SIDS-like symptoms in mice with serotonin signaling defects

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Sudden Infant Death Syndrome, or SIDS, is an extremely challenging thing to study. For years, it wasn't even clear whether the deaths of infants with no apparent abnormalities represented a distinct biological phenomenon. Over time, however, monitoring of infants revealed unexplained lapses in their regulation of body temperature and heart rate, and postmortem examinations suggested an association with defective signaling involving the neurotransmitter serotonin. Now, researchers exploring serotonin signaling in mice may have created the first animal model of SIDS; a description will appear in today's issue of Science.
It's not at all clear that SIDS was what the group were after, since serotonin is involved in a wide variety of neural process, and its signaling pathway is the focus of a lot of drug development. Still, if chance favors the prepared mind, the researchers appear to have been very well prepared.
Their work focused on creating a mouse strain where the activity of the serotonin pathway could be manipulated experimentally. To do so, they used the Htr1a receptor, which helps tone down serotonin signaling. When this receptor binds the neurotransmitter, it actually inhibits the function of other receptors, producing a net decrease in serotonin signaling. The authors placed the Htr1a gene under the control of regulatory proteins such that it would normally be expressed, but administration of a drug called tetracycline would shut the gene down; for the purposes of this discussion we'll call that genetic construct Tet-Htr1a.
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