These studies deal largely with neurochemical regulation in the brain.
Neurotransmitters, chemical substances that transmit nerve impulses across synapses in the brain, are crucial to normal brain function. The catecholamine hypothesis suggests that depression is caused by a deficit of norepinephrine at critical nerve terminals in the brain. Many antidepressants work by inhibiting the reuptake and/or breakdown of norepinephrine at receptor sites, such as monoamine oxidase inhibitors, or MAOIs. It is also believed that serotonin deficits, and abnormalities in the acetylcholine system may produce symptoms of depression. Acetylcholine seems to have a connection with monoamine transmitters. .
Neurophysiologic studies focus mainly on sleep patterns, and involve the use of an electroencephalogram, or EEG. Individuals suffering from depression often complain of insomnia or light, fitful sleep, all of which are consistent with the EEG results. Studies have shown that depressed persons have significantly decreased "deep sleep-, a shorter time before the onset of REM (the period when dreams and nightmares occur), and longer periods of REM than normal people.
Studies of neuroendocrine functions reveal that the abnormalities in various neuroendocrine target organs, such as the thyroid, adrenals, and pancreas in depressed patients have their roots in the hypothalamus, which is largely regulated by monoamine transmitters. .
Social and environmental circumstances may also play a role in causing depression. The issue is controversial, with conflicting research results. The results are difficult to interpret due to studies which were carried out either as if only biological factors should be considered as possible causes, or as if only psychosocial factors could influence the individual. Each theory was independent of the other and no effort was made to make a correlation between the two. Another difficulty presented is the effect of the depression itself on the life of the patient.
