Beneath the Surface: The Neurobiology of Depression
- 3 days ago
- 4 min read
Written by: Raghad AlGhamdi, BSc Clinical Psychology
Edited by: Fahad Hassan Shah
Many of us know what it feels like to be sad or unmotivated, but depression goes deeper than that. Depression is a mental health condition that affects all aspects of an individual’s life. In many cases, this can include a feeling of emptiness, loss of interest in activities that were once enjoyable, low energy levels, and difficulty concentrating, typically lasting for two weeks or more (American Psychiatric Association, 2024). While these experiences may seem purely emotional on the surface, depression is strongly linked to biological factors, specifically changes in brain function and chemistry. Understanding the underlying causes is important because it allows us to move from what depression feels like to what is actually happening inside the brain.
The emotional symptoms of depression reflect the quieter conflict occurring within the brain itself. To better understand this, researchers have been studying parts of the brain involved in emotion and cognition. One key region is the prefrontal cortex, specifically its two major subregions: the ventromedial prefrontal cortex and the dorsolateral prefrontal cortex. Both areas play a part in depression; they work together, yet interdependently. The ventromedial prefrontal cortex is primarily responsible for processing emotions and self-related thoughts. Research generally shows that this region has higher levels of activity in depressed individuals. On the other hand, the dorsolateral prefrontal cortex, which is involved in cognitive control and emotional regulation, is found to have lower levels of activity in depressed individuals. This imbalance between heightened emotional processing and lower levels of cognitive regulation helps explain why negative thoughts and feelings in depression can feel difficult to control (Koenigs & Grafman, 2009)
What many describe as a “chemical imbalance” in depression is more complicated than it sounds. Neurotransmitters play a central role in the neurobiological understanding of depression; however, they do not act simply by increasing or decreasing one type of neurotransmitter. A significant amount of research supports the association of multiple neurotransmitters with depression, including serotonin, norepinephrine, dopamine, glutamate, and glycine (Rădulescu et al., 2021). Serotonin, norepinephrine, and dopamine play large roles in regulating mood, motivation, reward processing, and cognitive control. Serotonin dysfunction has been associated with low mood and emotional instability, lower levels of norepinephrine with decreased energy levels and attention, and dopamine deficits with reduced reward sensitivity. In addition, glutamatergic and glycinergic systems are also shown to be disrupted in depressed individuals, with evidence suggesting that changes in glutamate signaling and NMDA receptor function can contribute to both cognitive and emotional aspects of depression (Rădulescu et al., 2021). Depression cannot be attributed to a singular chemical imbalance in one neurotransmitter system, but rather to the interaction among many neurotransmitter systems.
Depression does not merely change how an individual feels; it may also affect how they think and what they choose to remember. Depression has been associated with deficits in cognitive functioning, particularly related to executive and attentional control (Kircanski, Joormann, & Gotlib, 2012). This can make it difficult for individuals to manage their thoughts and redirect their attention from negative stimuli. In addition, there are various cognitive biases associated with depression. One of the most consistently supported findings is memory bias, which refers to the tendency to recall negative information (e.g., sad words, unpleasant experiences) more than positive information (Kircanski et al., 2012). Another notable feature is overgeneral memory. Depressed individuals have difficulty remembering specific details of past events and tend to generalize recollection of events in a much broader way. This pattern has been linked to reduced cognitive control, which may lead to a decrease in the ability to retrieve specific memories.
What if the depressed brain is not “broken”, but rather has difficulty adapting or changing? Neuroplasticity refers to the brain’s ability to adapt and modify throughout life by forming new neural connections and strengthening current neural connections. The process of neuroplasticity is decreased in individuals with depression, particularly within areas of the brain that are associated with mood, cognition, and reward. Depression treatments, such as pharmacological treatments and psychotherapy, work in part by restoring neuroplasticity (Wang et al., 2023). Antidepressants such as selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), and tricyclic antidepressants (TCAs) increase synaptic plasticity by increasing brain-derived neurotrophic factor (BDNF), which supports synaptic plasticity. This promotes new neural connections and supports new growth of neurons in the hippocampus over time (Wang et al., 2023). Therapies such as cognitive behavioral therapy improve brain function by creating new patterns of thinking and restructuring maladaptive thought processes (Wang et al., 2023). Therefore, depression could be viewed as an impairment of neuroplasticity, and its recovery involves rebuilding adaptive neural networks.
Depression is far more than its emotional presentation. It is deeply rooted in neurological and cognitive processes involving brain structure, function, and chemistry. While there have been significant advancements in research, there is still so much we do not understand about the “why” behind it all. Hopefully, as research evolves, we will be able to bridge the gap between science and emotional recovery.
References
American Psychiatric Association. (2024). What is depression? https://www.psychiatry.org/patients-families/depression/what-is-depression
Koenigs, M., & Grafman, J. (2009). The functional neuroanatomy of depression: Distinct roles for ventromedial and dorsolateral prefrontal cortex. Behavioural Brain Research, 201(2), 239–243. https://doi.org/10.1016/j.bbr.2009.03.004
Kircanski, K., Joormann, J., & Gotlib, I. H. (2012). Cognitive aspects of depression. Wiley Interdisciplinary Reviews: Cognitive Science, 3(3), 301–313. https://doi.org/10.1002/wcs.1177
Rădulescu, I., Drăgoi, A. M., Trifu, S. C., & Cristea, M. B. (2021). Neuroplasticity and depression: Rewiring the brain’s networks through pharmacological therapy (Review). Experimental and Therapeutic Medicine, 22(4), 1131. https://doi.org/10.3892/etm.2021.10565
Wang, Y.-B., Song, N.-N., Ding, Y.-Q., & Zhang, L. (2023). Neural plasticity and depression treatment. IBRO Neuroscience Reports. https://doi.org/10.1016/j.ibneur.2022.09.001
Yale Medicine. (2021, June 17). How Depression Affects the Brain. Yale Medicine. https://www.yalemedicine.org/news/neurobiology-depression
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