title: The relationship between neuronal plasticity and serotonergic neurons in the brainstem of SIDS victims.
abstract: BACKGROUND
  The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its cause is still unknown. Recently, the medullary serotonergic network deficiency theory has been proposed and an association between SIDS and neuronal plasticity has also been suggested. The growth-associated phosphoprotein 43 (GAP43) is a marker of synaptic plasticity and is critical for normal development of the serotonergic innervation. Therefore, the characteristics of GAP43-positive elements and their association with serotonergic neurons were here investigated in the brainstem of SIDS victims.
  
  
  METHODS
  The materials of this study included 26 cases of SIDS and 12 control cases. The brainstem material was collected and the immunohistochemistry of GAP43 and tryptophan hydroxylase (TrypH) carried out. The density of GAP43-positive neurons and dendrites and of TrypH-positive neurons were measured quantitatively. Nonparametric analyses of GAP43 between SIDS and non-SIDS and correlation analyses between GAP43 and TrypH were performed.
  
  
  RESULTS
  No significant difference in GAP43-associated findings was found between SIDS and non-SIDS nor any significant correlation between GAP43-associated findings and TrypH-positive neurons.
  
  
  CONCLUSIONS
  The results of this study were not in agreement with the association of GAP43 with SIDS and with serotonergic innervation in SIDS.
authors.affiliation: Department of Legal Medicine, Tokyo Women's Medical University School of Medicine, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan. tsawagu@research.twmu.ac.jp
authors.forename: Toshiko
authors.initials: T
authors.lastname: Sawaguchi
authors.forename: Franco
authors.initials: F
authors.lastname: Patricia
authors.forename: Hazim
authors.initials: H
authors.lastname: Kadhim
authors.forename: Jose
authors.initials: J
authors.lastname: Groswasser
authors.forename: Martine
authors.initials: M
authors.lastname: Sottiaux
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nishida
authors.forename: Andre
authors.initials: A
authors.lastname: Kahn
mesh_terms: D001933:Brain Stem / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D003712:Dendrites / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D004311:Double-Blind Method; D005260:Female; D019922:GAP-43 Protein / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000201:enzymology / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D017286:Polysomnography; D011446:Prospective Studies; D012701:Serotonin / Q000378:metabolism*; D018709:Statistics, Nonparametric; D013398:Sudden Infant Death / Q000209:etiology* / Q000473:pathology; D016683:Supine Position; D014365:Tryptophan Hydroxylase / Q000378:metabolism
chemical_list: D019922:GAP-43 Protein; D012701:Serotonin; D014365:Tryptophan Hydroxylase