Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices

Opitz, Thoralf; Richter, Petra; A.J., Carter,; Kozikowski, Alan P.; Shinozaki, H.; Reymann, Klaus G.

doi:10.1016/0306-4522(95)00195-o

Cited by 37 publications

(16 citation statements)

References 60 publications

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“…Similar preparations to the present one have shown efficacy with various types of drugs, including NMDA antagonists and calcium channel blockers [Schurr et al, 1995;Opitz et al, 1995;Fowler and Li, 1998]. In our study, MK-801 provided almost complete protection of function in the slices after 1 h after ischemia.…”

Section: Discussionsupporting

confidence: 71%

“…Preparation of hippocampal slices and recording of synaptic transmission has been well-documented [Kass and Lipton, 1982;Dong et al, 1988;Schurr et al, 1995], as has the insult of hypoxia, anoxia, hypoglycemia, or a combination of these factors on hippocampal slices [Kass and Lipton, 1982;Aitken and Schiff, 1986;Balestrino and Somjen, 1986;Dong et al, 1988;Fowler and Li, 1998;Schurr et al, 1995;Opitz et al, 1995]. Various drugs have been effective at reducing the damage to slices caused by these insults, including MK-801 [Schurr et al, 1995], pentobarbital [Aitken and Schiff, 1986], chlorpromazine [Balestrino and Somjen, 1986], t-ADA [Opitz, et al, 1995], sodium channel blockers [Fowler and Li, 1988;Fried et al, 1995], and several metabotropic glutamate receptor antagonists [Opitz, et al, 1995]. On the basis of the evidence of the effectiveness of glycine antagonists as a neuroprotective agent in in vivo animal models of ischemia [Warner et al, 1995;Bordi et al, 1997;Fabio et al, 1998], we tested several strychnine-insensitive glycine-modulatory site antagonists for their ability to protect rat hippocampal slices in an in vitro electrophysiologic model of ischemia.…”

Section: Introductionmentioning

confidence: 99%

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Effects of glycine antagonists in an acute in vitro electrophysiological model of ischemia

et al. 1999

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Effects of glycine antagonists in an acute in vitro electrophysiological model of ischemia

et al. 1999

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“…Thus, the activation of group II was found to decrease cell recovery from hypoxia. However, a beneficial role of pre-activation of group I, as well as their detrimental role if activated during hypoxic conditions, was reported [14]. …”

Section: Introductionmentioning

confidence: 99%

[60]Fullerene derivative modulates adenosine and metabotropic glutamate receptors gene expression: a possible protective effect against hypoxia

et al. 2014

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BackgroundGlutamate, the main excitatory neurotransmitter, is involved in learning and memory processes but at higher concentration results excitotoxic causing degeneration and neuronal death. Adenosine is a nucleoside that exhibit neuroprotective effects by modulating of glutamate release. Hypoxic and related oxidative conditions, in which adenosine and metabotropic glutamate receptors are involved, have been demonstrated to contribute to neurodegenerative processes occurring in certain human pathologies.ResultsHuman neuroblastoma cells (SH-SY5Y) were used to evaluate the long time (24, 48 and 72 hours) effects of a [60]fullerene hydrosoluble derivative (t3ss) as potential inhibitor of hypoxic insult. Low oxygen concentration (5% O2) caused cell death, which was avoided by t3ss exposure in a concentration dependent manner. In addition, gene expression analysis by real time PCR of adenosine A1, A2A and A2B and metabotropic glutamate 1 and 5 receptors revealed that t3ss significantly increased A1 and mGlu1 expression in hypoxic conditions. Moreover, t3ss prevented the hypoxia-induced increase in A2A mRNA expression.ConclusionsAs t3ss causes overexpression of adenosine A1 and metabotropic glutamate receptors which have been shown to be neuroprotective, our results point to a radical scavenger protective effect of t3ss through the enhancement of these neuroprotective receptors expression. Therefore, the utility of these nanoparticles as therapeutic target to avoid degeneration and cell death of neurodegenerative diseases is suggested.

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“…The mGluRs offer protection against anoxia (Maiese et al, 1995(Maiese et al, , 1996, nitric oxide (Maiese, 1997(Maiese, , 1998aVincent et al, 1997), excitotoxicity (Anneser et al, 1998), and hypoglycemia (Opitz et al, 1995). The cellular mechanisms that mediate neuronal protection by this group of receptors are not well defined but may rely on the regulation of several different signal transduction pathways.…”

Section: Introductionmentioning

confidence: 99%

Metabotropic glutamate receptor subtypes independently modulate neuronal intracellular calcium

et al. 1999

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Metabotropic glutamate receptors (mGluRs) modulate several G-protein-related signal transduction pathways including intracellular calcium (iCa(2+)) that control both neuronal development and demise. As an initial investigation, we characterized the ability of specific mGluR subtypes to modulate iCa(2+) by using Fura-2 microfluorometry in primary hippocampal neurons. Activation rather than inhibition of the metabotropic system with the group I and group II mGluR agonist 1S, 3R-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD), the specific group I agonist (S)-3,5-dihydroxyphenylglycine (DHPG), and the specific group II agonist (2S,1'S,2'S)-2-(carboxycyclopropyl)glycine (LCCG-I) increased iCa(2+) with increasing concentrations. In contrast, the group III mGluR agonist, L(+)-2-amino-4-phosphonobutyric acid (L-AP4) produced no significant increase in iCa(2+). Through the pharmacological modulation of individual mGluR subtypes, we further examined the role of iCa(2+) release by the mGluR system. Release of iCa(2+) by both 1S,3R-ACPD and LCCG-I was prevented only through the administration of the antagonists (2S)-alpha-ethylglutamic acid (EGlu; mGluR2 and mGluR3) and (2S,1'S,2'S,3'R)-2-(2'-carboxy-3'-phenylcyclopropyl)glycine (PCCG-IV; mGluR2), suggesting that the mGluR2 subtype was responsible for the release of iCa(2+). As a control, the group I antagonists, L(+)-2-amino-3-phosphonopropionic acid (L-AP3) and (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), prevented DHPG release of iCa(2+) but were ineffective against iCa(2+) release by 1S,3R-ACPD. Although extracellular calcium influx did not significantly contribute to the release of iCa(2+) by the mGluR system, pharmacological inhibition of calcium-induced calcium-release-sensitive calcium pools played a critical role in the release of iCa(2+). Further characterization of the cellular calcium pools modulated by the mGluR subtypes may provide greater insight into the mechanisms that mediate neuronal function.

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Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices

Cited by 37 publications

References 60 publications

Effects of glycine antagonists in an acute in vitro electrophysiological model of ischemia

Effects of glycine antagonists in an acute in vitro electrophysiological model of ischemia

[60]Fullerene derivative modulates adenosine and metabotropic glutamate receptors gene expression: a possible protective effect against hypoxia

Metabotropic glutamate receptor subtypes independently modulate neuronal intracellular calcium

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