Gamma-aminobutyric acid modulation of acetylcholine-induced contractions of a smooth muscle from an echinoderm (Sclerodactyla briareus)

• Published in: Invertebrate neuroscience 1999, Vol.4 (1), p.1-8
• Main Authors: Devlin, C L, Schlosser, W
• Format: Article
• Language: English
• Subjects: Acetylcholine - pharmacology; Animals; GABA Agonists - pharmacology; GABA Antagonists - pharmacology; GABA-A Receptor Agonists; GABA-A Receptor Antagonists; GABA-B Receptor Agonists; GABA-B Receptor Antagonists; gamma-Aminobutyric Acid - pharmacology; Muscle Contraction - drug effects; Muscle Contraction - physiology; Muscle, Smooth - drug effects; Muscle, Smooth - metabolism; Organ Culture Techniques; Receptors, GABA-A - drug effects; Receptors, GABA-A - metabolism; Receptors, GABA-B - drug effects; Receptors, GABA-B - metabolism; Sea Cucumbers - metabolism
• ISSN: 1354-2516; 1439-1104
• DOI: 10.1007/s101580050001

This study provides pharmacological evidence for the presence of GABAergic neurons innervating the longitudinal muscle of the body wall (LMBW) of holothurians. Gamma-aminobutyric acid (GABA) A and B receptor subtypes were both present in this system and regulated spontaneous contractions as well as responses to acetylcholine (ACh) that stimulated contraction of the LMBW. GABA dose-dependently relaxed the resting tone of the LMBW. GABA (10(-5) M) inhibited ACh-induced (10(-4) M) contractions by 20%. The GABA B agonist, baclofen, relaxed the LMBW, an effect potentiated by GABA. Pretreatment with baclofen (10(-4) M) inhibited ACh (10(-4) M) contractions of the LMBW by 50%. Phaclofen, a GABA receptor B antagonist, caused a dose-dependent increase in resting tension. Phaclofen-induced (10(-5) M) contractions were reversed by the addition of GABA or baclofen (10(-4) M) and potentiated by the addition of another GABA B receptor antagonist, 2-hydroxy-saclofen (10(-5) M). Pretreatment with phaclofen (10(-5) M) caused a marked potentiation of ACh-induced (10(-4) M) contractions by 101%. 2-Hydroxy-saclofen (10(-5) M) had a toxic effect on the LMBW, rendering it completely unresponsive either to ACh or to a second exposure to GABA, and so exhibiting cross-desensitization. Muscimol, a GABA A receptor agonist, had no effect on the resting tension of the LMBW. Curiously, pretreatment of the muscle with muscimol (10(-5) M) potentiated ACh-evoked (10(-4) M) contractions by nearly 20%. Bicuculline (10(-5) M), a GABA A receptor antagonist, generated large, sustained contractions and partially blocked GABA-induced (10(-4) M) relaxation. Like 2-hydroxy-saclofen, bicuculline (10(-5) M) had a profound cross-desensitizing effect on the LMBW to subsequent exposures to GABA and ACh. ACh was unable to potentiate the sustained contractions induced by bicuculline.