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Abnormalities of the dorsal motor nucleus of the vagus in sudden infant death syndrome

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dc.contributor.author Dentremont, Karen
dc.date.accessioned 2009-05-22T04:04:51Z
dc.date.available 2009-05-22T04:04:51Z
dc.date.copyright 1998 en
dc.date.issued 2009-05-22T04:04:51Z
dc.identifier.uri http://hdl.handle.net/2429/8070
dc.description.abstract Recent hypotheses concerning the pathogenesis of sudden infant death syndrome (SIDS) have focused on developmental abnormalities of the central nervous system, which are believed to produce cardiorespiratory instability in susceptible infants. The present study was designed to investigate developmental abnormalities in the dorsal motor nucleus of the vagus (DMV) in SIDS. Using serial histological sections of the brainstem from SIDS cases and agematched control cases without neurological disease, morphometric analyzes were performed to compare postnatal changes in 1) the total volume of the DMV, 2) the numerical density of neurons (Nv, cells per mm³), 3) the total number of neurons, and 4) mean neuronal profile area. In the SIDS cases there was a significant increase in the total volume of the DMV (33%), when compared to controls. In SIDS there was a significant decrease in the Nv of neurons (33%), although the total number of neurons did not differ significantly from controls. Mean neuronal profile areas were significantly greater in SIDS for both motor (31&) and non-motor (30%) neurons, when compared to controls. These changes are consistent with an overgrowth of the DMV during early postnatal development. Given the role of the DMV in the autonomic control of breathing and heart rate, this subtle developmental disorder likely contributes to the cardiorespiratory instability characteristic of susceptible infants. Given the possibility that increased expression of insulin-like growth factor I during early postnatal development might contribute to this overgrowth, morphometric analyses were performed on the DMV and hypoglossal nucleus (HN) in transgenic mice, which overexpress IGF-I postnatally, and in normal littermate controls on postnatal day 35. Morphometric variables included 1) the total volumes of the DMV and HN, 2) the Nv of neurons, 3) the total number of neurons, and 4) the mean neuronal profile areas. In transgenic mice there was a significant increase in the volumes of both the DMV (84%) and the HN (30%). The Nv of neurons was significantly reduced in both nuclei in transgenic mice. In the DMV, however, there was a significant increase in the total number of neurons (56%). In the HN, the total number of neurons did not differ significantly between transgenic mice and controls. Mean neuronal profile areas were significantly increased in transgenic mice in both the DMV (35%) and the HN (22%). Available evidence suggests that the increased neuron number in the DMV results from an antiapoptotic effect of IGF-I. In a third experiment, morphometric and stereological analyses were performed in the DMV of rats during normal postnatal development to determine the time course of the progressive and regressive phases of synaptogenesis. The initial phase of synapse proliferation occurred from birth to postnatal day 30, while the regressive phase of synapse elimination occurred after day 30. Recent hypotheses suggest that SIDS results from a failure to eliminate normally extraneous synapses from the brainstem. By knowing the age at which peak synaptic densities occur, one could introduce exogenous growth factors to prevent normal elimination of synapses. Preventing synapse elimination from the brainstem of the rat might be expected to produce an animal model of SIDS. (A scientific formula N[subscript V] used in this abstract could not be reproduced by the software.) en
dc.format.extent 14151467 bytes
dc.format.mimetype application/pdf
dc.language.iso eng en
dc.relation.ispartofseries UBC Retrospective Theses Digitization Project [http://www.library.ubc.ca/archives/retro_theses/]
dc.title Abnormalities of the dorsal motor nucleus of the vagus in sudden infant death syndrome en
dc.type Electronic Thesis or Dissertation
dc.degree.name Master of Science - MSc en
dc.degree.discipline Pathology en
dc.degree.grantor University of British Columbia
dc.date.graduation 1998-11 en
dc.degree.campus UBCV en


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