1982
DOI: 10.1016/0006-8993(82)90839-3
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Evidence for cysteine sulfinate as a neurotransmitter

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1983
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Cited by 66 publications
(24 citation statements)
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“…However, the inability of either the NMDA receptor antagonist, CPP, or the QUIS/KA receptor antagonist, CNQX, to block CSA-evoked release of endogenous transmitter, or indeed, of previously accumulated D-[3H]aspartate, is suggestive of depolarization being induced by electrogenic cotransport of Na + and CSA. This suggestion is consistent with data which reports the high-affinity nature of neuronal CSA transport (Recasens et al, 1982) and the inhibitory effects of acidic sulphur amino acids on D-[3H]aspartate uptake in synaptosomes and primary cultures of neurons and astrocytes (Griffiths et al, 1989). An alternative explanation for the excitatory actions of these compounds must include the involvement of another class of receptor.…”
Section: Discussionsupporting
confidence: 86%
See 1 more Smart Citation
“…However, the inability of either the NMDA receptor antagonist, CPP, or the QUIS/KA receptor antagonist, CNQX, to block CSA-evoked release of endogenous transmitter, or indeed, of previously accumulated D-[3H]aspartate, is suggestive of depolarization being induced by electrogenic cotransport of Na + and CSA. This suggestion is consistent with data which reports the high-affinity nature of neuronal CSA transport (Recasens et al, 1982) and the inhibitory effects of acidic sulphur amino acids on D-[3H]aspartate uptake in synaptosomes and primary cultures of neurons and astrocytes (Griffiths et al, 1989). An alternative explanation for the excitatory actions of these compounds must include the involvement of another class of receptor.…”
Section: Discussionsupporting
confidence: 86%
“…The endogenous location of a number of neuroactive sulphur amino acids has been reported (Do et al, 1986(Do et al, b, 1988Kilpatrick and Mozley, 1986) and it has been shown that certain of these compounds, such as HCA, L-homocysteine sulphinate (HSA) and Lcysteine sulphinate (CSA) are released by depolarization of slices from various regions of the rat brain in a Ca 2 +-dependent manner (Do et al, 1986 b). Furthermore the binding and high-affinity uptake of the excitatory amino acids Lglutamate and L-aspartate, are potently inhibited by a number of sulphur amino acids (Balcar and Johnston, 1972;Roberts, 1974;Recasens et al, 1982;Griffiths et al, 1989). Such observations have prompted conslderable recent interest in the study of neuroexcitant sulphur amino acids as transmitter candidates in the central nervous system.…”
Section: Introductionmentioning
confidence: 96%
“…In fact, neither of the excitatory amino acids activate adenylate cyclase activity in a cell free system from the hipppocampus under any conditions. As has been suggested (35,36), the stimulated formation of cAMP by 25,26,39). At present, the biochemical and pharmacological qualifications of ,"CSA neurones" are not clear.…”
supporting
confidence: 59%
“…Subsequent studies revealed uptake processes for these compounds in the central nervous system (Recasens et al, 1982;Wilson & Pastuszko, 1986) and their ability to release other transmitters from brain slices (Lehmann et al, 1988), cultured neurones (Dunlop et al, 1989a) and synaptosomes (Dunlop et al, 1989b). The possibility that one or more of these sulphur containing amino acids might be a central excitatory transmitter was apparently strengthened by reports that potassium depolarization caused their release from brain slices in a calcium-dependent manner (Do et al, 1986a,b).…”
Section: Introductionmentioning
confidence: 92%