Describe the proposed neurobiology of depression from the perspective of effective treatment with a selective serotonin reuptake inhibitor (SSRI).

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Discussion Question:
Describe the proposed neurobiology of depression from the perspective of effective treatment with a selective serotonin reuptake inhibitor (SSRI). That is, if an SSRI “works” to alleviate depressive symptoms, then what would account for the pathophysiologic mechanisms at work in depression? Describe the roles of atypical antipsychotics as mood stabilizers. Include proposed mechanism(s) of action and evidence for use.


The purpose of required threaded discussions is an interactive dialogue among instructors and students to assist the student in organizing, integrating, applying, and critically appraising one’s knowledge regarding the nursing profession and selected area of practice. Scholarly information obtained from current sources as well as professional communication is required. The articles should have been published within the past 5 years and be peer reviewed. In some cases, you will need to pull in content from the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

Application of information to advance practice nursing experiences promotes the analysis and use of principles, knowledge and information learned and related to real-life clinical situations. Interactive dialogue among instructors and peers fosters the development of a learning community as ideas, perspectives and knowledge is shared.

***Please respond to each classmate with at least 125 words and reference.***

Classmate 1 Discussion:
It is a well-established fact that selective serotonin reuptake inhibitors (SSRIs) take weeks to develop the clinical response to depression fully. The impact of SSRIs on mood is undeniable, leading to significant reductions in depressed mood and psychic anxiety, which in turn lead to cognitive symptoms. However, it is essential to consider the progression of symptom changes during treatment to gain a better understanding. Therefore, it is crucial to acknowledge that SSRIs mainly impact mood and that empirical evidence supports this claim.

Nerves communicate via chemical transmission. Pre- and postsynaptic events are regulated, forming CNS plasticity and learning. Synthesis, storage, regulated release of neurotransmitters, and termination of action induce final cellular responses through signal transduction.

The biology of major depression is a challenging scientific problem that has enormous clinical and social relevance. Antidepressant drugs have revolutionized our understanding of neuronal functioning and the possible mechanisms underlying depression. However, it is essential to acknowledge that any hypothesis for the pathophysiology of depression must consider the complexity of the regulation of CNS function and the many interactions with other brain systems. Despite significant progress in recent decades, we must recognize that there are still considerable challenges in understanding and treating severe depression. The cause of treatment-resistant depression is still unknown.

The introduction of atypical antipsychotic drugs in the early 1990s marked a significant breakthrough in the treatment of schizophrenia and affective disorders. Atypical antipsychotics are more effective than typical antipsychotics in treating not only positive symptoms but also harmful and cognitive symptoms of schizophrenia. Additionally, their multi-modal mechanism of action on neurotransmitters such as dopamine, serotonin, norepinephrine, and histamine makes them highly effective in treating mood and anxiety disorders. In summary, atypical antipsychotics are a game-changer in the field of psychiatric medication.

Atypical antipsychotic drugs are distinguished from typical agents by their pharmacological mechanisms of action. Specifically, atypical antipsychotics augment the transmission of 5-HT, norepinephrine, and dopamine while also reducing the inhibition of monoamine-secreting neurons by antidepressant drugs. Clinical observations corroborate these findings, demonstrating the efficacy of atypical antipsychotics in treating negative and cognitive symptoms of schizophrenia, as well as affective symptoms in mood and anxiety disorders. Such evidence suggests that parallel pathophysiological mechanisms may underlie negative symptoms in schizophrenia and mood disorders and that optimal treatment may require simultaneous modulation of the transmission of all three neurotransmitters.


Boschloo, L., Hieronymus, F., Lisinski, A., Cuijpers, P., & Eriksson, E. (2023). The complex clinical response to selective serotonin reuptake inhibitors in depression: A network perspective. Translational Psychiatry, 13(1). to an external site.

Brigitta, B. (2002). Pathophysiology of depression and mechanisms of treatment. Dialogues in Clinical Neuroscience, 4(1), 7–20. to an external site.

Grinchii, D., & Dremencov, E. (2020). Mechanism of action of atypical antipsychotic drugs in mood disorders. International Journal of Molecular Sciences, 21(24), 9532.

Classmate 2 Discussion:
The neurobiological relationship between neurogenesis, stress, and inflammation has been shown to underlie the spectrum of depressive symptoms. Selective serotonin reuptake inhibitors (SSRIs) are widely recognized for their significant therapeutic efficacy in treating depression. The central hypothesis behind the antidepressant mechanism of action is monoaminergic and involves serotonin as a neurotransmitter (Vahid-Ansari et al., 2019). SSRIs work by inhibiting or preventing serotonin from being utilized. This is achieved by SSRIs blocking serotonin transport and binding to the serotonin transporter (SERT). As a result, depressive symptoms are counteracted by the ability of serotonin to stay longer in the body due to the action of SSRIs. Serotonin regulates mood, anger, perception, appetite, attention, sexuality, and irritability (Knorr et al., 2019).

SSRIs have been found to have a therapeutic effect on the alleviation of depression symptoms. Pathophysiologic mechanisms associated with depression alleviation involve functional deficiencies associated with the brain’s monoaminergic transmitters, norepinephrine (NE), dopamine, or 5-HT (Spellman & Liston, 2020). Dysfunction in the central noradrenergic system has been considerably hypothesized to play a significant role in depression pathophysiology, specifically about the increased tyrosine activity and minimized metabolism of norepinephrine.

The roles associated with atypical antipsychotics as mood stabilizers involve the antagonistic nature of action at receptor subtypes and the 5-HT2A receptors blockade, which is regarded to facilitate improved dopamine secretion in the basal ganglia. Dopamine release is regarded to counterbalance the antagonism of D2 receptors in the regions of the brain associated with the control of the motor (Grinchii & Dremencov, 2020). Therefore, antipsychotic medications work by changing the chemistry of the brain and reducing psychotic symptoms, including depression. The proposed mechanism of action of atypical antipsychotics as mood stabilizers would involve a multimodal action mechanism putatively underlying the beneficial effect associated with atypical antipsychotics in anxiety and mood disorders for the modulation of serotonin (5-HT).


Grinchii, D., & Dremencov, E. (2020). Mechanism of action of atypical antipsychotic drugs in mood disorders. International Journal of Molecular Sciences, 21(24), 9532.

Knorr, U., Madsen, J. M., & Kessing, L. V. (2019). The effect of selective serotonin reuptake inhibitors in healthy subjects revisited: A systematic review of the literature. Experimental and Clinical Psychopharmacology, 27(5), 413.

Spellman, T., & Liston, C. (2020). Toward circuit mechanisms of pathophysiology in depression. American Journal of Psychiatry, 177(5), 381-390.

Vahid-Ansari, F., Zhang, M., Zahrai, A., & Albert, P. R. (2019). Overcoming resistance to selective serotonin reuptake inhibitors: targeting serotonin, serotonin-1A receptors and adult neuroplasticity. Frontiers in Neuroscience, 13, 404.

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