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

doi:10.1016/0006-8993(93)91592-G

Brain Research

Volume 619, Issues 1–2, 13 August 1993, Pages 22-28

https://doi.org/10.1016/0006-8993(93)91592-G Get rights and content

Abstract

The pharmacological specificity of the mGluR1α subtype of the metabotropic glutamate receptor (mGluR) was examined in a cloned baby hamster kidney cell line (BHK-ts13) measuring [³H]glutamate binding and inositol phosphate (PI) hydrolysis. PI-hydrolysis was maximally stimulated by quisqualate (1112±105%of basal), glutamate (1061±70%of basal), ibotenate (1097±115%of basal) andβ-N-methylamino-l-rmalanine (BMAA) (1010±104%of basal). In contrast, the maximal stimulation of PI-hydrolysis by(1S,3R)-1-amino-cyclopentane-1,3-dicar☐ylic acid (t-ACPD) was only673±78% of the basal level. The relative order of potency was quisqualate > glutamate > ibotenate > t-ACPD > BMAA. Agonist-stimulated PI-hydrolysis was attenuated (25±4%inhibition) byl-2-amino-3-phosphonopropionic acid and partially blocked (44±7%) by pertussis toxin treatment. Saturation binding studies with [³H]glutamate on membranes prepared from BHK-ts13 cells expressing the mGluR1α subtype showed that glutamate binds to a single affinity state of this receptor with a limited capacity (K_d = 296nM, B_max = 0.8pmol/mg protein). In competition experiments, [³H]glutamate was displaced by quisqualate, glutamate, ibotenate, t-ACPD and BMAA with a rank order of potency similar to that found for stimulation of PI-hydrolysis.

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

Abstract

J. Biol. Chem.

Neuron

FEBS Lett.

Trends Pharmacol. Sci.

Neurosci. Lett.

J. Biol. Chem.

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Virology

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Eur. J. Pharmacol.

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Biochem. Pharmacol.

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Neurosci. Lett.

Neuron

Eur. J. Pharmacol. Mol. Pharmacol. Sec.

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Lithium amplifies agonist dependent phosphatidylinositol responses in brain and salivary glands

Biochem. J.