Modulation of AMPA and NMDA responses in rat spinal dorsal horn neurons by trans-1-aminocyclopentane-1,3-dicarboxylic acid

Cerne, R.; Randić, Mirjana

doi:10.1016/0304-3940(92)90745-s

Cited by 99 publications

(40 citation statements)

References 17 publications

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“…IS,3R-ACPD has also been shown to potentiate NMDA receptor-mediated synaptic responses (Kinney & Slater, 1992;Collins, 1993). In the CAl region of the hip- and cerebellar Purkinje neurones IS,3R-ACPD has also been shown to potentiate responses to AMPA and kainate (Bleakman et al, 1992;Cerne & Randic, 1992;Glaum et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Signal transduction pathways involved in the acute potentiation of NMDA responses by 1S,3R‐ACPD in rat hippocampal slices

Harvey

Collingridge

1993

British J Pharmacology

134

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1 A grease-gap recording technique has been used to investigate the mechanisms underlying the acute potentiation of N-methyl-D-aspartate (NMDA) responses by aminocyclopentane-1S,3R-dicarboxylic acid (IS,3R-ACPD) in area CAI of rat hippocampal slices.2 1S,3R-ACPD (1OM), but not IR,3S-ACPD (1OEM), potentiated submaximal responses to NMDA (dose-ratio of 0.81 ± 0.02 (mean ± s.e.mean); n = 55), but not to a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), in a readily reversible manner. Potentiation also occurred in slices treated with 0.2 tLM tetrodotoxin, and in slices perfused with Mg2"-free medium.3 IS,3R-ACPD-induced potentiation was unaffected by the protein kinase inhibitors K-252b (0.1 tLM) and staurosporine (1 gM) and the intracellular Ca2+ store depletor, thapsigargin (10 gM). Coapplication of staurosporine and thapsigargin was also without effect. 4 IS,3R-ACPD-induced potentiation was unaffected by inhibitors of arachidonic acid formation, bromophenacyl bromide (50 tM) and RG80267 (100 gM). Arachidonic acid (10-50 gM) depressed reversibly NMDA-induced responses. The potentiation was unaffected by 8-bromo cyclic AMP (500 jAM) or the PKA inhibitor Rp-adenosine 3,5-cyclic monophosphothioate triethylamine (Rp-cAMPS; 50 jAM). 5 IS,3R-ACPD-induced potentiation was abolished in slices perfused with Ca2+-free medium. The potentiation was also blocked by phorbol-12,13-diacetate (1 gM), in a staurosporine-sensitive manner.6 It is concluded that the potentiation of NMDA responses by IS,3R-ACPD is not mediated by protein kinase A or C, by release of Ca2+ from intracellular stores or by arachidonic acid. It involves a Ca2+-sensitive process and is negatively regulated by protein kinase C.

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Section: Discussionmentioning

confidence: 99%

Signal transduction pathways involved in the acute potentiation of NMDA responses by 1S,3R‐ACPD in rat hippocampal slices

Harvey

Collingridge

1993

British J Pharmacology

134

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“…This is a particularly attractive hypothesis in the case of mGlu1 receptors, as these are restricted to corticothalamic synapses and because NMDA-receptor mediated responses have been shown to be modulated by activation of group I (i.e. mGlu1/mGlu5) receptors in several brain areas (Fitzjohn et al 1996;Doherty et al 1997;Pisani et al 1997;Martin et al 1998;Holohean et al 1999), as has modulation of AMPA-receptor-mediated responses (Cerne & Randic 1992;Bond & Lodge 1995;Jones & Headley 1995;Dev & Henley 1998;Calabresi et al 1999). In the VB, activation of mGlu1 receptors potentiates responses mediated via either AMPA or NMDA receptors in vivo ( gure 2) (Salt & Binns 2000), and it is probable that this is due to the direct effects of mGlu1 activation on neuronal membrane potential and resistance (McCormick & Von Krosigk 1992;Turner & Salt 1998) rather than a speci c interaction at the receptor level, or that the potentiation seen is a combination of these factors (Salt & Binns 2000).…”

