Question

You are developing a new drug to treat Major Depressive Disorder (MDD). You know that patients do not show clinical signs of improvement when they begin taking an SSRI. Your goal is to create a drug that will result in immediate improvement for patients, and can be used with SSRIs initially, and discontinued once the SSRI becomes fully effective.

What part of neuronal transmission would you target with your drug? Why would this alleviate the issue with SSRIs? (NOTE: Your answer should be logical and specific, and draw on what we have covered about communication between neurons this module/semester.It is not going to be a real drug)

Answer 1

To develop a drug that offers immediate improvement in treating MDD alongside SSRIs, targeting the monoamine receptors or monoamine oxidase could be effective. Fast-acting agonists or MAO inhibitors might offer immediate changes in neurotransmitter levels, providing rapid relief until SSRIs become fully effective.

Step-by-step explanation:

When developing a new drug to treat Major Depressive Disorder (MDD), targeting a component of the neuronal transmission that would offer an immediate improvement is challenging.

SSRIs, such as Prozac, Paxil, and Zoloft, work by blocking the reuptake of serotonin, but they often take weeks to show clinical improvement. Since the issue with SSRIs is the delayed response time, an effective drug could be one that acts faster by altering the availability of neurotransmitters immediately.

To achieve this, one promising area to target would be the monoamine receptors on the postsynaptic neuron. This could involve the design of a fast-acting agonist that would immediately bind to these receptors and elicit a quick response, mimicking the neurotransmitter's effects and providing rapid symptomatic relief.

This agonist could complement SSRIs by immediately improving neurotransmitter signaling until the SSRI kicks in, at which point the agonist could be tapered off.

Alternatively, fast-acting monoamine oxidase inhibitors (MAO inhibitors) might be another target. By inhibiting the enzyme responsible for neurotransmitter degradation, MAO inhibitors can also rapidly increase neurotransmitter levels in the synaptic cleft. However, they must be used cautiously due to potential side effects and the risk of interactions with SSRIs.

Lastly, other modulatory mechanisms such as sigma-1 receptor activation or glutamatergic system modulation could provide rapid antidepressant effects and could potentially be used alongside SSRIs. Critical to this hypothetical drug development would be ensuring safety and minimizing side effects when used in combination with other antidepressants.