by Jen L’Insalata

 Mood disorders are a broad category with symptoms ranging from mild dysphoria and grief to chronic and intense clinical depression. Symptoms include both psychological and physical components and can emerge as a reaction to stimuli or spontaneously. Psychological symptoms include diminished self-esteem, sadness, and diminished self-worth; while physical symptoms include alterations in sleep, appetite, and fatigue (Preston, O’Neal, & Talaga, 2013).

Psychological based depression is often reactive, stemming from a stressor either known or unknown to the individual. Biologically based depression does not develop as a response to a stimuli, rather a number of neurobiological conditions are altered which effect neurotransmission within the limbic system. While prolonged reactive depression can lead to biological changes, often individuals show predisposed vulnerability and biological markers (Preston, O’Neal, & Talaga, 2013).

Psycho therapeutic intervention is a primary treatment for reactive depression through which the individuals learns coping skills and is able to address the underlying factors.  Vegetative and neurovegitatve conditions observed in the physical manifestations such as diminished concentration, psychomotor agitation, and changes to sleep and appetite alert practitioners to biological depression (Preston, O’Neal, & Talaga, 2013).  Treatment for biological components of depression includes medication to help stabilize symptoms.

Biological Etiology

Depression symptoms are brought about by the malfunction of norepinephrine, serotonin and dopamine transmission thought out the neurons of the limbic system and hypothalamus. It is believed that a depletion of these neurotransmitters leads to symptom manifestation. The monoamine hypothesis suggests that neurotransmitter depletion can occur in several ways (Preston, O’Neal, & Talaga, 2013).

Excessive reuptake can deplete levels of norepinephrine, serotonin, and dopamine. In this instance, significant amounts of the neurotransmitter are released by the presynaptic neuron into the synapse. The neurotransmitters are rapidly reabsorbed by the presynaptic neuron resulting in a diminished quantity of neurotransmitters reaching and binding with receptors on the opposing postsynaptic nerve (Preston, O’Neal, & Talaga, 2013).

Another instance suggests that there is a decrease number of neurotransmitters released into the synapse. This is possibly due to the reduction of neurons being synthesized, the inability of the vesicle to adequately store or migrate neurons across the membrane of the presynaptic neuron (Preston, O’Neal, & Talaga, 2013). Still a final instance of neurotransmitter abnormalities can occur when the naturally occurring levels of monoamine oxidase become too active. This shouts down and degrades the neurotransmitters themselves (Preston, O’Neal, & Talaga, 2013) resulting in depression symptoms.

Medications

Antidepressants are used to treat the biological aspect of depression. When combined with psychotherapy, the pharmisudical treatment of depression is highly effective. There are many medications used to treat depression but the most commonly prescribed fall into three categories; Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs), and Tricyclic Antidepressants (TCAs).

Tricyclic Antidepressants (TCAs)

Tricyclic Antidepressants were first developed as an antipsychotic for the treatment of schizophrenia. The original TSA imipramine did not produce the desired antipsychotic effects but produced marked improvement with depressive symptoms. TSAs have a diverse philological profile and are considered a superior form of medicinal depression treatment. Action occurs at the two receptor transporters and three receptor proteins. This inhibits presynaptic reuptake of norepinephrine, serotonin, and blocks post synaptic adrenergic, muscarinic, and histamine H receptors (Hillhouse, & Porter, 2015).

For this reason, the medications prove effective and target many receptors on both end of the synapse. However there are many adverse side effects including unpleasant dry mouth and skin, blurred vison, bladder issues and even death. Additional symptoms involve a quick drop in blood pressure and light headedness. TCAs are considered toxic and can be lethal if the dosage is not accurate (Preston, O’Neal, & Talaga, 2013).

Selective Serotonin Reuptake Inhibitors (SSRIs)

Selective Serotonin Reuptake Inhibitors were developed in the 1960s with the aim of increasing the concentration in the synapse by the inhibition of the reuptake mechanisms of the presynaptic neuron. SSRIs bind the the reuptake receptors on the presynaptic neuron allowing adequate serotonin to bind with receptors on the post synaptic neuron (Hillhouse, & Porter, 2015).

SSRIs targets the serotonin receptor s and have very little effects on other receptors. This allows them to be as effective as TCAs with significantly fewer side effects. Most of the side effects observed have to do with the increase of serotonin and include mild nausea, insomnia, sedation, and restlessness. Over time, patients may experience a recurrence of symptoms that are similar to the initial depression they are being treated for. Patients may experience loss of energy, passivity, and decreased pleasure. Additional medication may be needed to augment some of the unwanted effects (Preston, O’Neal, & Talaga, 2013).

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) were developed and introduced in the early 1990s and are considered duel action antidepressants. As the name suggests, SNRIs target and inhibit the reuptake of both serotonin and norepinephrine. For this reason it is possible that SNRIs may be more effective then SSRIs in the treatment of depression but studies how there are significantly more unwanted side effects (Preston, O’Neal, & Talaga, 2013, & Hillhouse, & Porter, 2015).

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References

Hillhouse, T. M., & Porter, J. H. (2015). A brief history of the development of antidepressant drugs: From monoamines to glutamate. Experimental And Clinical Psychopharmacology, 23(1), 1-21. doi:10.1037/a0038550

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.