction with O-phthaldialdehyde.…”

Section: Amino Acid Analysismentioning

confidence: 99%

Measurement of endogenous amino acid losses in poultry

Siriwan¹,

Bryden

Mollah

et al. 1993

British Poultry Science

181

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1. Ileal endogenous amino acid losses were determined in broiler chickens and in cannulated cross-bred layer strain cockerels using either a nitrogen-free diet, regression analysis or a 48 h fast. 2. Endogenous amino acid flows to the ileum in fasted cockerels were significantly lower than those obtained both by feeding the nitrogen-free diet, and from regression analysis in either broilers or cockerels. Regression analysis gave the highest flows. 3. The apparent digestibility coefficients of amino acids in a diet containing 200 g/kg crude protein were lower in broilers (0.84) than in cockerels (0.88). When corrected, by regression analysis, for the contribution of endogenous amino acids, the true digestibility coefficients became 0.90 and 0.92 respectively.

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“…I N Aristar HCI, and samples analysed using a Locate amino acid analyser with DL-homocysteic acid as internal standard. Amino acids were detected fluorometrically as the 0-phthaldehyde derivatives (Lee et al, 1979). Tissue pellets were estimated for protein by the method of Lowry et al (1951).…”

Section: Endogenous Amino Acid Releasementioning

confidence: 99%

Pharmacological Studies on Lamotrigine, A Novel Potential Antiepileptic Drug

1986

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Lamotrigine (LTG) [3,5-diamino-6-(2,3-dichlorophenyl)-1,2,4-triazine] is a novel anticonvulsant chemically unrelated to current antiepileptic drugs and with a pharmacological profile similar to that of phenytoin. The effect of LTG has been compared with that of phenytoin, on the release of endogenous amino acids and radiolabelled acetylcholine evoked by veratrine or potassium, from slices of rat cerebral cortex in vitro. Both veratrine and potassium evoked a marked release of glutamate and gamma-aminobutyric acid (GABA), with a more moderate release of aspartate. LTG inhibited veratrine-evoked release of glutamate and aspartate, with ED50 values of 21 microM for both amino acids, but LTG was less potent in the inhibition of GABA release (ED50 = 44 microM). At concentrations up to 300 microM, LTG had no effect on potassium-evoked amino acid release or on spontaneous release. Also, LTG was some five times less potent in the inhibition of veratrine-evoked [3H]acetylcholine release (ED50 = 100 microM) than in glutamate or aspartate release. The total lack of effect of LTG on potassium-evoked release and the potent effect on veratrine-evoked release (at concentrations found in rat brain after anticonvulsant doses) strongly suggest that LTG acts at voltage-sensitive sodium channels to stabilise neuronal membranes and inhibit transmitter release, principally glutamate. The role of glutamate in the aetiology of epilepsy is discussed.

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Fluorometric microbore amino acid analyzer: The construction of an inexpensive, highly sensitive instrument using o-phthalaldehyde as a detection agent

Cited by 34 publications

References 9 publications

Vicious Cycle Involving Na⁺Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation

Vicious Cycle Involving Na⁺Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation

Measurement of endogenous amino acid losses in poultry

Pharmacological Studies on Lamotrigine, A Novel Potential Antiepileptic Drug

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Fluorometric microbore amino acid analyzer: The construction of an inexpensive, highly sensitive instrument using o-phthalaldehyde as a detection agent

Cited by 34 publications

References 9 publications

Vicious Cycle Involving Na+Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation

Vicious Cycle Involving Na+Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation

Measurement of endogenous amino acid losses in poultry

Pharmacological Studies on Lamotrigine, A Novel Potential Antiepileptic Drug

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Product

Resources

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Vicious Cycle Involving Na⁺Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation

Vicious Cycle Involving Na⁺Channels, Glutamate Release, and NMDA Receptors Mediates Delayed Neurodegeneration through Nitric Oxide Formation