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University of Ottawa
Jon Houseman

BIOLOGICAL THEORIES OF MOOD DISORDERS: THE GENETIC DATA: bipolar disorder is one of the mot heritable of disorders. Genes account for possibly 85% of variance in whether a person becomes manic. th Evidence favouring the hypothesis that bipolar disorder results from a dominant gene on the 11 chromosome. Within bipolar disorder, variation in the brain-derived neurotrophic factor (BDNF) gene appears to predict risk for developing rapid cycling. Some people seem to be genetically predisposed to the onset of MDD when confronted with a series of adverse life-events. Serotonin transporter gene-linked promoter region (5-HTTLPR), which is involved in modulating serotonin levels, is a significant predictor of first major depression onset following multiple adverse events. NEUROCHEMISTRY, NEUROIMAGING AND MOOD DISORDERS: The original theory posited that low levels of norepinephrine and dopamine lead to depression and high levels to mania. The serotonin theory suggests that serotonin, a neurotransmitter presumed to play a role in the regulation of norepinephrine, also produces depression and mania. However, the weight of the evidence does not completely support the notion that levels of neurotransmitters are critical in the mood disorders. Tricylclic drugs: i.e. imipramine, or Tofranil are group of antidepressant medications so named because their molecular structure is characterized by three fused rings. They prevent some of the reuptake of norepinephrine, serotonin and or dopamine by the presynaptic neuron after it has fired, leaving more of the neurotransmitter in the synapse so that transmission of the next nerve impulse is made easier. Monoamine oxidase (MAO) inhibitors: I.e. Tranylcypromine or Parnate are antidepressant drugs that keep the enzyme MAO from deactivating neurotransmitters, thus increasing the levels of serotonin, norepinephrine and or dopamine in the synapse. This action produces the same facilitating effect decried for tricylics, compensating for the abnormally low levels of these neurotransmitters in depressed people. Newer antidepressants, called selective serotonin reuptake inhibitors, i.e fluoxetine or Prozac, act more selectivel, specifically inhibiting the reuptake of serotonin. It now appears that the explanation of why these drugs work is not as straightforward as it seemed at first. Both tricyclics and MAO inhibitors take from seven to 14 days to relieve depression, but by that time, the neurotransmitter level has already returned to its previous state. Another approach to further evaluate the theories involved measuring metabolites of these NT, the by-products of the breakdown of serotonin, norepinephrine, and or dopamine found in urine, blood serum, and the cerebrospinal fluid. The problem with such measurements is that they are not direct reflections of levels of NT in the brain; metabolites measured in this way could reflect NT anywhere in the body. Further, the expected high or low metabolites were not found consistently, thus, many people with depression or mania did not have disturbances in absolute levels of NT. It would seem, then, that a simple change in the level of norepinephrine or serotonin or dopamine is not a sufficient explanation for why people become depressed and/or manic. One line of research examined whether antidepressants alter the chemical messengers that a postsynaptic receptor sends into the postsynaptic neuron. If receptors are overly sensitive they should respond to very small amounts of a neurotransmitter in the synaptic cleft. Drugs that increase dopamine levels have triggered manic behaviour in people with bipolar disorder, suggesting the possibility that dopamine receptors are overly sensitive. Research on Bipolar disorder is also moving away from the older norepinephrine theory. One major reason is that lithium, the most widely used and effective treatment for bipolar disorder is useful in treating both the manic and depressive episodes of the disorder, suggesting that it acts by affecting some neurochemical that can either increase or decrease neural activity. Current research is focusing on G-proteins. High levels of these have been found in patients with mania and low levels in patients with depression, suggesting that the therapeutic effects of lithium may be due to its ability to regulate G-proteins. The amygdyla, hippocampus, prefrontal cortex, and the anterior cingulated are the main brain structures implicated in MDD and bipolar disorder. Several neuroimiging studies concluded that: • Structural imaging show that recurrent depression and long duration untreated depression are related to decreased hippocampal volume and neurocognitive impairment. • Functional imaging show that induction of dysphoria in healthy volunteers increases glucose metabolism in cingulated area 25, and response to treatment of depression with paroxetine was evident in a reduction of hyper-metabolism in cingulated area 25. A (MAO-A) is an enxyme that metabolizes monoamine such as serotonin, norep, and dopamine. Elevated MAO-A density is the primary monoamine-lowering process during major depression. THE NEUROENDOCRINE SYSTEM: The HPA-axis is though
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