Question

You suspect that a drug called Xtreme influences the life cycle of Substance X. You apply the drug to a region of the brain where presynaptic axon terminals release Substance X and observe that an abundance of Substance X lingers in the synaptic cleft. Which of the following possible targets of Xtreme could result in an abundance of Substance X in the synaptic cleft (select ALL that apply):

*this is all of the knowledge given*
a) Xtreme disrupts X-AT, which transports Substance X across the neuronal membrane
b) Xtreme disrupts V-XAT, which packages Substance X into synaptic vesicles
c) Xtreme disrupts X-ase, which enables extracellular breakdown of Substance X
d) Xtreme disrupts voltage-gated calcium channels at the presynaptic axon terminal
e) Xtreme disrupts X-CAT, which synthesizes Substance X

Answer 1

Targets of Xtreme that could result in an abundance of Substance X in the synaptic cleft include disruption of X-AT (reuptake), X-ase (degradation), and voltage-gated calcium channels (release). Disruption of these could inhibit reuptake, prevent degradation, or alter neurotransmitter release, leading to accumulation of Substance X.

Step-by-step explanation:

If a drug called Xtreme causes an abundance of Substance X to linger in the synaptic cleft, several mechanisms might be affected. Here are the possibilities that align with this observation:

• Xtreme disrupts X-AT, which transports Substance X across the neuronal membrane, could cause Substance X to accumulate in the synaptic cleft if reuptake is inhibited.
• Xtreme disrupts V-XAT, which packages Substance X into synaptic vesicles, might not directly cause accumulation in the synaptic cleft but could affect the availability of Substance X for release.
• Xtreme disrupts X-ase, which enables extracellular breakdown of Substance X, would lead to an accumulation of Substance X in the synaptic cleft by preventing its degradation.
• Xtreme disrupts voltage-gated calcium channels at the presynaptic axon terminal, might cause changes in the release of Substance X into the synaptic cleft, since calcium influx triggers vesicle fusion and neurotransmitter release.
• Xtreme disrupts X-CAT, which synthesizes Substance X, would impact the levels of Substance X but might not cause immediate accumulation in the synaptic cleft unless there is an excess of Substance X already present and ready for release.

Therefore, the most likely targets of Xtreme that could result in an abundance of Substance X in the synaptic cleft are X-AT, X-ase, and voltage-gated calcium channels. Targeting these structures or enzymes could inhibit reuptake, prevent degradation, or alter release respectively, leading to increased levels of Substance X in the synaptic cleft.