Effects of uptake carrier blockers SK&amp;F 89976-A and l-trans-PDC on in vivo release of amino acids in rat hippocampus

Zuiderwijk, M.; Veenstra, Ersot; Silva, F.H. Lopes da; Ghijsen, W.E.J.M.

doi:10.1016/0014-2999(96)00284-1

Cited by 29 publications

(17 citation statements)

References 29 publications

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“…Because the chemical structure of theanine is similar to glutamic acid, some studies of theanine were concerned with its relationship to glutamic acid function and metabolism (Oda et al 1980;Kakuda et al 2002a;Sugiyama et al 2003;Tsuge et al 2003). L-trans-2,4-PDC, EAAT1-4 inhibitor, is known to inhibit glutamic acid reuptake in the rat hippocampus in a Ca 2þ -dependent manner and does not participate in GABA re-uptake (Zuiderwijk et al 1996). In this study, we showed that perfusion of L-trans-2, 4-PDC caused significant dopamine release and increased the glutamic acid concentration in the interstitium.…”

Section: Discussionmentioning

confidence: 58%

Effects of theanine, r-glutamylethylamide, on neurotransmitter release and its relationship with glutamic acid neurotransmission

Yamada

Terashima

Ōkubo

et al. 2005

Nutritional Neuroscience

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t Theanine, r-glutamylethylamide, is one of the major amino acid components in green tea and many researchers have compared theanine's effects with glutamic acid because the chemical structure is similar. In the previous study, we demonstrated that theanine can pass brain-blood barrier and may play as an agonist or an antagonist of some receptors. In this study, we investigated the effects of theanine on neurotransmitter release in the rat brain striatum by in vivo brain microdialysis and examined whether theanine affected glutamate transporters by comparing it with a glutamate transporter blocker, L-trans-Pyrrolidine-2,4-dicarboxylic acid (L-trans-2,4-PDC). Because we investigated whether the effects of theanine is similar to L-trans-2,4-PDC on the brain neurotransmission, we measured dopamine release and some amino acids release which are known as excitatory or inhibitory neurotransmitters from neurons by theanine or L-trans-2,4-PDC perfusion into the rat brain striatum. L-trans-2,4-PDC or theanine perfusion into the brain striatum caused dopamine release from dopaminergic neurons. In addition, L-trans-2,4-PDC perfusion increased glutamic acid, aspartic acid and, whereas theanine perfusion prevented aspartic acid release and increased glycine release. These results suggested that the mechanism of dopamine release caused by theanine is different from glutamate transporter blockers or glutamic acid. Further, L-trans-2,4-PDC cause excitatory neurotransmission, whereas theanine may inhibit excitatory neurotransmission and cause inhibitory neurotransmission via glycine receptors.

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Section: Discussionmentioning

confidence: 58%

Effects of theanine, r-glutamylethylamide, on neurotransmitter release and its relationship with glutamic acid neurotransmission

Yamada

Terashima

Ōkubo

et al. 2005

Nutritional Neuroscience

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“…It is conceivable that the tonic Glu release in the dark may be elevated by inhibiting Glu uptake (Zuiderwijk et al, 1996;Semba and Wakuta, 1998;Nyitrai et al, 1999;Waagepetersen et al, 2001). Thus, our findings might indicate distinguishable functions for the different transporters present in the rat retina (Arriza et al, 1997;Eliasof et al, 1998;Pow et al, 2000).…”

Section: Discussionmentioning

confidence: 94%

Light‐induced changes in glutamate release from isolated rat retina is regulated by cyclic guanosine monophosphate

Barabás

Kovács

Kovacs

et al. 2001

J of Neuroscience Research

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Isolated rat retina was preloaded with [(14)C]glutamate and subsequently superfused to follow release of glutamate (Glu). After 20 min of superfusion in the dark, exposure of the [(14)C]Glu preloaded rat retina to a single train of white light pulses reduced Glu efflux significantly in the absence as well as in the presence of low (4 microM) and high (0.5 mM) concentrations of the Glu uptake inhibitor trans-L-pyrrolidine-2,4-dicarboxylate (t-PDC). The dark-light response was the highest in the presence of 4 microM t-PDC by establishing a plateau at 75% +/- 7% of the tonic Glu release in the dark (100%). Displaying transient to saturating responses with increasing relative luminance, time series of four trains of white light pulses arrived at a plateau of 85% +/- 10%. The cyclic guanosine monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast (200 microM) antagonized the effect of the light series, leading to a plateau of 115% +/- 9%. Exposure of the retina to the guanylyl cyclase inhibitor LY83583 (30 and 100 microM) showed fast, transient responses characterized by peaks at 90% +/- 1% and 80% +/- 3%, respectively.

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“…1987; Millan et al. 1991; Sved and Curtis 1993; Mitrovic and Johnston 1994; Zuiderwijk et al. 1996).…”

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confidence: 99%

The effects of local perfusion of DAMGO on extracellular GABA and glutamate concentrations in the rostral ventromedial medulla

Schepers¹,

Mahoney²,

Zapata³

et al. 2007

Journal of Neurochemistry

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Electrophysiological data suggest an involvement of rostral ventromedial medulla (RVM) GABA and glutamate (GLU) neurons in morphine analgesia. Direct evidence that extracellular concentrations of GABA or GLU are altered in response to mu opioid receptor (MOP‐R) activation is, however, lacking. We used in vivo microdialysis to investigate this issue. Basal GABA overflow increased in response to intra‐RVM perfusion of KCl (60 mmol/L). Reverse microdialysis of the MOP‐R agonist d‐Ala(2),NMePhe(4),Gly‐ol(5)]enkephalin (DAMGO) (20–500 μmol/L) produced a concentration‐dependent decrease of RVM GABA overflow. Behavioral testing revealed that concentrations that decreased GABA levels increased thermal withdrawal thresholds. A lower agonist concentration that did not increase GABA failed to alter thermal thresholds. DAMGO did not alter GLU concentrations. However, KCl also failed to modify GLU release. Since rapid, transporter‐mediated uptake may mask the detection of changes in GLU release, the selective excitatory amino acid transporter inhibitor pyrrolidine‐2,4‐dicarboxylic acid (tPDC, 0.6 mmol/L) was added to the perfusion medium for subsequent studies. tPDC increased GLU concentrations, confirming transport inhibition. KCl increased GLU dialysate levels in the presence of tPDC, demonstrating that transport inhibition permits detection of depolarization‐evoked GLU overflow. In the presence of tPDC, DAMGO increased GLU overflow in a concentration‐dependent manner. These data demonstrate that MOP‐R activation decreases GABA and increases GLU release in the RVM. We hypothesize that the opposing effects of MOP‐R on GLU and GABA transmission contribute to opiate antinociception.

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Effects of uptake carrier blockers SK&F 89976-A and l-trans-PDC on in vivo release of amino acids in rat hippocampus

Cited by 29 publications

References 29 publications

Effects of theanine, r-glutamylethylamide, on neurotransmitter release and its relationship with glutamic acid neurotransmission

Effects of theanine, r-glutamylethylamide, on neurotransmitter release and its relationship with glutamic acid neurotransmission

Light‐induced changes in glutamate release from isolated rat retina is regulated by cyclic guanosine monophosphate

The effects of local perfusion of DAMGO on extracellular GABA and glutamate concentrations in the rostral ventromedial medulla

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