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Mechanism of Action of Cymbalta

Mechanism of Action of Cymbalta




Mechanism of Action of Cymbalta

The active agent in Cymbalta is Duloxetine, a selective inhibitor that has found enormous relevance in treating stress urinary incontinence and depressive episodes. It has also been integrated into pain management therapies, including tingling caused by diabetic neuropathy. An underlying factor in the contemporary utilization is its mechanism of action, where it acts as a dual inhibitor by attaching itself to transport sites of norepinephrine (NE) and serotonin (5-hydroxytryptamine, 5-HT). The functioning is founded on a widely accepted concept that imbalance among neurotransmitters is the primary factors in the etiology of psychiatric disorders such as depression (Karpa, Cavanaugh, & Lakoski, 2002).

The mechanism of action is based on excitatory postsynaptic, where the neuron initiates a spike train that causes depolarization in adjacent neurons. The rapid rises resulting from the flow of positively charged ions culminates to potentiation of noradrenergic and serotonergic activity in the CNS. While it achieves a balanced inhibition of NE and 5-HT, it does not affect any activity for dopamine, α-adrenergic, opioid, histamine, and muscarinic receptors. By drastically altering the reuptake of NE and 5-HT from both presynaptic adrenergic and serotonergic nerve terminals, duloxetine enables the postsynaptic receptors to be continually stimulated by the two neurotransmitters (Tendolkar, Van Wingen, Urner, Verkes, & Fernández, 2011). Duloxetine disrupts the neurological processes, where it affects the way brain cells and nerves communicate with each other. The disruption of serotonergic reuptake has a blunting effect on the emotional reactivity, where duloxetine curtails neural activity in the putamen, subgenual cingulate cortex, and the middle frontal gyrus, regions that play a primary role in regulating emotions (Drevets, Savitz, & Trimble, 2008). Duloxetine also targets affective neurocircuitry, where the attenuation downregulates the circuitry, disrupting successful memory formation. Similarly, the noradrenergic inhibition affects amygdala, which is primary in the activation of emotional memory. The inhibitory roles decrease effects of life events on mood, including normalizing biased processing.


Drevets, W. C., Savitz, J., & Trimble, M. (2008). The subgenual anterior cingulate cortex in mood disorders. CNS Spectrums13(8), 663.

Karpa, K. D., Cavanaugh, J. E., & Lakoski, J. M. (2002). Duloxetine pharmacology: profile of a dual monoamine modulator. CNS drug reviews8(4), 361-376.

Tendolkar, I., Van Wingen, G., Urner, M., Verkes, R. J., & Fernández, G. (2011). Short-term duloxetine administration affects neural correlates of mood-congruent memory. Neuropsychopharmacology, 36(11), 2266-2275.

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