Presynaptic inhibition in Aplysia involves a decrease in the Ca2+ current of the presynaptic neuron.
By voltage clamping presynaptic cell L10 and using pharmacologic separation techniques, we have analyzed the specific ionic currents in the presynaptic cell that correlate with presynaptic inhibition while assaying transmitter release with intracellular recordings from postsynaptic cells. We have found that presynaptic inhibition can be elicited in conditions in which the Na+ and the various K+ channels are pharmacologically blocked and depolarizing current pulses produce only an inward Ca2+ current. Both inward currents and tail currents at and above the K+ reversal potential were always less inward during presynaptic inhibition. The changes in conductance associated with presynaptic inhibition were voltage sensitive and paralleled the voltage sensitivity of the Ca2+ channel. We therefore conclude that presynaptic inhibition is caused by a direct transmitter-mediated decreased of presynaptic Ca2+-channel conductance.
D000818:Animals; D001048:Aplysia; D002118:Calcium / Q000502:physiology*; D004553:Electric Conductivity; D007473:Ion Channels / Q000187:drug effects; D008564:Membrane Potentials; D009433:Neural Inhibition; D009474:Neurons / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism; D011188:Potassium / Q000502:physiology; D013569:Synapses / Q000502:physiology*
D007473:Ion Channels; D018377:Neurotransmitter Agents; D011188:Potassium; D002118:Calcium