Talk:Metabotropic glutamate receptor

Latest comment: 6 years ago by InternetArchiveBot in topic External links modified

Error check edit

There is a statement in Metabotropic glutamate receptor,

"Rather than having much direct effect on postsynaptic potential, mGluRs serve to modulate the function of other receptors (Chu and Hablitz, 2000). "

I believe this to be in error. Though I cannot access the full article by Chu and Hablitz, metabotropic receptors do not modify other receptors. They usually modulate cAMP which leads to changes in ion channels - and through this they do change the postsynaptic potential. --RichG 10:33, 13 October 2005 (UTC)Reply


You're right that it's not correct to suggest that they don't have any role in postsynaptic potential, so I'll that part of the sentence out. Their modulatory role, however, is REALLY well supported, including their ability to modify other receptors. Check it out:
  • Metabotropic glutamate receptors provide intrinsic modulation of the lamprey locomotor network. Brain Research Reviews, Volume 40, Issues 1-3, October 2002, Pages 9-18 Abdeljabbar El Manira, Petronella Kettunen, Dietmar Hess and Patrik Krieger
  • Metabotropic glutamate mGlu5 receptor-mediated modulation of the ventral striopallidal GABA pathway in rats. Interactions with adenosine A2A and dopamine D2 receptors. Neuroscience Letters, Volume 324, Issue 2, 17 May 2002, Pages 154-158 Zaida Díaz-Cabiale, Meritxell Vivó, Alberto Del Arco, William T. O'Connor, Michael K. Harte, Christa E. Müller, Emili Martínez, Patrizia Popoli, Kjell Fuxe and Sergi Ferré
  • Metabotropic glutamate receptor 5 mediates the potentiation of N-methyl-D-aspartate responses in medium spiny striatal neurons. Neuroscience, Volume 106, Issue 3, 27 September 2001, Pages 579-587. A. Pisani, P. Gubellini, P. Bonsi, F. Conquet, B. Picconi, D. Centonze, G. Bernardi and P. Calabresi
  • Activation of metabotropic glutamate receptor 1 inhibits glutamatergic transmission in the substantia nigra pars reticulata. Neuroscience, Volume 105, Issue 4, 22 August 2001, Pages 881-889. M. Wittmann, G. W. Hubert, Y. Smith and P. J. Conn

plus, these quotes from articles I'll have listed in the references:

  • "The mGluRs modulate excitatory synaptic transmission in various regions of the brain (Endoh, 2004)"
  • "Glutamate ... activates both ionotropic and metabotropic glutamate receptors (mGluRs). The former is involved in fast synaptic transmission whereas the latter play a modulatory role (Chu and Hablitz, 2000)."
  • "[D]istinct functional roles for group I mGluR subtypes have been demonstrated for medium spiny neurons, either in synaptic plasticity or in the modulation of NMDA receptor activity (Bonsi, 2005)."
With this and the fact that I'll take out the "much role in postsynaptic potential" part, would you say it's fair to remove the 'dubious' tag? --Delldot 20:28, 13 October 2005 (UTC)Reply
  • Ok, good work! Apparently mGluR do indeed modulate other receptors. I appreciate the lesson. This is cutting edge stuff. --RichG 01:45, 14 October 2005 (UTC)Reply


Broken link? edit

Does this link work for anyone else? Should we remove it or replace it?

