Exam 18: Affective Disorders: Antidepressants and Mood Stabilizers

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Using a selective serotonin reuptake inhibitor (SSRI), such as fluoxetine (Prozac), as an example: An acute effect would be to inhibit serotonin reuptake from the synaptic cleft, and potentially provide more serotonin receptor activation. However, given the existence of presynaptic auto-inhibitory receptors that inhibit serotonin release, one may initially get a cancelling out of effects, so no net difference in serotonin activation of postsynaptic receptors occurs. With chronic administration, if the presynaptic receptors desensitize, then the net effect will be more serotonin activation of postsynaptic serotonin receptors. This could take several weeks to occur. This is just one theory about the time lag for the therapeutic effect of antidepressant drugs.

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The monoamine hypothesis of mood disorders suggests that a deficit in the functioning of monoamines such as serotonin and norepinephrine contributes to the production of depression. Evidence in favor includes the production of depression in some patients who have taken reserpine for treating high blood pressure. Reserpine depletes the stores of serotonin and norepinephrine by inhibiting their uptake into synaptic vesicles. Conversely, administration of a monoamine oxidase inhibitor (MAOI), which inhibits metabolism of biogenic amines, can cause an elevation in mood. Evidence against this hypothesis includes the observation that measurements of biogenic amine metabolites in cerebrospinal fluid (CSF), which can reflect biogenic amine activity in the brain, have not been consistent in showing differences between those with and without depression. Also, since drugs such as reserpine and MAOIs affect several biogenic amines (serotonin, dopamine, norepinephrine, epinephrine), specifying which transmitter(s) may be of particular significance for depression would require additional studies.