This patient, a 35 year old mother of 3, who just gave birth 8 weeks ago began to notice depressive symptoms about a month ago. Her obstetrician notices her sadness and anxiety and prescribed a low dose of Zoloft. Five weeks later, some of her symptoms have improved, but the patient says she feels worse. She now complains of worrisome weight loss and lack of sleep. Her obstetrician referred her to the psychiatric provider for treatment of possible postpartum depression (PPD).

Neurobiological Theory

Several treatments for depressive symptoms such as those that accompany PPD exist. The discovery that a reduction monoamines—norepinephrine, serotonin, and dopamine—may be a cause of depression was made in the 1950s. Since then, pharmacologic therapy for the treatment of depression has focused on increasing the brain monamine concentration. Norepinephrine, serotonin, and dopamine are neurotransmitters and are normally found in low concentrations in gamma aminobutyric acid (GABA), a neurotransmitter that blocks impulses between nerve cells in the brain. Goldberg, Bell and Pollard (2014) writing in Perspectives of Medicinal Chemistry list evidence that a deficiency of GABA may contribute to depression including magnetic resonance spectroscopy of parts of the brain show that tissue GABA is decreased in depression. Also, “in animal models, phenelzine, an inhibitor and substrate of monoamine oxidase (MAO), elevates cortical GABA levels” (Goldberg, Bell, & Pollard, 2014, p. 1). This long-held understanding that GABA levels are a factor in depression and the treatment of depression is the basis for the monoamine hypothesis of depression.

The medications that are effective on GABA levels enhance the short-term functions of the monoamines by inhibiting the functions of their transporters. Jeon and Kim (2016) of the International Journal of Molecular Sciences say that when selective serotonin reuptake inhibitors (SSRIs) were introduced, there was even more support for the hypothesis (Jeon & Kim, 2016, p. 3). However, when a patient with depressive symptoms begins treatment with an SSRI, there is a time lapse of 3 to 4 weeks before there is a response to the treatment, even though monoamine levels increase immediately. The monoamine receptor sensitivity hypothesis was created to address the limitation. This hypothesis says that the monoamines are secreted all the time and are increased by the treatment, which also activates the synapses to transmit, but the number of monoamine receptors are decreased due to the treatment also. “In other words, depression is induced by monoamine receptor up-regulation” (Jeon & Kim, 2016, p. 3). This hypothesis explains the 3 to 4 week time frame for treatment effects to begin, and it is usually the first choice for treatment of depression. ‘

These hypotheses are discussed here in a simplified way, but they are really quite groundbreaking. Mulinari (2012) of the Journal of the History of the Neurosciences explains that the hypotheses are a merger of data, concepts, standardized experimental techniques and animal models. The development of the antidepressants that arose from these hypotheses is also innovative because they affect the communication patterns between neurons in the brain that are facilitated by the neurotransmitters that the medications affect (Mulinari, 2012, p. 380). Mulinari (2012) also says that recent discoveries about antidepressant drugs are also revolutionary, “most importantly on the notion that TCAs block the uptake of monoamines from the intersynaptic space between neurons, and that MAOIs increase levels of available monoamines by inhibiting an enzyme that metabolizes monoamines” (Mulinari, 2012, p. 380). This then leads to the type of treatment that may be best for the patient who is experiencing depressive symptoms.

Pharmacological Intervention

One possible pharmacological intervention for this patient is an SSRI such as Zoloft. She has already been prescribed a low dose of Zoloft (usually 25 to 50 mg), but perhaps increasing the dose would be more effective. This can be done gradually, increasing the dose by 25 mg per week until she is taking 100 mg to 200 mg of Zoloft per day; however, it is not recommended to go over 200 mg per day. Yet, Zoloft is not the only possible pharmacological treatment for PPD.

A common treatment for PPD is an SSRI. If the patient were breastfeeding, an SSRI would not be a good option, but since she is not, it should be considered. Pawluski, Lonstein, and Fleming (2017) of Trends in Neurosciences explain that SSRIs may not be as effective on PPD as it is on other types of depression because “SSRIs may act on the maternal brain to reverse the behavioral effects of repeated stress by increasing synaptic density in the prefrontal cortex and the nucleus accumbens, and by increa