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Metabotropic Glutamate Receptor (mGluR)‐Mediated Potentiation of Cyclic AMP Responses Does Not Require Phosphoinositide Hydrolysis: Mediation by a Group II‐Like mGluR by Danny G. Winder; P. Jeffrey Conn is a Neuroscience article available to read on EtoBox.
What is Metabotropic Glutamate Receptor (mGluR)‐Mediated Potentiation of Cyclic AMP Responses Does Not Require Phosphoinositide Hydrolysis: Mediation by a Group II‐Like mGluR about?
Abstract: Metabotropic glutamate receptors (mGluRs) in the CNS are coupled to a variety of second messenger systems, the best characterized of which is activation of phosphoinositide hydrolysis. Recently, we found that activation of mGluRs in rat brain slices by the selective mGluR agonist 1‐aminocyclopentane‐1__S__,3__R__‐dicarboxylic acid (1__S__,3__R__‐ACPD) potentiates cyclic AMP (cAMP) responses elicited by activation of other receptors coupled to G~s~. It has been suggested that mGluR‐mediated potentiation of cAMP responses is secondary to activation of phosphoinositide hydrolysis. However, preliminary evidence suggests that this is not the case. Therefore, we designed a series of experiments to test more fully the hypothesis that mGluR‐mediated potentiation of cAMP responses is secondary to phosphoinositide hydrolysis. Inhibitors of both protein kinase C and intracellular calcium mobilization failed to antagonize 1__S__,3__R__‐ACPD‐stimulated potentiation of cAMP responses. Further, coapplication of phorbol esters and 1__S__,3__R__‐ACPD induced a cAMP response that was greater than additive. Finally, (__RS__)‐3,5‐dihydroxyphenylglycine, a selective agonist of mGluRs coupled
Who reads Metabotropic Glutamate Receptor (mGluR)‐Mediated Potentiation of Cyclic AMP Responses Does Not Require Phosphoinositide Hydrolysis: Mediation by a Group II‐Like mGluR?
It is typically read by researchers, students, and practitioners in Neuroscience.
- Author
- Danny G. Winder; P. Jeffrey Conn
- Publisher
- John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)
- Published
- 1995
- Language
- EN
- Field
- Neuroscience (Life Sciences)