Thanks, delldot | talk 21:00, 14 January 2007 (UTC)Reply

Oh, never mind, I got to it through the web archive. [1] delldot | talk 22:09, 25 January 2007 (UTC)Reply

Suggestions edit

I read with great interest the “Metabotropic Glutamate Receptor” Page of Wikipedia and would like to make following suggestions:

- It is rather difficult to find book references, as for exemple ref. 36 of the History section. Citation of the original papers would considerably facilitate the task of interested readers. The original papers for ref 36 are below. In view of their contents I would suggest the following: "The first demonstration that glutamate could induce the formation of molecules belonging to a major second messenger system was in 1985, when it was shown that it could stimulate the formation of inositol phosphates.(Sladeczek F, Pin J-P, Récasens M, Bockaert J, Weiss S 1985. Glutamate stimulates inositol phosphate formation in striatal neurons. Nature 317, 717-719). This finding allowed in 1987 to yield an explanation for oscillatory ionic glutamate responses and to provide further evidence for the existence of metabotropic glutamate receptors (Sugiyama H., Ito I, Hirono C 1987. A new glutamate receptor linked to inositol phospholipids metabolism. Nature 325, 531-533). In 1991 the first metabotropic glutamate receptor of the seven transmembrane domain family was cloned (Masu M., Tanabe Y., Tsuchida K., Shigemoto R., Nakanishi S. 1991. Sequence and expression of a metabotropic glutamate receptor. Nature 349, 760-765)."

- The following addition could be an interesting extension to the actual complexity of metabotropic responses: "More recent reports on ionotropic glutamate receptors able to couple to metabotropic transduction systems (Dingledine R, Borges K, Bowie D, Traynelis SF, 1999. The glutamate receptor Ion channels. Pharmacol. Rev. 51, 7-61. Wang Y, Small DL, Stanimirovic DB, Morley P., Durkin JP. 1997 Nature 389, 502-504 and references citing Wang et al. in Nature on-line) suggest that metabotropic responses of glutamate might not be limited to seven transmembrane domain metabotropic glutamate receptors.”


In the Function and structure chapter, I would suggest to modify the paragraph: “Unlike ionotropic receptors, metabotropic receptors are not directly linked to ion channels, but may affect them by activating biochemical cascades. In addition to producing excitatory and inhibitory postsynaptic potentials, mGluRs serve to modulate the function of other receptors (such as NMDA receptors), changing the synapse’s excitability.” “…….producing excitatory and inhibitory postsynaptic potentials……” is surely documented by the cited references, but might be misleading for a non-specialist because the straightforward way for “producing excitatory and inhibitory postsynaptic potentials” is glutamate induced opening of ionotropic receptor channels.

My suggestion would be: "Unlike ionotropic receptors, metabotropic receptors of the seven transmembrane domain family are no ion channels. They activate signalling cascades, leading to biochemical modification of other proteins, as for exemple ion channels. This can lead to changes in the synapses’ excitability by, for exemple, presynaptic inhibition of neurotransmission (Sladeczek F, Momiyama A, Takahashi T 1992. Presynaptic inhibitory action of metabotropic glutamatereceptor agonist on excitatory transmission in visual cortical neurons. Proc. Roy. Soc. Lond. B 1993 253, 297-303), or modulation and even induction of postsynaptic responses (2, 5-7)."


The paragraph succeeding the above in the mGluR-page describes GroupI mGluR-responses and would therefore fit better in the corresponding chapter. —Preceding unsigned comment added by Defincom (talkcontribs) 16:56, 26 October 2008 (UTC) Defincom (talk) 14:35, 7 December 2008 (UTC)Reply

I think these are all fine suggestions, you should go ahead and implement them! Let me know if there's anything I can do to help. delldot ∇. 05:09, 27 October 2008 (UTC)Reply
Just a note that as a rule, Wikipedia policy prefers secondary references (such as review papers) to primary references, because they lend themselves less to "original interpretation". But on a technical topic like this, it might not be possible to find secondary references that address all the key issues, so you should go ahead and use primary refs if you feel that you need them. Looie496 (talk) 05:50, 27 October 2008 (UTC)Reply

Protein Domain edit

This page has been marked in the category 'Protein Domains' but other than mentioning that the specific protein the article refers to has at least 7 of them, there appears to be no reason for it to be on the list. I would suggest we remove it from the protein domains category. Ta, Abergabe (talk) 15:12, 24 June 2010 (UTC)Reply

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