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Partial uncoupling of neurotransmitter release from [Ca2+]i by membrane hyperpolarization
1The Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Department of Neurobiology, The Hebrew University, Jerusalem 91904, Israel.
Journal of Neurophysiology
|June 16, 1999
Summary
This study reveals how intracellular calcium and membrane potential influence neurotransmitter release at the crayfish neuromuscular junction. Hyperpolarizing pulses reduce release by decreasing calcium sensitivity, not just calcium levels.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Neurotransmitter release is crucial for synaptic transmission.
- Intracellular calcium ([Ca2+]i) and presynaptic membrane potential are key regulators of this process.
- Understanding these regulatory mechanisms is vital for comprehending neural communication.
Purpose of the Study:
- To investigate the dependence of evoked and asynchronous neurotransmitter release on [Ca2+]i and presynaptic membrane potential.
- To elucidate the role of hyperpolarizing postpulses (HPPs) in modulating neurotransmitter release dynamics.
- To test the hypothesis that HPPs alter the sensitivity of the release machinery to calcium.
Main Methods:
- Experiments were conducted on single-release boutons of the crayfish opener neuromuscular junction.
- Depolarizing pulse trains were used to manipulate presynaptic membrane potential and [Ca2+]i.
- Evoked and asynchronous release were measured concurrently with [Ca2+]i changes.
- The effects of hyperpolarizing postpulses (HPPs) on release parameters were analyzed.
Main Results:
- Both evoked and asynchronous release increased sigmoidally with rising [Ca2+]i.
- HPPs reduced [Ca2+]i, evoked release, and asynchronous release.
- Evoked release terminated earlier following HPPs.
- The reduction in release by HPPs was greater than could be explained by [Ca2+]i reduction alone.
Conclusions:
- Neurotransmitter release is modulated by both calcium levels and the sensitivity of the release machinery.
- HPPs decrease neurotransmitter release by reducing the calcium sensitivity of the release apparatus.
- This calcium desensitization mechanism contributes to the rapid termination of evoked release.
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