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4 edition of Analysis of presynaptic metabotropic glutamate and adenosine A1 receptors found in the catalog.

Analysis of presynaptic metabotropic glutamate and adenosine A1 receptors

Louise Jane Blythe

Analysis of presynaptic metabotropic glutamate and adenosine A1 receptors

by Louise Jane Blythe

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Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

Thesis (M.Sc.) -- University of Toronto, 1998.

SeriesCanadian theses = -- Thèses canadiennes
The Physical Object
FormatMicroform
Pagination2 microfiches : negative. --
ID Numbers
Open LibraryOL18884956M
ISBN 100612339521
OCLC/WorldCa46584444

Conn PJ, Battaglia G, Marino MJ, Nicoletti F () Metabotropic glutamate receptors in the basal ganglia motor circuit. Nat Rev Neurosci 6, – [19] Testa CM, Standaert DG, Young AB, Penney JB Jr. () Metabotropic glutamate receptor mRNA expression in the basal ganglia of the rat. J Neuro – [20]. L- glutamate is the major excitatory neurotransmitter in the central nervous system and activates both ionotropic and metabotropic glutamate receptors. Glutamatergic neurotransmission is involved in most aspects of normal brain function and can be perturbed in many neuropathologic conditions.

Neuropeptide Y inhibits this effect through stimulation of glutamate release and consequent activation of metabotropic glutamate receptors that stimulate adenosine release. Then, A1 receptors are stimulated and inhibit osmotic swelling via regulation of K + and Cl − channels (Uckermann et al., ). The metabotropic glutamate receptors, or mGluRs, are a type of glutamate receptor that are active through an indirect metabotropic process. They are members of the group C family of G-protein-coupled receptors, or GPCRs. Like all glutamate receptors, mGluRs bind with glutamate, an amino acid that functions as an excitatory neurotransmitter.

between ionotropic and metabotropic glutamate receptors was trans‑ACPD (1S,3R isomer) The ligand contributed considerably to the study of metabotropic glutamate receptors despite its lack of subtype selectivity.2,3,5 A limited number of molecules possess agonist activity across all mGlu receptors. RESEARCH ARTICLE Open Access Control of glutamate release by complexes of adenosine and cannabinoid receptors Attila Köfalvi1†, Estefanía Moreno2†, Arnau Cordomí3†, Ning-Sheng Cai4, Victor Fernández-Dueñas5,6, Samira G. Ferreira1, Ramón Guixà-González3, Marta Sánchez-Soto4, Hideaki Yano4, Verònica Casadó-Anguera2, Rodrigo A. Cunha1,7, Ana Maria Sebastião8,9, Francisco.


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Analysis of presynaptic metabotropic glutamate and adenosine A1 receptors by Louise Jane Blythe Download PDF EPUB FB2

Adenosine A1 and Class II Metabotropic Glutamate Receptors Mediate Shared Presynaptic Inhibition of Retinotectal Transmission CHUNYI ZHANG AND JOHN T. SCHMIDT Department of Biological Sciences and Neurobiology Research Center, University at Albany, State University of New York, Albany, New York Zhang, Chunyi and John T.

Schmidt. In the present study, we use both the isolated nerve-tectum preparation and cultured goldfish retinal ganglion cells for parallel studies on presynaptic inhibition and calcium channel modulation, and report that activation of A1 adenosine receptors and group II metabotropic glutamate receptors both inhibit N-type calcium channels to produce the Cited by: A1 receptors, cells were transiently transfected with 10 mg of cDNA encoding the rat metabotropic glutamate receptors and/or rat adenosine A1 receptor (ratio ; pcDNA containing LacZ reporter was used to equilibrate the amount of total DNA) by calcium phosphate precipita-tion (19).

The cells were used for experimentation at either 24 or 48 h. Schild analysis yielded a Kd value of nM for antagonism of CPA by the adenosine A1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine). Both baclofen and adenosine reduced the magnitude of paired-pulse depression of IPSCs, and neither blocked currents evoked by GABA, which was pressure-ejected from by:   Here we report a molecular interaction between metabotropic glutamate receptor type 1α and the adenosine A1 receptor, two members of different GPCR families.

This interaction suggests that both receptors may form part of a signaling complex in vivo that could play a critical role in fine-tuning neurotransmission at glutamatergic by: Adenosine A1 and class II metabotropic glutamate receptors mediate shared presynaptic inhibition of retinotectal transmission.

Zhang C(1), Schmidt JT. Author information: (1)Department of Biological Sciences and Neurobiology Research Center, University at Albany, State University of New York, Albany, New YorkUSA.

Interactions between adenosine receptors and ionotropic excitatory amino‐acid transmission (via N‐methyl‐ D ‐aspartate (NMDA) receptors) have previously been reported from our laboratory (Bartrup & Stone, ; Nikbakht & Stone, ), and there have been reports of interactions between adenosine and metabotropic glutamate.

