Neurochemical Signaling in Depression: Impact of Target-Based Pharmaceuticals

Depression is a chronic, devastating, and frequently occurring disease. Clinical studies have shown the association of depression with atrophy as well as degeneration of nerve cells and glial cells, which contribute to the size and function of specific brain regions that regulate the status of the mind, including depression. The currently available pharmacotherapies can be helpful in the treatment of psychosomatic disorders, including depression. Since these drugs display a very slow reaction and are required to be taken for a prolonged period, they often induce many side effects, which pose challenges in chemotherapy of the disease. The vascular endothelial growth factor A (VEGF) and the brainderived neurotrophic factor (BDNF) are known to play key roles in regulating the pathophysiology of depression. While searching for better options of treatment, rapid-acting antidepressants, such as the antagonist ketamine and N-methyl-D-aspartate NMDA receptor (NMDAR), are gaining more attention, which affects an array of signaling pathways. An evolutionary hypothesis suggests that the plasticity of neuronal routes is likely to be involved in the pathogenesis and hence the treatment of depression. It has been shown that due to the improper functioning of the neuronal system, adaptive plasticity can contribute to the pathogenesis of depression. Due to the use of medicines that promise choices for the treatment of depressive patients for dramatic improvement, there is an urgent need to develop novel tools about the mechanism of action of these rapid-acting antidepressants affecting the brain, particularly their interaction with the neuronal cell signaling pathways and their special effects on the neural circuits in the brain.