The more spells of clinical depression a woman had, the smaller the hippocampus was. Stress, which plays a role in clinical depression, may be a key factor here, since experts believe stress can suppress the production of new neurons (nerve cells) in the hippocampus (author, date).
A 2003 study in Behavioral Neuroscience found that when neurogenesis is blocked in mice, the benefits of antidepressants seem to fade (Drew, Denny, & Hen, 2010, p. 446-454). Mice showed less anxious or depressed behavior (became braver about getting food from a brightly lit place) after they were given antidepressants for four weeks (Drew, Denny, & Hen, 2010, p. 446-454).These treated mice had 60% more dividing cells in the hippocampus. However, the drug treatment failed to reduce anxious behavior in the mice when researchers blocked their new cell growth by dousing the hippocampus with x-rays (Drew, Denny, & Hen, 2010, p. 446-454). .
Researches like France, Lysaker, and Robinson (2007) who support a cognitive-behavioral perspective, admits that chemical imbalances (e.g. serotonin, monoamines, and depletion in SSRI neurotransmitters) contribute to clinical depression, but they do not believe a chemical imbalance is the only cause of clinical depression. For example, antidepressants repair or increase the levels of serotonin (a mood chemical) that changes or masks the symptoms of clinical depression, but never really eliminates the symptoms of clinical depression. In addition, France et al. (2007) suggests with the use of antidepressants, adding psychotherapy to the treatment plan may prove to be more effective in reducing or even eliminating the symptoms of clinical depression. .
Dr. Amen and Dr. Gray (date) ( as cited in Pourbabaee, n.d.) showed that when there is an imbalance in serotonin, the limbic system changes as a result. For example, an imbalance of serotonin in the limbic system can result in symptoms of clinical depression such as negative thoughts, chronic distress, and hopelessness (Pourbabaee, n.
