SIDS tied to serotonin dysfunctions

New evidence supports extensive abnormalities in the brainstem serotonin system in sudden infant death syndrome (SIDS), according to research published in JAMA this week. The study was based on a comparison of frozen medullae from SIDS infants and from infants who died of other causes. "We have expanded upon previously identified abnormalities in the medullary serotonin system in SIDS cases," first author David S. Paterson of Children's Hospital Boston and Harvard Medical School, Boston told The Scientist. Paterson said the research team pinpointed a specific subtype of serotonin receptor in the serotonin medullary system, which projects to the brainstem and spinal chord and regulates arousal, blood pressure, breathing, heart rate, and temperature."We knew there was a deficit in the serotonin receptors in the medulla in SIDS cases, but we didn't know what subtypes of receptors were involved," said Paterson. "Here, we identified the serotonin receptor 5-HT1A subtype, an autoreceptor that is important in controlling serotonin neuron function. We also counted the serotonin neurons within the medulla and we found a significantly higher number of serotonin neurons in SIDS cases compared to controls." The results showed that although there was a higher number of neurons, those neurons had less 5-HT1A autoreceptor, which evinced a problem with the self-regulatory mechanisms in the serotonin neurons in SIDS. According to Eugene E. Nattie, a professor of physiology at Dartmouth College in New Hampshire, this paper is "a very important step forward" because it provides a constellation of three abnormalities that can be used in animal models to study how the serotonin system can be disrupted to contribute to sudden death. "These are very interesting clues," he said.The paper also supports the "triple-risk model," which proposes that sudden death occurs in infants who simultaneously have an underlying vulnerability, are under an exogenous stressor, and are at a critical developmental period. "All of the babies in our study were exposed to at least one risk factor [male gender, sleep position, bed sharing, or illness within one week of death, among others]; they were all within the critical developmental period [the first year of life], and all of them had the brainstem abnormalities," said Paterson. The results also hint at the causes of the increased vulnerability of boys to SIDS. "We saw that the 5-HT1A receptor binding in boys was significantly lower than in girls," Paterson said. "Perhaps these differences between boys and girls predispose boys to the syndrome."Debra E. Weese-Mayer, an expert in pediatric respiratory medicine from Rush University Medical Center in Chicago, told The Scientist the JAMA paper is an important step forward, but noted some reservations. "It advances us in our understanding of the serotonergic role in SIDS, but it's limited in the number of samples. In the neuropathological studies, there are only 16 SIDS cases and seven controls; those are very small numbers," she said. "There's a bigger number for the genetic studies, but the actual cases in which they did the serotonin 1A are very few." Wesse-Mayer, who has an editorial in the JAMA issue, also pointed out that the paper studies older babies, and that it has a very small number of African-Americans, a population known to be at a higher risk. She attributes this bias to a limited source of tissues. "We hope that the paper together with the editorial will get people to think about the importance of having tissue banks such as the NIH-funded University of Maryland Brain and Tissue Bank, which provides researchers with tissues donated by parents," she said. Graciela Flores mail@the-scientist.comLinks within this article:Paterson DS et al., "Multiple serotonergic brainstem abnormalities in SIDS," JAMA, 296:2124-2132. http://jama.ama-assn.org/cgi/content/abstract/296/17/2124?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=paterson+and+SIDS&searchid=1&FIRSTINDEX=0&resourcetype=HWCITPanigrahy A, et al., "Decreased serotonergic receptor binding in rhombic lip-derived regions of the medulla oblongata in the sudden infant death syndrome," J Neuropathol Exp Neurol. 59:377-384, 2000. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10888367&itool=iconabstr&query_hl=2&itool=pubmed_docsum | [PubMed]Eugene E. Nattie http://www.dartmouth.edu/~physiol/faculty/nattie.htmlDebra E. Weese-Mayer http://rush.photobooks.com/directory/profile.asp?dbase=main&setsize=10&pict_id=0002910Weese-Mayer, D.E., "Sudden infant death syndrome. Is serotonin the key factor?" JAMA, 296:2143-2144. http://jama.ama-assn.org/cgi/content/extract/296/17/2143?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=paterson+and+SIDS&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

SIDS tied to serotonin dysfunctions

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