SYNAPTIC NEUROCHEMISTRY OF HUMAN STRIATUM DURING DEVELOPMENT - CHANGES IN SUDDEN-INFANT-DEATH-SYNDROME

There is evidence of abnormalities in the brainstem monoamine-containi ng neurons in infants with sudden infant death syndrome (SIDS). By tak ing advantage of the rich innervation of the human basal ganglia by mo noaminergic afferents from cell bodies in the brainstem, we studied th e synaptic chemistry of catecholamine and associated neurons of the pu tamen obtained postmortem from 14 SIDS infants, eight age-matched cont rol infants, and older control subjects of various ages. We found sign ificantly lower concentrations of dopamine and higher homovanillic aci d/DA ratios in samples from SIDS infants compared with age-matched con trol infants. Noradrenaline and 5-hydroxytryptamine were lower in SIDS compared with control subjects, but the difference did not reach stat istical significance. There was no clear evidence that dihydroxyphenyl acetic acid and 5-hydroxyindoleacetic acid were altered. Immunoblot an alysis of striatal tissue showed that samples from infants with SIDS, which exhibited lower DA, also had lower tyrosine hydroxylase protein. Other transmitter-specific neuronal markers were also assessed, inclu ding enzymes associated with cholinergic and GABA-containing neurons. We found significantly decreased choline acetyltransferase activities. However, GABA, glutamate, or somatostatin concentrations or monoamine oxidase activities were unchanged in SIDS. We also noted age-dependen t changes in brain weights and some synaptic markers by comparing the age-matched infants with older control subjects. Analysis of variance revealed that homovanillic acid, dihydroxyphenylacetic acid, and monoa mine oxidase B activities were increased with age. DA and choline acet yltransferase were also found to be positively correlated in putamen. Our findings suggest developmental changes in some transmitter-specifi c neurons in SIDS that may result from apneic episodes or chronic hypo xia induced before death.