Depression is a common disease which causes the patient to suffer from behaviors and thoughts which are negative and also by certain changes in bodily activities. These physical changes are called neurovegetative signs like body aches, crying spells, low libido, insomnia and weight fluctuations. There are different kinds of depressive disorders like manic depression, clinical depression, dysthymic disorder, postpartum depression, chronic depression and others. There are no specific causes of depression, it is caused by a combination of factors which are psychological, biochemical, genetic and environmental (Lunbeck Institute 2). It is therefore a complex disorder which has no specific treatment which is able to cure all cases of depression. It is also a relatively common disorder; scientists estimate that approximately 10-20 percent of the population will suffer from a depression at some point in their lives (Stevens 15).
Brain Involvement in Depression
The limbic system and the forebrain are the parts of the brain which are involved in depression. The limbic system is responsible for regulating stress, emotions, sexual and physical drives. Parts of the limbic system which are involved in emotional responses are the hypothalamus, hippocampus and amygdala. Studies suggest that certain parts of the forebrain may be involved in depression, though it is not verified that disturbances in these parts causes depression or they become affected when the disease is already present (Marshall and Bangert 361). The cerebral cortex is a part of the forebrain which is involved in the thinking process. It is assumed that abnormalities in this region may be responsible for negative feelings and thoughts that are characteristic of depression.
The pituitary gland and hypothalamus are the hormonal control centers in the brain and are thought to increase levels of certain hormones which are involved in the maintenance of a depressed state. The hypothalamus produces CRF (Corticotropin Releasing Factor), which is involved in the initiation of some forms of depression. CRF acts by stimulating the pituitary glands to produce ACTH (adenocorticotrophic hormone) which stimulates adrenal glands into releasing cortisol. Cortisol acts by depressing an individual mood, studies
indicate that about 50% of depression patients have high levels of cortisol (McNeal and Cimbolic 361).
The Role of Neurones and Neurotransmitters
A neuron is composed of an axon, which is the cell body and many branched dendrites. Chemical messages in the brain are transported through these neurons. A chemical message begins as an electric impulse picked up by a dendrite which then travels through the axon. In the axon the electric impulse is changed into a chemical impulse (Stevens 17). These chemical impulses are known as neurotransmitters which are released by axons so that messages are transferred from one neuron to another. When a neighboring dendrite picks up the neurotransmitter it changes it back into an electric impulse and undergoes the same process. In this way, the chemical impulse passes from one neuron to the next through a synapse. A synapse is a narrow gap which separates neurons.
Neurotransmitters are transmitted in a manner which is orderly. They are also shaped in a specific manner which ensures that after they pass through a neuron and synapse, they are also able to fit onto receptors of neighboring neurons. When the neurotransmitter is received by a receptor on a neuron, it may be converted into an electric impulse which traverses the neuron or it may be stopped at that stage. In both cases, the transmitter is released from the receptor and it gets back into the synapse. Once in the synapse, the neurotransmitter may be removed in either one of two strategies. It may be broken down by the enzyme monoamine oxidase or the neuron which released it in a process called reuptake. Neurotransmitters which are relevant in clinical depression are serotonin, dopamine and norepinephrine (Lunbeck Institute 1).
Monoamine Theory of Depression
The Monoamine Theory of Depression attributes the development of depression to dysfunctions in activity of monaoamines especially serotonin (5-HT) and/or norepinephrine. It was formulated in 1950 after it was found that treating hypertensive patients with reserpine could cause depression (Newholme and Leech, 250). The action of reserpine was to cause depletion of neurons of serotonin and noradrenaline which are monoamine transmitters. Reserpine treatment therefore caused neurotransmission of noradrenergic and serotonergic neurons resulting n a shortage of these monoamines. This theory was supported when the actions of antidepressants was used. Antidepressants which are tetracyclic and tricyclic interfere with the monoamine reuptake from the synapse after transmission has taken place. This causes levels of monoamines to fall causing depression. MAOIs (monoamine oxidase inhibitors) act by inhibiting the monoamine oxidase enzyme which breaks down noradrenaline and serotonin and therefore affects levels of these hormones (Newholme and Leech 252).
Treating depression can be done by increasing the concentration of monoamines in the synaptic cleft. This can be done through the following means: increasing the synthesis of monoamines; increasing the rate of exocytosis; and inhibiting the removal of monoamines from the synapse. Therapeutic drugs which inhibit removal of monoamines have been developed. An example is Specific Serotonin Reuptake Inhibitors (SSRIs). The most commonly prescribed SSRI is known by the brand name Prozac (Marshall and Bangert 346).
