Capsaicin blocks synaptically activated potassium conductance in snail neurone.
The effect of capsaicin was studied on non-cholinergic inhibitory postsynaptic currents (IPSC). The experiments were performed on an identified snail neurone using the single electrode voltage-clamp technique. The IPSC decayed with a bi-exponential time course. Capsaicin (200 microM) reversibly blocked both components of the transmitter-activated potassium conductance similarly to other potassium channel blockers such as Ba2+, quinine or 4-aminopyridine. Externally applied TEA+ exclusively attenuated the slow phase. Capsaicin prolonged the action potential duration and decreased the membrane outward current in the postsynaptic neurone.
D015761:4-Aminopyridine; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D002211:Capsaicin / Q000494:pharmacology*; D004553:Electric Conductivity; D006372:Helix, Snails; D007473:Ion Channels / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects*; D011188:Potassium / Q000378:metabolism*; D011803:Quinine / Q000494:pharmacology; D013569:Synapses / Q000187:drug effects* / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects
D000631:Aminopyridines; D007473:Ion Channels; D011803:Quinine; D015761:4-Aminopyridine; D011188:Potassium; D002211:Capsaicin