Skip to Content
Merck
  • Medullary Serotonin Neuron Abnormalities in an Australian Cohort of Sudden Infant Death Syndrome.

Medullary Serotonin Neuron Abnormalities in an Australian Cohort of Sudden Infant Death Syndrome.

Journal of neuropathology and experimental neurology (2017-09-20)
Fiona M Bright, Roger W Byard, Robert Vink, David S Paterson
ABSTRACT

Serotonin (5-hydroxytryptamine [5-HT]) neurons in the medulla oblongata project extensively to key autonomic and respiratory nuclei in the brainstem and spinal cord regulating critical homeostatic functions. Multiple abnormalities in markers of 5-HT function in the medulla in sudden infant death syndrome (SIDS) have been reported, informing the hypothesis that at least a subset of SIDS cases is caused by deficits in 5-HT function resulting in impaired homeostatic responses to potentially life-threatening events during sleep. To investigate medullary 5-HT defects in SIDS further, we undertook qualitative analysis immunohistochemical assessment of 5-HT neuron expression within the medulla of SIDS infants (n41) and nonSIDS controls (n = 28) in an independent cohort from Forensic Science South Australia. Compared with controls SIDS cases had significantly higher 5-HT neuron numbers and density in addition to significantly altered 5-HT neuron morphology. Thus, for the first time, we replicated and corroborated previous observations of a significant abnormality in medullary 5-HT neuron expression in SIDS in a separate independent SIDS cohort. This study further supports the hypothesis that medullary 5-HT defects contribute to the pathogenesis of a subset of SIDS victims and provides additional evidence of a more complex abnormality in 5-HT neuron dysfunction specifically within the different caudal and rostral medullary 5-HT domains.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-Tryptophan Hydroxylase/Tyrosine Hydroxylase/Phenylalanine Hydroxylase Antibody, clone PH8, clone PH8, Chemicon®, from mouse