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Dive into the research topics where Mary Richards is active.

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Featured researches published by Mary Richards.


British Journal of Pharmacology | 1995

Human muscarinic receptors expressed in A9L and CHO cells: activation by full and partial agonists.

Mary Richards; Paul L.M. van Giersbergen

1 A comparative study of receptor activation by ten full and partial muscarinic agonists was undertaken on the five subtypes of human muscarinic receptors expressed at similar receptor densities in Chinese hamster ovary (CHO‐K1) cells. In addition, m1, m2 and m3 receptors were expressed in mouse fibroblast A9L cells in order to compare the influences of cell type on agonist activation of these receptors.


Biochemical Pharmacology | 1997

Activation of neurotensin receptors and purinoceptors in human colonie adenocarcinoma cells detected with the microphysiometer

Mary Richards; Paul L.M. van Giersbergen; André Zimmermann; Brigitte Lesur; Jan Hoflack

Activation of endogenous neurotensin (NT) receptors and P2-purinoceptors expressed by human colonic adenocarcinoma HT-29 cells increased extracellular acidification rates that were detected in the microphysiometer. NT (pGlu-Leu-Tyr-Glu-Asn-Lys-Pro-Arg-Arg-Pro-Tyr-Ile-Leu), NT[8-13] (Arg-Arg-Pro-Tyr-Ile-Leu), NT[9-13] (Arg-Pro-Tyr-Ile-Leu), and NT1 (N alpha methyl-Arg-Lys-Pro-Trp-Tle-Leu [Tle = tert-leucine]) were full agonists, whereas XL 775 (N-[N-[2-[3-[[6-amino-1-oxo-2-[[(phenylmethoxy)carbonyl]-amino]hex yl]amino]phenyl]-3-(4-hydroxyphenyl)-1-oxo-2-propenyl]-L-isoleucyl]-L-le ucine) was a partial agonist for activating NT receptors expressed by HT-29 cells. Desensitization induced by NT was rapid and monophasic with 85% of the initial response lost by a 30-s exposure. Once initiated, the rate and extent of desensitization were similar for different concentrations of a given agonist, for agonists of different potencies, and for agonists of different efficacies, which suggests that desensitization may be independent of receptor occupancy or agonist efficacy. Resensitization was a much slower process, requiring 60 min before the full agonist response to NT was recovered. ATP, via P2-purinoceptors, also activated cellular acidification rates in a concentration-dependent manner. ATP induced a biphasic desensitization of purinoceptors with a loss of ca. 50% of the initial stimulation detectable between 30 and 90 s of exposure to the agonist. Desensitization of NT receptors did not influence the activation of P2-purinoceptors by ATP, suggesting there was no heterologous desensitization between the two types of receptors. Superfusion with NT receptor agonists for 15 min at concentrations that did not elicit changes in extracellular acidification rates blocked, in a concentration-dependent manner, the agonist response induced by 100 nM NT. This may reflect sequestration of the receptor. These results suggest that the high agonist affinity state of NT receptors may modulate receptor sequestration, whereas activation of the low agonist affinity state may be linked to cellular metabolism. Comparison of our results with published data found differences as well as similarities of NT responses among three lines of HT-29 cells.


Life Sciences | 1995

Differences in agonist potency ratios at human m1 muscarinic receptors expressed in A9L and CHO cells

Mary Richards; Paul L.M. van Giersbergen

A9L mouse fibroblast and Chinese hamster ovary (CHO) cells appear to differ in their complement of guanine-nucleotide binding proteins (G proteins) and/or isoform of effectors that lead to inositol-monophosphate formation. The influence of these cellular components on receptor activation was examined by comparing agonist-induced inositol monophosphate formation via human muscarinic m1 receptors expressed in the two cell lines. The rank order of agonist potencies of five full agonists differed in the two cell lines. In addition, differences in agonist potency ratios for two of the five agonists (carbachol and methacholine) suggest that the agonists differ in their activation of m1 receptors and this is reflected in differences in G protein coupling. The results provide biological evidence that muscarinic agonists differentially activate m1 receptors and that, at least for the systems examined in this study, receptor-effector coupling in a given system may depend on the structure of the agonist.


European Journal of Pharmacology | 1991

EFFECTS OF CYPROHEPTADINE AND PIZOTIFEN ON CENTRAL MUSCARINIC RECEPTORS

Mary Richards

The affinities of cyproheptadine, pizotifen and (+/-)-quinuclidinyl xanthane-9-carboxylate hemioxylate (QNX) were determined at muscarinic autoreceptors and postsynaptic (IP1 formation) receptors in rat hippocampal slices. The affinity values for QNX were 8.2 and 8.5 respectively. Cyproheptadine and pizotifen were less potent than QNX. Pizotifen was slightly (2-fold) less active at antagonizing IP1 formation than blocking the autoreceptors whereas cyproheptadine was equally active at antagonizing the two hippocampal muscarinic receptors.


Biochemical Pharmacology | 1991

Pharmacology and second messenger interactions of cloned muscarinic receptors

Mary Richards


Archive | 1992

Diaryl piperazineacetamides as antimuscarinic agents.

Hijfte Luc Van; Mary Richards; Marcel Hibert; Jan Hoflack; Susanne Trumpp-Kallmeyer; Gilbert Marciniak


Archive | 1994

Diaryl piperazinoacetamide compounds as antimuscarinic agents

Hijfte Luc Van; Mary Richards; Marcel Hibert; Jan Hoflack; Susanne Trumpp-Kallmeyer; Gilbert Marciniak


Archive | 1995

5H-Dibenzo (A,D) cycloheptenes as muscarinic receptor antagonists

Marcel Domaine Des Grands-prés Hibert; Luc Van Hijfte; Mary Richards; Paul Moser


Life Sciences | 1995

Synthesis and biological evaluation of MDL 74,019DG, a centrally active M1 versus M2 selective muscarinic receptor antagonist

L. Van Hijfte; V. Zerr; Marcel Hibert; G. Marciniak; Paul Moser; P. Moran; Mary Richards; P.L.M. van Giersbergen


Life Sciences | 1993

Activation by full and partial agonists of M1 to M5 human muscarinic receptors expressed in A9L or CHO cells

Mary Richards; P.L.M. van Giersbergen; C.R. Jones

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Marcel Hibert

University of Strasbourg

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