Final answer:
The monoamine hypothesis posits that depression is associated with underactivity at serotonin and norepinephrine synapses, and has been influential in the development of antidepressant drugs. Therapies targeting these neurotransmitters can alleviate symptoms, although the complete etiology of depression likely involves additional factors.
Step-by-step explanation:
According to the monoamine hypothesis of depression, underactivity at serotonin and norepinephrine synapses underlies depression. The monoamine hypothesis suggests that a deficit in certain neurotransmitters, specifically serotonin (5-HT) and norepinephrine (NE), is responsible for the clinical features of depression. These neurotransmitters play key roles in regulating mood, motivation, and a range of other physiological processes. Medications such as monoamine oxidase inhibitors and selective serotonin reuptake inhibitors work to increase the levels of these monoamines in the synaptic cleft, which can alleviate depressive symptoms in some patients.
While the monoamine hypothesis has been influential in the development of treatments for depression, it is also acknowledged that the etiology of depression is complex and may involve other factors such as genetics, environmental influences, and alterations in neural circuitry. Furthermore, the delayed effects of antidepressants suggest that simply increasing neurotransmitter levels may not fully address the underlying causes of depression.