(RS)-alpha-methyl-4-carboxyphenylglycine neither prevents induction of LTP nor antagonizes metabotropic glutamate receptors in CA1 hippocampal neurons

Chinestra, Patrick; Aniksztejn, Laurent; Diabira, Diabé; Ben‐Ari, Yehezkel

doi:10.1152/jn.1993.70.6.2684

Cited by 109 publications

(51 citation statements)

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“…The GABA B and adenosine A 1 receptor-induced presynaptic inhibition of EPSPs is of a rapid onset and fully reversible within 5-10 min after agonist application. 22,57 The depression of the fEPSPs produced by activation of the presynaptic metabotropic glutamate receptor, however, lasts more than 15 min after the termination of agonist application, 5,10,35 which is comparable to that elicited by LFS (see Fig. 2 for comparison).…”

Section: Discussionmentioning

confidence: 78%

Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus

et al. 1998

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Abstract--Long-term depression, depotentiation and long-term potentiation of field excitatory postsynaptic potentials in the CA1 field of the hippocampus were studied in slices from two-, 12-, 24-and 36-week-old rats. Long-term potentiation was induced by stimulating afferent fibres for 1 s at 100 Hz. Long-term depression was induced either by stimulating the afferent pathways twice for 15 min at 1 Hz (protocol 1), giving in total 1800 pulses, or by stimulating the fibres at 5 min intervals twice at 1 Hz for 5 min followed by 5 min stimulation at 5 Hz (protocol 2), giving in total 2100 pulses. We found significant long-term depression in slices of all groups stimulated with protocol 1; however, the magnitude of long-term depression in slices from 24-and 36-week-old rats was significantly lower than that in slices from two-and 12-week old rats, although there was no such difference in the magnitude of long-term potentiation between slices. Stimulation protocol 2 induced long-term depression only in slices from twoand 12-week-old rats. Comparison of the dynamic range of transmission plasticity in slices from two-and 36-week-old rats, calculated as the difference between the nearly saturated long-term potentiation and nearly saturated depotentiation, revealed a significantly smaller dynamic range in slices from 36-week-old rats in comparison with slices from two-week-old animals. The decrease in the dynamic range in slices from 36-week-old rats was due to a diminished capacity to depotentiate the nearly saturated long-term potentiation and not due to a decreased long-term potentiation expression in these slices. In contrast to long-term depression, in which the slope of the field excitatory postsynaptic potentials consistently and significantly decreased below the baseline level, the nearly saturated depotentiation did not decrease below the original, pre-long potentiation baseline level.The results demonstrate that increasing age reduces expression of long-term depression and the dynamic range of transmission plasticity.1998 IBRO. Published by Elsevier Science Ltd.

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Section: Discussionmentioning

confidence: 78%

Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus

et al. 1998

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“…This has previously been reported by some groups (Bashir et al, 1993;Bortolotto et al, 1995;Richter-Levin et al, 1994;Riedel et al, 1995), and not by others (Chinestra et al, 1993;Manzoni et al, 1994;Selig et al, 1995). Also work from mGluR5 knockout mice have shown that NMDA-receptor mediated LTP is impaired in these animals (Jia et al, 1998;Lu et al, 1997).…”

Section: Discussionmentioning

confidence: 81%

“…The involvement of the mGluRs in hippocampal LTD has been well established (Bolshakov and Siegelbaum, 1994;Fitzjohn et al, 1999;O'Mara et al, 1995;Snyder et al, 2001), however their contribution to LTP has been a subject of unresolved debate (Bashir et al, 1993;Bortolotto et al, 1995;Chinestra et al, 1993;Manzoni et al, 1994;Richter-Levin et al, 1994;Riedel et al, 1995;Selig et al, 1995). To date, eight mGluR subtypes, designated mGluR1 to mGluR8, have been cloned from the mammalian brain.…”

Section: Introductionmentioning

confidence: 99%

Evidence for a role for the group I metabotropic glutamate receptor in the inhibitory effect of tumor necrosis factor-α on long-term potentiation

