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Depression is a mental illness that can have serious implications if left untreated. Studies involving a neurotrophic factor called brain derived neurotrophic factor (BDNF) and its associated signaling pathways have solidified our understanding of the pathophysiology of depression. The objective of this literature review is to gain a better understanding of the mechanism by which reduced levels of BDNF are implicated in depression and how antidepressants facilitate the treatment of depression by increasing BDNF levels. The specific approach is to learn about the key involvements of BDNF and its receptor TrkB (tropomyosin receptor kinase B) and how their interactions and subsequent intracellular signaling cascades bring about enhanced neuroplastic changes. In this literature review, we searched for past review articles focusing on BDNF. We collected data using PubMed and created a summary of our findings. The results showed that stress and depression through the reduction of BDNF levels contribute to neuroplastic changes while antidepressants through enhanced BDNF levels are able to generate positive neuroplastic outcomes and thereby help resolve depressive symptoms. In this paper, we will delve into how a better understanding of the neural circuitry involving BDNF will enable us to both understand how current antidepressants work in the limbic regions of the brain as well as search for novel rapid-acting antidepressants to use in clinical practice.

Neuroplasticity and the Biological Role of Brain Derived Neurotrophic Factor in the Pathophysiology and Management of Depression