Neurochemical characterization of cysteine sulfinic acid, an excitatory amino acid, in hippocampus.

Baba, Akemichi

doi:10.1254/jjp.43.1

Cited by 10 publications

(2 citation statements)

References 31 publications

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“…After forskolin and other stimulatory agents were added, incubation was carried out at 37°C for 10 min. CSA, an excitatory amino acid neurotransmitter candidate (Iwata et al, 1982ab;Recasens et al, 1982;Baba, 1987) was mainly used as an agonist in the present study, because it was the most potent amino acid examined in stimulating cyclic AMP production (Baba et al, , 1983. Cyclic AMP content in the slices was determined as described elsewhere .…”

Section: Assay Of Cyclic Ampmentioning

confidence: 99%

Inhibition by Forskolin of Excitatory Amino Acid‐Induced Accumulation of Cyclic AMP in Guinea Pig Hippocampal Slices

Baba

Nishiuchi

Uemura

et al. 1988

Journal of Neurochemistry

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The effect of forskolin on the excitatory amino acid-induced accumulation of cyclic AMP was examined in hippocampal preparations of the guinea pig. Forskolin at concentrations of 0.1-10 microM remarkably enhanced the stimulatory effects of histamine and adenosine, whereas it markedly attenuated the stimulation induced by cysteine sulfinate, an excitatory amino acid. Forskolin reduced the maximal response to cysteine sulfinate without affecting the apparent ED50. At a concentration of 1 microM, forskolin also inhibited the stimulatory effects of glutamate, N-methyl-DL-aspartate, and veratridine without affecting those of kainate and quisqualate. Pretreatment of the slices with 0.1 mM N-ethylmaleimide partially prevented the attenuation by forskolin of cysteine sulfinate-induced accumulation of cyclic AMP without affecting the stimulation induced by cysteine sulfinate. Forskolin at concentrations of less than 1 microM did not affect GTP-stimulated activity and Cl- -dependent activity of adenylate cyclase of the hippocampal membranes.

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Section: Assay Of Cyclic Ampmentioning

confidence: 99%

Inhibition by Forskolin of Excitatory Amino Acid‐Induced Accumulation of Cyclic AMP in Guinea Pig Hippocampal Slices

Baba

Nishiuchi

Uemura

et al. 1988

Journal of Neurochemistry

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“…In the mammalian CNS, only a few amino acidsaspartate (Asp), glutamate (Glu), y-aminobutyric acid (GABA), and glycine (G1y)-are established as neurotransmitters (for review, see Fonnum, 1978;Watkins and Evans, 1981;Fagg and Foster, 1983). However, the list of amino acids and small peptides as neurotransmitter candidates is still growing: the sulfur-containing amino acids (Curtis and Watkins, 1960;Mewett et al, 1983;Do et al, 1986~) cysteinesulfinic acid (for review, see Rkcasens et al, 1982;Iwata and Baba, 1983;Baba, 1987;Turski et al, 1987), cysteic acid, homocysteinesulfinic acid, homocysteic acid (Do et al, 1986u,b), and taurine (for review, see Oja et al, 1985); 0-danine (Sandberg and Jacobson, 198 1;Toggenburger et al, 1982); and N-acetylaspartylglutamate (Coyle et al, 1986;Zollinger et al, 1988). Furthermore, there are good reasons to wonder whether Asp, Glu, or both are the only endogenous neurotransmitters of all socalled acidic amino acid pathways.…”

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confidence: 99%

Cysteine: Depolarization‐Induced Release from Rat Brain In Vitro

Keller

Zollinger

et al. 1989

Journal of Neurochemistry

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Compounds released on depolarization in a Ca2+-dependent manner from rat brain slices were screened to identify candidates for neuroactive substances. Lyophilized superfusates were analyzed by reversed-phase HPLC after derivatization with 9-fluorenyl N-succinimidyl carbonate. One of the compounds that showed an increase of concentration in superfusates in the presence of iodoacetamide was identified as the cysteine (Cys) derivative, S-carboxamidomethylcysteine, by fast atom bombardment mass spectrometry and other methods. This stable Cys derivative originates from endogenous, extracellular Cys. The finding led to a method for quantification of Cys in superfusates by immediate cooling of the superfusates to 0 degrees C and reaction of Cys with N-ethylmaleimide. Depolarization-induced Ca2+-dependent release of Cys was most prominent in the neocortex, followed by the mesodiencephalon, striatum, and cerebellum. This suggests that Cys is released from a neuronal compartment and might be involved in neurotransmission.

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