Serotonin Receptors Don't Always Activate the Same Way
> 1/3/2008 2:16:49 PM

Serotonin is a crucial neurotransmitter. There are a number of synthetic drugs designed to trigger serotonin receptors and thus restore the brain to a healthy balance. These drugs are used to treat major disorders such as depression and schizophrenia, and there has been so much success with them that many more are in development. Those rushing to develop must pause, though, to read a study published last week by the Ohio State University Medical Center.

This study, lead by Dr. Laura Bohn, questioned the assumption that all activations of serotonin receptors have the same effect. The prevailing belief had been that anything that triggers the receptor will induce it to produce the same signal. Dr. Bohn focused on the A2 receptor, which is the target of many medications. She compared natural serotonin to a hallucinogen called DOI, which was created to mimic serotonin.

Both serotonin and DOI triggered serotonin receptors in a way that looked identical to normal electrical observation. But while they both produced G-proteins, only serotonin produced beta-arrestin. This observation was tested in mice designed to lack beta-arrestin. The result was a perfect lesson in the danger of assuming that similar symptoms or benefits are caused by identical chemical pathways. Both serotonin and DOI cause head-twitching, and earlier researchers assumed that they did this in the same way. However, mice without beta-arrestin twitched when given serotonin but not DOI, demonstrating that serotonin relies on other mechanisms.

This observation is critical because it means that it is not enough to create a drug that triggers serotonin receptors. As with almost anything else in the brain, it is not that simple. Researchers need to realize that serotonin can be activated in different ways, and they need to figure out what ways are most important for treatment and ensure that their  medication has that capability.

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