AI Article Synopsis
- The study investigated changes in membrane potential that trigger neurotransmitter release in the crayfish neuromuscular junction by recording from the axon near presynaptic terminals.
- The researchers found that depolarizing the presynaptic terminal with current pulses activated a calcium-activated potassium conductance (gK(Ca)), which reduced depolarization and was sensitive to specific ion manipulations.
- There is also a delayed rectifier potassium conductance (gK) at the presynaptic terminal, both of which play key roles in repolarizing the membrane during action potentials.
Article Abstract
Membrane potential changes that typically evoke transmitter release were studied by recording intracellularly from the excitor axon near presynaptic terminals of the crayfish opener neuromuscular junction. Depolarization of the presynaptic terminal with intracellular current pulses activated a conductance that caused a decrease in depolarization during the constant current pulse. This conductance was identified as a calcium-activated potassium conductance, gK(Ca), by its disappearance in a zero-calcium/EGTA medium and its block by cadmium, barium, tetraethylammonium ions, and charybdotoxin. In addition to gK(Ca), a delayed rectifier potassium conductance (gK) is present in or near the presynaptic terminal. Both these potassium conductances are involved in the repolarization of the membrane during a presynaptic action potential.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2229067 | PMC |
| http://dx.doi.org/10.1085/jgp.98.6.1161 | DOI Listing |
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