Norepinephrine is usually quickly removed from the synapse and pumped back into the cell that released it in order to turn off and reset the system. By blocking the removal of norepinephrine, tricyclics appear to prolong or intensify norepinephrine's message to the post-synaptic cells. However, the fundamental biochemical effect of antidepressants on the brain that is responsible for their benefit remains a mystery. It is thought that the change in neuroamine signaling at the synapse caused by anti-depressants "may set off a cascade of events involving second messenger systems that eventually results in the improvement of the symptoms of depression" (Enna, 1991, 187). Unfortunately, how these medications truly operate remains largely unknown.

Another group of anti-depressants is called selective serotonin re-uptake inhibitors, first introduced in 1988. Unlike the tricyclics, these new anti-depressants have little direct effect on norepinephrine in the brain; instead, they block the re-uptake of serotonin which gives this class its name, sometimes referred to as SSRIs. As with the tricyclics, the effect of serotonin in the synapse seems to occur at the receptors, and there is some evidence that "serotonin is actually the more important neurotransmitter in the treatment of depression" (Kendler, 1992, 720). The development of these new agents which help with depression but which seem to work differently from the tricyclics has provided more clues to the underlying biology of many mood disorders.

Since the early 1990's, an entirely new series of anti-depressants emerged that are neither tricyclics nor selective serotonin re-uptake inhibitors. Most of these agents do not share common features, yet they do generally effect norepinephrine, serotonin and other neurotransmitters. One of them is iproniazid, developed initially for the treatment of tuberculosis. This drug causes inactivation of an enzyme in the body that metabolizes amine compounds in the nervous system. This enzyme called monoamine oxidase "gobbles up molecules of norepinephrine, serotonin and other neurotransmitters" (Enna, 1991, 234). The inactivating effect of iproniazid on the enzyme gives this class its name -- monoamine oxidase inhibitors, or MAOIs.

Another anti-depressant is known as valproate which is generally used for bi-polar depression; however,...

Yet it is understood that valproate improves neuronal transmission in the brain that is mediated by the neurotransmitter gamma-aminobutyric acid (GABA) which seems to have an inhibitory or modulating effect on many brain circuits. An additional agent is known as lamotrigine which is used almost primarily for bi-polar disorder. With this anti-depressant, the release of the neurotransmitter glutamate is inhibited which then causes the stimulation of various neural circuits. Lamotrigine is also thought to affect at least one of the same second-messenger systems as lithium does, being the inositol triphosphate system.
CONCLUSION:

The biochemical systems within the human brain are extremely complex, much like the workings of an advanced computer with intricate wiring networks and related systems. But unlike a computer, the human brain is a living entity and the moods and emotions generated by the brain are greatly affected by certain types of chemical systems. Therefore, under certain conditions, these chemical systems become disrupted and are then treated with anti-depressants that work by boosting and increasing parts of the monoamine system that controls positive emotions while toning down those areas that control negative emotions. Of course, anti-depressants achieve these results in varying ways, sometimes completely by accident or through unknown interactions that still remain a mystery despite more than fifty years of extensive research which only proves that the human brain is an entity unto itself with doorways that have yet to be opened.