Catecholaminergic neurons in the diencephalon and basal ganglia of SIDS.
The catecholaminergic systems of sudden infant death syndrome victims were examined in the diencephalon and basal ganglia, in addition to the midbrain, pons, and medulla oblongata, using the immuno-histochemical method involving tyrosine hydroxylase. A significant decrease in tyrosine hydroxylase immunoreactivity was demonstrated in the basal ganglia of sudden infant death syndrome victims between 2 to 12 months of age compared with age-matched control subjects. This change in the basal ganglia may be a secondary finding induced by chronic hypoxia or repeated ischemia in sudden infant death syndrome but suggests impairment of the development of the neuronal connection from the brainstem to the upper cardiorespiratory control in sudden infant death syndrome.
Ozawa
Y
Y
Department of Mental Retardation and Birth Defect Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
Obonai
T
T
Itoh
M
M
Aoki
Y
Y
Funayama
M
M
Takashima
S
S
D001479:Basal Ganglia / Q000378:metabolism / Q000473:pathology*; D016022:Case-Control Studies; D002395:Catecholamines / Q000378:metabolism*; D004027:Diencephalon / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D007223:Infant; D008297:Male; D009474:Neurons / Q000378:metabolism*; D013398:Sudden Infant Death / Q000175:diagnosis* / Q000473:pathology; D014446:Tyrosine 3-Monooxygenase / Q000276:immunology
D002395:Catecholamines; D014446:Tyrosine 3-Monooxygenase