This tendency was especially evident among people high in autonomy. Depression and martial discord
Constant seeking of reassurance is a critical variable in depression. Even when reassured, they are
only temporarily satisfied. Their negative self-concept causes them to doubt the truth o the feedback
they have received, and their constant efforts to be reassured come to irritate others.
Social skills deficits may be a cause and consequence of depression.
PSYCHOLOGICAL THEORIES OF BIPOLAR DISORDER:
patients with bipolar depression have elevated levels of the dysfunctional attitudes described by
Beck, as well as problems in autobiographical memory and the ability to generate solutions in problem-
solving task. The manic phase of the disorder is seen as a defence against a debilitating psychological
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
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
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
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
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
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
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.