Biochemical Correlates of Depression Research clearly points to a link between depression and biochemical abnormalities in the brain. While much is still to be discovered, evidence strongly suggests that abnormalities in the synaptic transmitter systems of the brain can cause depression. Two neurotransmitters thought to have significant importance are norepinephrine and serotonin. Depression is usually associated with the reduction in levels of serotonin and norepinephrine, although other neurotransmitters may be involved. Reduced levels of serotonin in the synapse have been associated to cause depression. However, many other factors are involved.
Recent studies suggest that a complex system, involving second messenger systems, in which secondary chemicals affect the synthesis and transport of primary neurotransmitters, such as serotonin also play a role. But, it was the research into primary neurotransmitter systems that led the revolution in the treatment of depression during the mid 1950 s with the appearance of the first effective antidepressant medications. The interaction between different neurotransmitters and depression is highly complicated and unclear. In agreement with the serotonin deficiency hypothesis of depression, there is evidence that depressed people have a deficiency of tryptophan, a serotonin precursor. However, while some depressed people respond best to drugs that affect mostly serotonin, others respond more to drugs that affect catecholamines. Thus it seems that there are several biochemically different forms of depression.
In the early 1960 s researchers proposed that depression could be due to a deficiency of activity at catecholamine synapses and evidence was in favor of the catecholamine hypothesis of mania and depression. Hence, drugs were formulated to allow catecholamines to stay longer in the synapse. For example, the tricyclic drugs worked by preventing the presynaptic neuron from reabsorbing catecholamines after release, thereby causing the catecholamines to remain longer in the synaptic cleft. Other drugs, such as monoamine oxidase inhibitors, blocked the enzyme monoamine oxidase, which metabolizes catecholamines into inactive forms. The first effective medications for the treatment of depression were monoamine oxidase (MAO) inhibitors. MAO inhibitors increase serotonin levels and norepinephrine levels by blocking their degradation by MAO enzymes.
Then, beginning in the late 1980 s, a new family of antidepressants called selective serotonin reuptake inhibitors (SSRI) became available. The SSRIs target serotonin, the primary neurotransmitter believed to be involved in the development of depression. It is believed that insufficient amounts of serotonin in synaptic clefts may cause depression. SSRI inhibit the reuptake of serotonin from the synaptic cleft, allowing increased amounts of the neurotransmitter to be available.
SSRIs include the well known Prozac drug Antidepressant drugs have led to a breakthrough in the treatment of depression and demonstrate the existence of the biochemical aspect of mood disorders. One of the major revelations of the 20 th century has been the discovery that mental states and disorders of the mind and mood are not completely psychological in nature, but is related to the biological state of the individual as well, especially with regards to neuro chemical imbalances in the brain.