Mg²⁺ (magnesium ions) can influence neurotransmitter release by acting as a competitive blocker of certain calcium channels, specifically those that are voltage-gated. Here is how Mg²⁺ blocks the effect of extracellular calcium on neurotransmitter release:
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Competition with Ca²⁺: Mg²⁺ can compete with extracellular calcium ions (Ca²⁺) for binding sites on voltage-gated calcium channels. When these channels open in response to membrane depolarization, the flux of Ca²⁺ into the neuron is crucial for triggering neurotransmitter release. Elevated Mg²⁺ concentrations can reduce the influx of Ca²⁺ by blocking these channels.
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Alteration of Channel Conductance: At certain concentrations, Mg²⁺ can block the conductance of calcium channels. This makes it more difficult for Ca²⁺ to enter the presynaptic neuron during action potentials, thereby reducing the amount of intracellular calcium available for triggering synaptic vesicle fusion and neurotransmitter release.
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Influencing the Resting Membrane Potential: Mg²⁺ can also affect the resting membrane potential of neurons. A higher intracellular concentration of Mg²⁺ can stabilize the membrane potential, making it less likely that the neuron will reach the threshold for action potentials, and hence less likely to release neurotransmitters.
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Role in Synaptic Plasticity: In certain contexts, such as long-term potentiation (LTP) and long-term depression (LTD), Mg²⁺ plays a role in modulating synaptic efficacy. It often acts to prevent excessive activation of glutamate receptors (like NMDA receptors), which require removal of Mg²⁺ for calcium influx, linking its effects on both synaptic transmission and plasticity.
In summary, Mg²⁺ blocks the impact of extracellular calcium on neurotransmitter release primarily by competing with Ca²⁺ at calcium channels, thereby reducing calcium influx upon neuronal excitation, influencing synaptic transmission efficiency.
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