Section: Sensory Responses Of Thalmic Relay Neurons In Vivo: Recruitmmentioning

confidence: 99%

Glutamate receptor functions in sensory relay in the thalamus

Salt

2002

Phil. Trans. R. Soc. Lond. B

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It is known that glutamate is a major excitatory transmitter of sensory and cortical afferents to the thalamus. These actions are mediated via several distinct receptors with postsynaptic excitatory effects predominantly mediated by ionotropic receptors of the a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and N-methyl-d-aspartate varieties (NMDA). However, there are also other kinds of glutamate receptor present in the thalamus, notably the metabotropic and kainate types, and these may have more complex or subtle roles in sensory transmission. This paper describes recent electrophysiological experiments done in vitro and in vivo which aim to determine how the metabotropic and kainate receptor types can in uence transmission through the sensory thalamic relay. A particular focus will be how such mechanisms might operate under physiological conditions.

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“…Group I mGlu receptor agonist-evoked responses are enhanced in the spinal cord of hyperalgesic animals and are reversed by the administration of NMDA receptor antagonists (Boxall and Lancaster, 1998). NMDA currents in dorsal horn neurons are potentiated by the activation of group I mGlu receptors (Bleakman et al, 1992;Cerne and Randic, 1992;Bond and Lodge, 1995). The ionotropic function of NMDA receptor in vivo is subject to phosphorylation, which is initiated by mGlu/G-proteinlinked mechanisms during injury-induced spinal dorsal horn plasticity (Guo et al, 2004).…”

Section: G Painmentioning

confidence: 99%

“…Activation of group I mGlu receptors in motoneurons and dorsal horn neurons induces transient membrane depolarizations and modulates excitation meditated by ionotropic glutamate receptors (Bleakman et al, 1992;Cerne and Randic, 1992;Jones and Headley, 1995;Ugolini et al, 1997Ugolini et al, , 1999Zhong et al, 2000;Neugebauer, 2002), alters spike frequency accommodation, and decreases the firing threshold of these neurons and/or the amplitude and duration of afterhyperpolarizations (Cao et al, 1995;King and Liu, 1996;Morisset and Nagy, 1996;Russo et al, 1997). Group I mGlu receptor activation also induces rhythmic oscillations of the membrane potential and long-term changes in the excitability of sympathetic neurons (Spanswick et al, 1995;Nolan and Logan, 1998).…”

Section: Distribution and Role Of Metabotropic Glutamate 1 Receptors mentioning

confidence: 99%

Metabotropic Glutamate 1 Receptor: Current Concepts and Perspectives

Ferraguti

Crepaldi

Nicoletti³

2008

Pharmacol Rev

192

205

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Almost 25 years after the first report that glutamate can activate receptors coupled to heterotrimeric G-proteins, tremendous progress has been made in the field of metabotropic glutamate receptors. Now, eight members of this family of glutamate receptors, encoded by eight different genes that share distinctive structural features have been identified. The first cloned receptor, the metabotropic glutamate ( mGlu) receptor mGlu1 has probably been the most extensively studied mGlu receptor, and in many respects it represents a prototypical subtype for this family of receptors. Its biochemical, anatomical, physiological, and pharmacological characteristics have been intensely investigated. Together with subtype 5, mGlu1 receptors constitute a subgroup of receptors that couple to phospholipase C and mobilize Ca(2+) from intracellular stores. Several alternatively spliced variants of mGlu1 receptors, which differ primarily in the length of their C-terminal domain and anatomical localization, have been reported. Use of a number of genetic approaches and the recent development of selective antagonists have provided a means for clarifying the role played by this receptor in a number of neuronal systems. In this article we discuss recent advancements in the pharmacology and concepts about the intracellular transduction and pathophysiological role of mGlu1 receptors and review earlier data in view of these novel findings. The impact that this new and better understanding of the specific role of these receptors may have on novel treatment strategies for a variety of neurological and psychiatric disorders is considered

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Modulation of AMPA and NMDA responses in rat spinal dorsal horn neurons by trans-1-aminocyclopentane-1,3-dicarboxylic acid

Cited by 99 publications

References 17 publications

Signal transduction pathways involved in the acute potentiation of NMDA responses by 1S,3R‐ACPD in rat hippocampal slices

Signal transduction pathways involved in the acute potentiation of NMDA responses by 1S,3R‐ACPD in rat hippocampal slices

Glutamate receptor functions in sensory relay in the thalamus

Metabotropic Glutamate 1 Receptor: Current Concepts and Perspectives

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