Differing actions of β-(2-thienyl)-γ-aminobutyric acid in central and peripheral preparations
Identifieur interne : 002516 ( Istex/Curation ); précédent : 002515; suivant : 002517Differing actions of β-(2-thienyl)-γ-aminobutyric acid in central and peripheral preparations
Auteurs : Jennifer Ong [Australie] ; David I. B. Kerr [France] ; Pascal Berthelot [France] ; Claude Vaccher [France] ; Nathalie Flouquet [France] ; Michel Debaert [France]Source :
- European Journal of Pharmacology [ 0014-2999 ] ; 1992.
English descriptors
- KwdEn :
- Agonist, Agonist activity, Agonists wcrc, Analogue, Antagonist, Baclofen, Berthelot, Control level, Different preparations, Full agonist, Gaba, Ileum, Krebs medium, Krebs solution, Neocortical slices, Partial agonism, Partial agonist, Phenyl ring, Present study, Receptor, Receptor agonist, Receptor antagonist, Receptor antagonists, Spontaneous activity, Spontaneous discharges.
- Teeft :
- Agonist, Agonist activity, Agonists wcrc, Analogue, Antagonist, Baclofen, Berthelot, Control level, Different preparations, Full agonist, Gaba, Ileum, Krebs medium, Krebs solution, Neocortical slices, Partial agonism, Partial agonist, Phenyl ring, Present study, Receptor, Receptor agonist, Receptor antagonist, Receptor antagonists, Spontaneous activity, Spontaneous discharges.
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
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<front><div type="abstract" xml: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.</div>
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