5-Hydroxytryptamine facilitates GABA-induced depolarization in bullfrog primary afferent neurons.
Intracellular and voltage-clamp recordings were made from sensory neurons in bullfrog dorsal root ganglia (DRG). Bath-application of 5-hydroxytryptamine (5-HT, 10 microM to 1 mM) reversibly increased the amplitude of depolarizing responses to gamma-aminobutyric acid (GABA) and muscimol. 5-HT also increased the amplitude of chloride current activated by GABA. An analysis with dose-response curves revealed that 5-HT potentiated the maximum GABA current (Vmax), while it produced no significant change in the apparent dissociation constant (Km). It is suggested that 5-HT increases the sensitivity of the GABAA receptor, acting on an allosteric site for the receptor-ionophore complex.
Akasu
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Department of Physiology, Kurume University School of Medicine, Japan.
D000818:Animals; D005727:Ganglia, Spinal / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009118:Muscimol / Q000494:pharmacology; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D011892:Rana catesbeiana / Q000502:physiology*; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology; D012701:Serotonin / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D011963:Receptors, GABA-A; D009118:Muscimol; D012701:Serotonin; D005680:gamma-Aminobutyric Acid