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The Monoamine Theory of Depression
Neurons communicate with one another through neurotransmitter.When a presynaptic neuron fires [ex. Serotonin], the signal is passed along the receiving neuron by the binding of that neurotransmitter to receptors on the post-synaptic neuron. There are two ways a signal between two neurons ends after the neurotransmitter is delivered to the receptor; Either it is metabolized by Monoamine Oxidase , Or it is recycled back into the pre-synaptic/firing cell.
Antidepressants work by inhibiting the means by neurochemical signals are ended after firing a signal. Antidepressants work by elevating synaptic content of certain neurotransmitters, namely the monoamines: Serotonin, Dopamine, and Norepinephrine.
Monoamine Reputake inhibitors block reuptake channels, not permitting fired neurotransmitters to be recycled back into the firing nerve cell thereby letting the chemical signal go on longer.
Monoamine Oxidase Inhibitors work by blocking the enzyme which metabolize neurotransmitters, after they are fired, in order that the signal ends.
The Serotonin Theory of Depression states that depression is due to a lack of serotonergic neurotransmission. Hence, drugs are used which inhibit the reputake of serotonin, in order to raise its levels in the synaptic cleft.
For example, SSRI = Selective Serotonin Reuptake Inhibitors; selectively block serotonin transporter recycle channels; thereby increasing synaptic serotonin content; thereby turning up serotonin neuro-transmission. The Monoamine Theory of Depression is not born out of an understanding of what is wrong with the brain that is causing depression; but rather merely from the hypothesized activity of the anti-depressant.
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