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In the Central Nervous System (CNS) neurons communicate with one other through the release of neurotransmitter from presynaptic neurons which bind to receptors located on postsynaptic neurons.

Although neurotransmission most often occurs from pre- to postsynaptic partners, retrograde neurotransmission also occurs via the release of endocannabinoids from the postsynaptic neuron.

Endocannabinoids are hydrophobic signaling molecules which bind to presynaptic receptors that subsequently cause a slow reduction in neurotransmitter release.

What is/are the mechanism(s) for this presynaptic form of inhibition?

Select ALL that apply.


Endocannabinoids bind ionotropic CB1 receptors causing an influx of $K^{ + }$ which subsequently lowers membrane potential.


Endocannabinoids bind G-Protein Coupled Receptors which subsequently cause secondary signaling that inhibits $Ca^{2 + }$ influx. Since $Ca^{ 2+ }$ is necessary for vesicle fusion, this inhibition effectively reduces neurotransmitter release.


Endocannabinoids bind CB1 receptors which lead to a secondary signaling cascade which activates voltage gated $K^{ + }$ channels. Increased $K^{ + }$ flux lowers membrane potential, leading to an increase in the threshold for neurotransmitter release.


Endocannabinoids bind and inhibit voltage gated $Na^{ + }$ channels. The resulting decrease in $Na^{ + }$ influx causes a decrease in neurotransmitter release.

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