High performance liquid chromatographic determination of subpicomole amounts of amino acids by precolumn fluorescence derivatization with o-phthaldialdehyde

Lindroth, Peter; Mopper, Kenneth

doi:10.1021/ac50047a019

Cited by 1,816 publications

(775 citation statements)

References 19 publications

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“…Endogenous glutamate analysis GLU was measured by precolumn derivatization with o-phthaldialdehyde and separation by reversed phase HPLC coupled to fluorimetric detection (Lindroth and Mopper 1979), according to the method described by Calò et al (1997) and modified by Morari et al (1998). Fifteen microlitres of o-phthaldialdehyde/mercaptoethanol reagent (0.4 M borate, 0.04 M o-phthaldialdehyde, 0.4 M 2-mercaptoethanol, pH 10.4) were added to 15 lL aliquots of sample.…”

Section: Microdialysis Experimentsmentioning

confidence: 99%

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Marti

Mela

Bianchi

et al. 2002

Journal of Neurochemistry

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Dual probe microdialysis was employed in conscious rats to investigate whether endogenous dopamine is involved in the stimulation of glutamate release in the substantia nigra pars reticulata following striatal NMDA receptor activation. Intrastriatal perfusion with NMDA (1 and 10 lM) facilitated nigral glutamate release (dizocilpine-and tetrodotoxin-sensitive). The D 2 dopamine receptor antagonist raclopride increased spontaneous nigral glutamate release and caused a leftward shift in the NMDA sensitivity, lowering NMDA effective concentrations to submicromolar levels. Conversely, the D 1 antagonist SCH23390 prevented the effect of NMDA (1 lM) and caused a rightward shift in the NMDA sensitivity. It was tested whether the antagonist effects were due to dopamine receptor blockade or increased tone on D 1 /D 2 receptors. SCH23390 prevented the raclopride-induced enhancement of spontaneous but not NMDA-evoked glutamate release while raclopride left unchanged the SCH23390-induced inhibition. The physiopathological relevance of the dopaminergic modulation was strengthened by perfusing NMDA in the dopaminedepleted striatum of hemiparkinsonian rats. Nigral glutamate responsiveness to NMDA was enhanced as with raclopride. We conclude that endogenous striatal dopamine regulates both spontaneous and NMDA-induced nigral glutamate release via an opposite control mediated by D 1 facilitatory and D 2 inhibitory receptors. Alterations of this control may subserve the motor symptoms of Parkinson's disease.

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Section: Microdialysis Experimentsmentioning

confidence: 99%

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Marti

Mela

Bianchi

et al. 2002

Journal of Neurochemistry

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“…Vol. 5, No.3, 1985 Amino acids were measured with liquid chromatog raphy after precolumn derivatization with o-phthaldialde hyde (OPA) (Lindroth and Mopper, 1979), The OPA derivatives were separated on a 5 fLm Nucleosil C-18-column (x 200 4-6 mm) using gradient elution with increasing methanol (30-100%) in Na-phosphate buffer (50 mM, pH 5,25). The system consisted of a Varian LC 5000 chromatograph, a Schoeffel FS 970 fluorimeter, and a Waters WISP 710 B autoinjector equipped with an ad ditional pneumatic valve to perform automatic derivati zation and sample injection into the main stream without interruption of the normal flow.…”

Section: Determination Of Free Amino Acidsmentioning

confidence: 99%

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

Hagberg

Lehmann

Sandberg³

et al. 1985

J Cereb Blood Flow Metab

660

246

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Brain ischemia was induced for 10 or 30 min by clamping the common carotid arteries in rabbits whose vertebral arteries had previously been electrocauterized. EEG and tissue content of high energy phosphates were used to verify the ischemic state and to evaluate the degree of postischemic recovery. Extracellular levels and total contents of amino acids were followed in the hippocampus during ischemia and 4 h of recirculation. At the end of a 30-min ischemic period, GABA had increased 250 times, glutamate 160 times, and aspartate and taurine 30 times in the extracellular phase. The levels returned to normal within 30 min of reflow. A delayed increase of extracellular phosphoethanolamine and ethanolamine peaked after 1–2 h of reflow. Ten minutes of ischemia elicited considerably smaller but similar effects. With respect to total amino acids in the hippocampus, glutamate and aspartate decreased to 30–50% of control while GABA appeared unaffected after 4 h of reflow. Alanine, valine, phenylalanine, leucine, and isoleucine increased severalfold. The importance of toxic extracellular levels of excitatory amino acids, as well as of high extracellular levels of inhibitory amino acids, are considered in relation to the pathophysiology of neuronal cell loss during cerebral ischemia.

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“…The ammonium concentrations of this supernatant as well as of the culture medium obtained in the first centrifugation step were determined by reversed-phase highperformance liquid chromatography (HPLC) using a protocol based on the method described by Lindroth and Mopper [21]. Ammonium was labeled by pre-column derivatization using ortho-phthaldialdehyde (OPA).…”

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confidence: 99%

Ammonium Toxicity in Bacteria

et al. 2006

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Abstract. Although an excellent nitrogen source for most bacteria, ammonium was-in analogy to plant and animal systems-assumed be detrimental to bacteria when present in high concentrations. In this study, we examined the effect of molar ammonium concentrations on different model bacteria, namely, Corynebacterium glutamicum, Escherichia coli, and Bacillus subtilis. The studied bacteria are highly resistant to ammonium. When growth was impaired upon addition of molar (NH 4 ) 2 SO 4 concentrations, this was not caused by an ammonium-specific effect but was due to an enhanced osmolarity or increased ionic strength of the medium. Therefore, it was concluded that ammonium is not detrimental to C. glutamicum and other bacteria even when present in molar concentrations.Ammonium (in this communication, the term ''ammonium'' is used in a general sense, including NH 4 + and NH 3 ; distinct ammonium species are indicated by chemical formula) is the preferred nitrogen source for most bacteria and fungi, and also plants acquire ammonium as a nitrogen source from the soil [35]. When present in high concentrations, diffusion of NH 3 , which is in equilibrium with NH 4 + , across the cytoplasmic membrane into the cell is sufficient to promote growth. In a situation of ammonium limitation, diffusion becomes negligible and special carriers are synthesized in bacteria, fungi, and plants (for a recent review, see [36]).However, ammonium is a paradoxical nutrient, because it is notorious for its cytotoxic effects. Furthermore, active transport of ammonium can to lead to a harmful energy-wasting futile cycling when accumulated ammonium diffuses across the cytoplasmic membrane back into the medium. Sensitivity to ammonium is discussed to be a universal phenomenon; however, it is well investigated only in plant and animal systems [36], whereas the situation in bacteria is less clear.

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High performance liquid chromatographic determination of subpicomole amounts of amino acids by precolumn fluorescence derivatization with o-phthaldialdehyde

Cited by 1,816 publications

References 19 publications

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

Ammonium Toxicity in Bacteria

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High performance liquid chromatographic determination of subpicomole amounts of amino acids by precolumn fluorescence derivatization with o-phthaldialdehyde

Cited by 1,816 publications

References 19 publications

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D1 and D2 receptors

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D1 and D2 receptors

Ischemia-Induced Shift of Inhibitory and Excitatory Amino Acids from Intra- to Extracellular Compartments

Ammonium Toxicity in Bacteria

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Product

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Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors