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Differing actions of β-(2-thienyl)-γ-aminobutyric acid in central and peripheral preparations

Identifieur interne : 002516 ( Istex/Corpus ); précédent : 002515; suivant : 002517

Differing actions of β-(2-thienyl)-γ-aminobutyric acid in central and peripheral preparations

Auteurs : Jennifer Ong ; David I. B. Kerr ; Pascal Berthelot ; Claude Vaccher ; Nathalie Flouquet ; Michel Debaert

Source :

RBID : ISTEX:C81244B2BA40632FA881487CBC18CD35AA5D6938

English descriptors

Abstract

Abstract: In the guinea-pig isolated ileum, β-(2-thicnyI)-γ-aminobutyric acid (BTG; 100–500 μM reversibly and competitively (pA2 = 4.3 ± 0.1) antagonised the baclofen-induccd (5–100 μM) depression of cholinergic twitch contractions, but not that to adenosine or morphine. By contrast, in rat neocortical slice preparations, BTG (100–500 μM) acted as an agonist, abolishing the frequency and amplitude of spontaneous discharges, sensitive to 2-hydroxysaclofen (100–500 μM). BTG exhibits differential actions at G ABAB receptors in brain and periphery.

Url:
DOI: 10.1016/0014-2999(92)90784-2

Links to Exploration step

ISTEX:C81244B2BA40632FA881487CBC18CD35AA5D6938

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<ce:title>Differing actions of β-(2-thienyl)-γ-aminobutyric acid in central and peripheral preparations</ce:title>
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<ce:given-name>Jennifer</ce:given-name>
<ce:surname>Ong</ce:surname>
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<ce:given-name>Pascal</ce:given-name>
<ce:surname>Berthelot</ce:surname>
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<ce:sup>a</ce:sup>
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<ce:author>
<ce:given-name>Claude</ce:given-name>
<ce:surname>Vaccher</ce:surname>
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<ce:given-name>Nathalie</ce:given-name>
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<ce:given-name>Michel</ce:given-name>
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<ce:textfn>Department of Anaesthesia and Intensive Care, The University of Adelaide, Adelaide, South Australia 5000, Australia</ce:textfn>
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<ce:text>Correspondence to: J. Ong, Department of Anaesthesia and Intensive Care, The University of Adelaide, Adelaide, South Australia 5000. Australia. Tel. 61 (8) 228-5163, fax 61 (8) 232-3283.</ce:text>
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<ce:simple-para id="SP0005">In the guinea-pig isolated ileum, β-(2-thicnyI)-γ-aminobutyric acid (BTG; 100–500 μM reversibly and competitively (pA
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= 4.3 ± 0.1) antagonised the baclofen-induccd (5–100 μM) depression of cholinergic twitch contractions, but not that to adenosine or morphine. By contrast, in rat neocortical slice preparations, BTG (100–500 μM) acted as an agonist, abolishing the frequency and amplitude of spontaneous discharges, sensitive to 2-hydroxysaclofen (100–500 μM). BTG exhibits differential actions at G ABA
<ce:inf>B</ce:inf>
receptors in brain and periphery.</ce:simple-para>
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<ce:text>Baclofen</ce:text>
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<ce:text>Neocortical slices</ce:text>
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<ce:keyword>
<ce:text>(rat)</ce:text>
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<abstract lang="en">Abstract: In the guinea-pig isolated ileum, β-(2-thicnyI)-γ-aminobutyric acid (BTG; 100–500 μM reversibly and competitively (pA2 = 4.3 ± 0.1) antagonised the baclofen-induccd (5–100 μM) depression of cholinergic twitch contractions, but not that to adenosine or morphine. By contrast, in rat neocortical slice preparations, BTG (100–500 μM) acted as an agonist, abolishing the frequency and amplitude of spontaneous discharges, sensitive to 2-hydroxysaclofen (100–500 μM). BTG exhibits differential actions at G ABAB receptors in brain and periphery.</abstract>
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