Cumiskey¹,

Butler²,

Moynagh³

et al. 2007

Brain Research

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Pro-inflammatory cytokines are known to be elevated in several neuropathological states that are associated with learning and memory. We have previously demonstrated in our laboratory that the inhibition of long-term potentiation (LTP) in the dentate gyrus region of the rat hippocampus, by tumor necrosis factor (TNF)-α, represents a biphasic response, an early phase dependent on p38 mitogen activated protein kinase (MAPK) activation and a later phase, possible dependent on protein synthesis. Many of the factors involved in the early modulation of LTP by TNF-α have yet to be elucidated. This study investigated if metabotropic glutamate receptors (mGluRs) are functionally linked to the inhibitory effect of TNF-α on LTP in the rat dentate gyrus in vitro. We report that the impairment of early-LTP by TNF-α is significantly attenuated by prior application of the group I/II mGluR antagonist MCPG and more specifically the mGluR5 antagonist MPEP. Since TNF-α is now known to cause transient increases in intracellular Ca 2+ levels from ryanodine-sensitive stores, we explored the possibility that disruption of intracellular Ca 2+ homeostasis could be involved.Ryanodine was found to significantly reverse the inhibition of LTP by TNF-α. From these studies we propose that the TNF-α inhibition of LTP is dependent upon the activation of TNFR1 and mGlu5-receptors. Importantly this study provides the first proof of the involvement of ryanodine-sensitive intracellular Ca 2+ stores in TNF-α mediated inhibition of LTP. IntroductionThe pro-inflammatory cytokine tumor-necrosis factor (TNF)-α is elevated in the brain in a number of neuropathological states including trauma, ischemia, Parkinson's disease, multiple sclerosis and HIV-associated dementia (Iida et al., 2000;Kassiotis and Kollias, 2001;Sriram et al., 2002). The signaling mechanism underlying the ability of TNF-α to cause the cognitive dysfunction associated with many of these conditions has been probed, but to date no clear mechanistic understanding has been reached. TNF-α and IL-1β at pathophysiological levels have been shown by many authors to inhibit long-term potentiation (LTP) in the CA1 and the dentate gyrus regions of the rat hippocampus (Cunningham et al., 1996;Murray and Lynch, 1998;Tancredi et al., 1992) but not by others (Stellwagen and Malenka, 2006). IL-1β has been shown to depress NMDAreceptor mediated field potentials in the dentate gyrus (Coogan B R A I N R E S E A R C H 1 1 3 6 ( 2 0 0 7 ) 1 3 -1 9 ⁎ Corresponding author.

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“…Several studies have shown that the mGluR antagonist, MCPG, can block high frequency stimulation-induced long-term potentiation at the Schaffer collateral-CA1 synapse (7,(26)(27)(28)(29)(30). Several other groups have reported that they cannot block long-term potentiation under apparently identical conditions (31)(32)(33)(34)(35). The lack of truly selective pharmacology of these mGluR compounds could in part help explain problems in using these drugs to study synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

Direct effects of metabotropic glutamate receptor compounds on native and recombinant N -methyl- d -aspartate receptors

Contractor

Gereau

Green

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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The actions of glutamate in the central nervous system are mediated through interaction with fast activating ionotropic receptors and G protein-coupled metabotropic glutamate receptors (mGluRs). Studies of these receptors have relied on the availability of agonists and antagonists selective for each receptor class. Compounds that were thought to be selective for mGluRs have been extensively used to study the role of these receptors in the brain. Their use has implicated mGluRs in a wide range of physiological and pathological processes including the modulation of N-methyl-D-aspartate (NMDA) receptors and NMDA receptordependent processes. We report that some of the most commonly used mGluR compounds act as antagonists on NMDA receptors at concentrations commonly used to activate or block mGluRs. In addition, several of the drugs also act as agonists at higher concentrations due at least in part to high levels of contaminant amino acids. Our results indicate that caution should be used when using these drugs to study the roles of mGluRs in various NMDA-dependent processes. The antagonist effects were dependent on the concentration of the NMDA receptor coagonists, preventing reappraisal of previously published work.

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(RS)-alpha-methyl-4-carboxyphenylglycine neither prevents induction of LTP nor antagonizes metabotropic glutamate receptors in CA1 hippocampal neurons

Cited by 109 publications

References 0 publications

Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus

Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus

Evidence for a role for the group I metabotropic glutamate receptor in the inhibitory effect of tumor necrosis factor-α on long-term potentiation

Direct effects of metabotropic glutamate receptor compounds on native and recombinant N -methyl- d -aspartate receptors

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