Australian researchers have observed the chemical processes facilitated by certain anti-depressant medications on the cellular level for the first time, recording these interactions with an unprecedented degree of detail. Their insights will almost certainly help speed the development of more effective drugs.

The study behind the new report published in the Journal of Neuroscience concerned only SNRI (serotonin and norepinephrine reuptake inhibitors) drugs, the most popular of which is Effexor. Unlike more common SSRIs such as Prozac and Zoloft, these drugs work to elevate existing levels of both serotonin, the "pleasure hormone," and norepinephrine, an unrelated neurotransmitter.

According to data collected from the rodents in this study, these drugs actually stimulate neurogenesis by creating new masses of cells in the hippocampus, an area of the brain closely tied to emotion and memory retention.

By inhibiting the re-uptake, or return, of these two transmitters to the neurons that created them, the drugs create a flood of both in the brain. This wealth of transmitters then undergoes a chemical reaction to activate stem cells in the hippocampus, prompting them to create new matter. This supercharging of the hippocampus actually works to improve mood. Were it not for this interaction, the drugs would not work in the same way.

The fact that researchers did not consider SSRI's like Prozac and Zoloft (which are the most popular antidepressants) certainly negates the amount of attention this report will receive. It also raises further questions about how, exactly, these other drugs work.

The study's implications go well beyond depression, however, especially since a decreased rate of neurogenesis is the primary factor behind dementia. It would seem that the chemical process that allows these SNRIs to create new cells may also counteract the development of age-related dementia. Perhaps most importantly, it allows future research to focus on refining the exact mechanism that stimulates neurogenesis.