Lecture 11 (mood disorders) Flashcards
What is the prevalence of mood disorders in blood relatives?
The prevalence of mood disorders is approximately three times higher among blood relatives of persons with clinically diagnosed unipolar depression than in the population at large.
What is the difference between mono- and dizygotic twins in depression?
Monozygotic co-twins of a twin with unipolar major depression are about twice as likely to develop major depression as are dizygotic twins.
Which gene is maybe involved in depression?
The serotonin-transporter gene.
It is a gene involved in the transmission and reuptake of serotonin, which is one of the key neurotransmitters involved in depression.
What is the HPA-axis?
Hypothalamic-pituitary-adrenal axis.
What is wrong with the HPA-axis in people with depression?
In depressed individuals, a reduced feedback mechanism of cortisol concentrations on the HPA axis causes increased cortisol levels after a particularly stressful situation has ended.
What is the connection between stress in infancy and the HPA-axis?
Stress in infancy and early childhood can promote long-term changes increasing the reactivity of the HPA axis.
Damage in which part of the brain often leads to depression?
Damage to the left but not the right, anterior or prefrontal cortex.
Which areas of the cortex show decreased volume in people with depression?
Several areas of the prefrontal cortex.
Which part of the brain can get decreased volume following prolonged depression?
Hippocampus.
Do the activation of amygdala increase or decrease with depression?
Increase.
The monoamine hypothesis?
A hypothesis that suggested that depression was at least sometimes due to an absolute or relative depletion of one or all of these neurotransmitters (dopamine, norepinephrine, and serotonin) at important receptor sites in the brain.
What are the neurotransmitters from the monoamine hypothesis known to be involved in today?
Regulation of behavioral activity, emotional expression, and vegetative functions – all important for mood disorders.
The neurotrophin hypothesis?
Neurotrophins aid in the survival, growth, and connections of neurons. Most people with depression have lower level of this than normal people. This leads to a smaller than normal hippocampus in people with depression, impaired learning, and reduced production of new hippocampal neurons. Many studies suggest that antidepressant drugs increase these levels.
The point is that new neurons in the hippocampus is produced, which leads to new learning, which is important for antidepressant effects.
The mechanism of tricyclics?
They block the transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after their release.
The mechanism of monoamine oxidase inhibitors?
Block the enzyme monoamine oxidase, a presynaptic enzyme that metabolizes catecholamines and serotonin into inactive forms.
