A pharmacological characterization of the mGluR1α subtype of the metabotropic glutamate receptor expressed in a cloned baby hamster kidney cell line

  title={A pharmacological characterization of the mGluR1$\alpha$ subtype of the metabotropic glutamate receptor expressed in a cloned baby hamster kidney cell line},
  author={Christian Thomsen and Eileen R. Mulvihill and Betty Haldeman and Darryl S. Pickering and David R. Hampson and Peter D. Suzdak},
  journal={Brain Research},
CPCCOEt, a noncompetitive metabotropic glutamate receptor 1 antagonist, inhibits receptor signaling without affecting glutamate binding.
It is proposed that the interaction of CPCCOEt with Thr815 and Ala818 of mGluR1 disrupts receptor activation by inhibiting an intramolecular interaction between the agonist-bound extracellular domain and the transmembrane domain.
Enhanced type 1alpha metabotropic glutamate receptor-stimulated phosphoinositide signaling after pertussis toxin treatment.
Changing changes in the concentration-effect curves for mGluR agonists are consistent with a model in which the receptor associates with PTX-sensitive inhibitory (Gi/o) and PTx-insensitive stimulatory (Gq/11) G proteins that can each influence PIC activity.


Cloning of a cDNA for a glutamate receptor subunit activated by kainate but not AMPA
The cloning and expression of a functional rat glutamate receptor subunit cDNA, GluR6, which has a very different pharmacology from that of the GluLl–GluR4 class and exhibits an outwardly rectifying current–voltage relationship.
Activation of polyphosphoinositide metabolism as a signal‐transducing system coupled to excitatory amino acid receptors in astroglial cells
Astroglia cultured from newborn rat cerebra are used to demonstrate that glutamate provokes an accumulation of inositol phosphates in a time‐ and concentration‐dependent manner, suggesting a feedback role for protein kinase C in phospholipase C action.
Activation of the metabotropic glutamate receptor attenuates N-methyl-D-aspartate neurotoxicity in cortical cultures.
Concomitant activation of the ACPD receptor may serve as a protective mechanism against neurotoxicity that could be produced by brief intense NMDA receptor activation during normal or abnormal brain function.