Glutamate is a major excitatory neurotransmitter which induces synaptic transmission through activation of glutamate receptors, which are separated into two broad groups: metabotropic glutamate receptors (mGluRs) and ionotropic glutamate receptors. Ionotropic glutamate receptors include the ligand-gated AMPA, NMDA, and kainate receptors.

Given the remarkably slow desensitization of presynaptic A 1 receptors (Wetherington & Lambert, ), ambient adenosine will provide a sustained inhibition of transmitter release, thereby preserving transmitter glutamate, and protecting cells from possible glutamate toxicity.

Its neuromodulatory role relies on a balanced activation of inhibitory A 1 receptors (A1R) and facilitatory A 2A receptors (A2AR), mostly controlling excitatory glutamatergic synapses: A1R impose a tonic brake on excitatory transmission, whereas A2AR are selectively engaged to.

These receptors are termed ionotropic glutamate receptors (iGluRs). The subsequent discovery of metabotropic glutamate receptors (mGluRs) revealed that glutamate can also mediate slow synaptic potentials, modulate ion channels, and directly couple to GTP binding proteins. G-protein-coupled receptors (GPCRs) may form heteromeric complexes and cooperatively mediate cellular responses.

Although heteromeric GPCR complexes are suggested to occur in many neurons, their contribution to neuronal function remains unclear.

We address this question using two GPCRs expressed in cerebellar Purkinje cells: adenosine A1 receptor (A1R), which. We address this question using two GPCRs expressed in cerebellar Purkinje cells: adenosine A1 receptor (A1R), which regulates neurotransmitter release and neuronal excitability in central neurons, and type-1 metabotropic glutamate receptor (mGluR1), which mediates cerebellar long-term depression, a form of synaptic plasticity crucial for cerebellar motor learning.

Evidence for heteromeric receptor complexes comprising adenosine A2A and metabotropic glutamate 5 (mGlu5) receptors in striatum has raised the possibility of synergistic interactions between striatal A2A and mGlu5 receptors.

We investigated the role of striatal A2A receptors in the locomotor stimulant and antiparkinsonian properties of mGlu5 antagonists using. Fabiano P. Menezes, Rosane S.

Da Silva, in Reproductive and Developmental Toxicology (Second Edition), Distribution and Signaling of Adenosine Receptors.

The adenosine receptors A 1, A 2A, A 2B, and A 3 are clustered on the P 1 purinergic receptor family (Ralevic and Burnstock, ).The P 1 receptors are expressed on the whole body. The high-affinity adenosine A 1 receptor is mainly. It has been hypothesized that heteromers of adenosine A2A receptors (A2AR) and cannabinoid CB1 receptors (CB1R) localized in glutamatergic nerve terminals mediate the integration of adenosine and endocannabinoid signaling involved in the modulation of striatal excitatory neurotransmission.

Previous studies have demonstrated the existence of A2AR-CB1R heteromers in artificial cell systems. We propose that the attenuation of the inhibitory effects of adenosine caused by activation of metabotropic glutamate receptors might have pathophysiological relevance in situations, such as hypoxia and ischaemia, in which marked release of both excitatory amino acids (Benveniste et al., ) and adenosine (Berne et al., ) occurs.

Scanziani M, Salin PA, Vogt KE et al () Use-dependent increases in glutamate concentration activate presynaptic metabotropic glutamate receptors. Nature PubMed CrossRef Google Scholar Schoepp DD, Goldsworthy J, Johson BG et al () 3,5-dihydroxyphenylglycine is a highly selective agonist for phosphoinositide linked metabotropic.

Co-Activation of Metabotropic Glutamate Receptor 3 and Beta-Adrenergic Receptors Modulates Cyclic-AMP and Long-Term Potentiation, and Disrupts Memory Reconsolidation Adam G Walker 1, 2 na1.

The aim of the present review was to summarize the described mechanisms of interaction and crosstalking between adenosine and metabotropic glutamate receptors, mainly of group I, in both in vitro and in vivo systems, and their possible use for the design of novel ligands for the treatment of neurodegenerative diseases.

Presynaptic metabotropic glutamate receptors (mGluRs) modulate the release of transmitter from most central synapses. However, difficulties in recording from presynaptic structures has lead to an incomplete understanding of the mechanisms underlying these fundamental processes.

By recording directly from presynaptic reticulospinal axons and postsynaptic motoneurons of the lamprey spinal .Akihisa Mori, in International Review of Neurobiology, Presynaptic A 2A –A 1 receptor interaction. Adenosine A 2A and A 1 receptor heterodimer-induced reciprocal interaction has recently been discussed in the regulation of corticostriatal glutamatergic transmission onto MSNs (Schwarzchild, Agnati, Fuxe, Chen, & Morelli, ).This was suggested from data indicating A 2A –A 1.Adenosine receptors are GTP binding (G) protein‐coupled receptors (GPCRs) widely expressed at nerve terminals and postsynaptic cells.

Endogenous adenosine is rapidly converted from ATP (Dunwiddie et al. ), which is released from nerve terminals (Silinsky & Hubbard, ; Jo & Schlichter, ), neuronal somata, or glia (Latini & Pedata, ) in response to neuronal activity.