Article date: February 1984
By: Michel Désarmenien, Paul Feltz, Guiseppe Occhipinti, Francesca Santangelo, Remy Schlichter in Volume 81, Issue 2, pages 327-333
Intracellular recordings from adult rat dorsal root ganglion neurones were performed in vitro and the coexistence of two γ‐aminobutyric acid (GABA) receptors on the membrane of identified Aδ and C primary afferents was demonstrated.
Transient applications of GABA (10−6 − 10−2m) evoked dose‐dependent depolarizations and increased membrane conductance. The responses were mimicked by muscimol, isoguvacine, THIP and 3 amino propane sulphonic acid (3 APS); they were blocked by bicuculline and picrotoxin. Pentobarbitone induced an increase of GABA‐induced depolarizations.
Perfusion of tetraethylammonium (TEA, 7.5 mm) and intracellular injection of Cs+ ions unmasked the Ca2+ component of action potentials, which appeared as long‐lasting plateau depolarizations. Such action potentials were shortened in the presence of methoxyverapamil (D600, 5 × 10−6‐ 10−5m) and in a medium without Ca+ ions.
Prolonged (5–10 min) perfusion of GABA (10−9‐10−5m) shortened the Ca2+ component of action potentials. This effect was mimicked by baclofen (10−7‐5 × 10−6m) and muscimol (5 × 10−7‐10−5m) and was not affected by bicuculline perfusion (5 × 10−6‐10−5m). Isoguvacine (2.5 × 10−5m) did not affect action potential duration.
It is concluded that two GABA receptors coexist on the membrane of slow conducting primary afferents: the bicuculline‐sensitive GABAA receptor mediates depolarizations and the bicuculline‐insensitive GABAB receptor shortens the calcium component of action potentials.
Intracellular recordings from adult rat dorsal root ganglion neurones were performed in vitro and the coexistence of two γ‐aminobutyric acid (GABA) receptors on the membrane of identified Aδ and C primary afferents was demonstrated.
Transient applications of GABA (10−6 − 10−2m) evoked dose‐dependent depolarizations and increased membrane conductance. The responses were mimicked by muscimol, isoguvacine, THIP and 3 amino propane sulphonic acid (3 APS); they were blocked by bicuculline and picrotoxin. Pentobarbitone induced an increase of GABA‐induced depolarizations.
Perfusion of tetraethylammonium (TEA, 7.5 mm) and intracellular injection of Cs+ ions unmasked the Ca2+ component of action potentials, which appeared as long‐lasting plateau depolarizations. Such action potentials were shortened in the presence of methoxyverapamil (D600, 5 × 10−6‐ 10−5m) and in a medium without Ca+ ions.
Prolonged (5–10 min) perfusion of GABA (10−9‐10−5m) shortened the Ca2+ component of action potentials. This effect was mimicked by baclofen (10−7‐5 × 10−6m) and muscimol (5 × 10−7‐10−5m) and was not affected by bicuculline perfusion (5 × 10−6‐10−5m). Isoguvacine (2.5 × 10−5m) did not affect action potential duration.
It is concluded that two GABA receptors coexist on the membrane of slow conducting primary afferents: the bicuculline‐sensitive GABAA receptor mediates depolarizations and the bicuculline‐insensitive GABAB receptor shortens the calcium component of action potentials.
DOI: 10.1111/j.1476-5381.1984.tb10082.x
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