PS215 Unit 3 Neurotransmitters and Drugs Paper Example

Serotonin, Reuptake and a Six-Week Wait: A PS215 Unit 3 Neurotransmitters and Drugs Paper

[Student Name]

Purdue University Global

PS215: Neuroscience

Unit 3 Neurotransmitters and Drugs Paper

[Instructor Name]

[Date]

The stroke survivor and his treatment are composite; the research cited is real.

The Case

Two months after his stroke, Harold, a retired choir director, stopped attending his speech therapy sessions with any energy, slept late, said through his limited speech that he was useless, and lost interest in the choir recordings he had always played. His physician diagnosed post-stroke depression, which develops in about one survivor in three and is linked with slower recovery (Robinson & Jorge, 2016), and prescribed sertraline, a selective serotonin reuptake inhibitor.

Serotonin and Its System

Serotonin is made by neurons whose cell bodies sit in the raphe nuclei of the brainstem but whose axons reach almost every part of the brain, including the frontal cortex, limbic regions and hippocampus. Released into the synapse, it binds more than a dozen receptor types, some excitatory and some inhibitory, which is one reason it influences so many functions, from mood and sleep to appetite. Its action ends mainly through reuptake: a transporter protein on the releasing neuron pulls serotonin back inside to be reused (Kandel et al., 2021).

What the Drug Does

Sertraline binds the serotonin transporter and blocks it, so serotonin stays longer in the synapse and continues to act on receptors. Blockade is measurable on the very first day of treatment.

The chemical effect starts in hours, but the improvement takes weeks, so the chemical effect cannot be the whole story.

The Delay

Harold's mood did not change for the first three weeks, and his family began to doubt the medication. By about the sixth week, he was more engaged in therapy and asked for his recordings again. This delay is typical, and it is one of the main reasons researchers no longer explain depression simply as a serotonin shortage. If more serotonin in the synapse were enough, improvement would follow the first dose.

Current explanations focus on what happens over the following weeks. Sustained serotonin at the synapse leads to adaptive changes in receptors, including desensitization of autoreceptors that normally limit serotonin release, which eventually allows more release. Antidepressant treatment is also associated with increased brain-derived neurotrophic factor and with growth of new connections in regions such as the hippocampus, changes that take weeks (Castrén, 2013). In this view, the drug creates conditions for the brain to change, and experience, including therapy, shapes what changes.

Side Effects and Cautions

Because serotonin acts throughout the body, the drug can cause nausea, sleep changes and, in some patients, increased bleeding risk, a consideration after stroke that the physician monitored. These effects often appear before benefits, which can make the first weeks discouraging.

What the Case Shows

The case shows a neurotransmitter system working at several time scales: the drug changes chemistry in hours, receptors adapt over weeks, and the brain's capacity to rewire, supported by therapy, carries the recovery. Harold's speech therapy and his antidepressant were working on the same brain, which may be why his engagement in therapy improved along with his mood.

References

Castrén, E. (2013). Neuronal network plasticity and recovery from depression. JAMA Psychiatry, 70(9), 983-989. https://doi.org/10.1001/jamapsychiatry.2013.1

Kandel, E. R., Koester, J. D., Mack, S. H., & Siegelbaum, S. A. (2021). Principles of neural science (6th ed.). McGraw Hill.

Robinson, R. G., & Jorge, R. E. (2016). Post-stroke depression: A review. American Journal of Psychiatry, 173(3), 221-231. https://doi.org/10.1176/appi.ajp.2015.15030363