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Serotoninergic receptor 1A in the sudden infant death syndrome brainstem medulla and associations with clinical risk factors

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Abstract

The immunoreactivity of the serotoninergic receptor subtype 1A (5HT1AR) was quantitatively analyzed in the human infant brainstem medulla (caudal and rostral levels). We hypothesized that immunoreactivity of 5HT1AR would be reduced in infants diagnosed with sudden infant death syndrome (SIDS). In particular that those infants with known clinical risk factors (including cigarette smoke exposure, bed sharing and sleep position) would have greater changes than those without clinical risks. Comparing SIDS (n = 67) to infants who died suddenly with another diagnosis (non-SIDS, n = 25), we found decreased 5HT1AR immunoreactivity in the majority of the nuclei studied at the rostral medulla level including dorsal motor nucleus of the vagus (DMNV), nucleus of the solitary tract, vestibular, and inferior olivary nucleus (ION). There was a significant relationship with all risk factors for 5HT1AR, especially for DMNV, suggesting that 5HT1ARs are highly vulnerable to various insults within the SIDS DMNV. This study not only provides further evidence of abnormalities within the brainstem serotoninergic system of SIDS infants, but also shows that these changes may be associated with exposure to clinical risk factors.

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Acknowledgments

This research was funded by the SIDS Foundation of South Australia, NH&MRC (#302006), and A/Prof. Waters was supported by an NH&MRC Practitioner Fellowship (#206507). The authors thank the staff of the Department of Forensic Medicine, Glebe, NSW, Australia, for their co-operation in this study, and acknowledge the facilities as well as scientific and technical assistance from the staff of the NANO Major National Research Facility at the Electron Microscope Unit, University of Sydney.

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Correspondence to Rita Machaalani.

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Machaalani, R., Say, M. & Waters, K.A. Serotoninergic receptor 1A in the sudden infant death syndrome brainstem medulla and associations with clinical risk factors. Acta Neuropathol 117, 257–265 (2009). https://doi.org/10.1007/s00401-008-0468-x

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  • DOI: https://doi.org/10.1007/s00401-008-0468-x

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