Manic depression (bipolar disorder) is characterized by mood swings from elation to depression. Studies suggest that this may be caused by an electrolyte imbalance or abnormality. In some patients, it is found that there are abnormal patterns in the Na+K+ATPase activity where it is reduced in periods of depression. In these cases, lithium has proven to restore the activity of the Na+K+ATPase activity. Lithium has also been found to increase levels of serotonin by increasing its uptake and synthesis.
Circadian Rhythms
Another theory to explain the depression arose from the observation that depression can be treated by sleep deprivation. It has also been observed that many antidepressant drugs act by reducing or eliminating REM sleep and patients of depression exhibit sleep patterns which are abnormal. The patients experience a reduced period of time until REM begins, experience more REM and have sleep cycles which are disrupted. Studies suggest that a depressogenic substance may be released as the patient sleeps, which is deactivated in wakefulness (Cheah 15). Typical patterns of depression patients indicate that depression is at its peak in the morning and reduces as the day goes on. This would be consistent with the assumption that the depressogenic substance was being broken down as the day wears on (Cheah 16).
The Endocrine System and Hormones
The endocrine system is composed of numerous glands which release hormones. These hormones regulate sexual development and responses to stress. Studies have shown that despite having healthy glands, depression patients have abnormal concentrations of hormones in their blood (Marshall and Bangert 345). It has also been noted that patients with certain endocrine disorders become depressed while some patients of depression develop endocrine disorders despite having healthy endocrinal glands. Changes in hormonal levels are usually interrelated with brain chemistry changes observed during depression. The hypothalamus controls secretion of neurotransmitters which are associated with depression that also function in the hormonal functions. These are dopamine, serotonin and norepinephrine. Clinical depression may also be a sign of disorders in the endocrinal glands. Examples include thyroid conditions like Addison’s disease and Cushing’s syndrome.
Cortisol is a hormone which is secreted by adrenal glands which are found in excessive quantities in their blood (Stevens 19). It is believed that this hormone is related to depression because its levels decline till normal once the depression disappears. The hypothalamus controls the levels of cortisol in the blood plasma. The hypothalamus produces CRH (Corticotrophic Releasing Hormone) which stimulates the release of ACTH (adrenocorticotrophic hormone). ACTH causes the release of cortisol into the blood. In cases of depression, the hypothalamus causes the pituitary to continue to release CRH despite the levels of cortisol in the blood.
In cases of post partum depression, it has been found that biochemical triggers may be responsible for bipolar illness during pregnancy. This has been associated with the abrupt decrease of sex hormones (oestrogenes and progesterones) in the plasma in the postpartum period. Since these sex steroids are lipid soluble, it is believed that changes in their plasma concentrations are related to parallel fluctuations in their brain concentrations. Sex hormone receptors are located in the limbic region of the forebrain where they modify genetic expression. In the postpartum period, changes are observed in the receptor functions of brain oestrogen. Studies therefore advance the theory that if indeed the withdrawal of sex steroids is responsible for post partum depression, this would be mediated through pathways of the monoamine neural system (McNeal and Cimbolic 361)
Works Cited
Cheah Ui-Hoon. "Rhythm and blues :Doctors are realising depression has much to do with the body's circadian rhythms.. " The Business Times 12 Mar. 2011,ABI/INFORM Trade & Industry, ProQuest. Web. 25 May. 2011.
Lunbeck Institute. Depression.Web. 25 May 2011. http://www.brainexplorer.org/depression/depression_aetiologi.shtml
Marshall, William and Bangert S. Clinical Biochemistry: Metabolic and Clinical Aspects.New York: Churchill Livingstone, 1995. Print.
McNeal, Elizabeth T, and Cimbolic, Peter. "Antidepressants and Biochemical Theories of Depression. " Psychological Bulletin 99.3 (2003): 361. ABI/INFORM Global, ProQuest. Web. 25 May. 2011.
Newsholme, Eric, and Anthony Leech. Functional Biochemistry in Halth and Disease.New Jersey: Wiley Blackwell, 2010. Print
Stevens, Lawrence. The Myth of Biological Depression.Web. 25 May 2011. http://www.antipsychiatry.org/depressi.htm
