Neurochemical and morphological effects of neonatal anoxia on monoamin
e systems were studied after 100% N2 exposure for 25 min at 30 h postn
atally (postnatal day 2-P2). At 20 min after anoxia, reductions of tis
sue levels of cerebellar noradrenaline (NA) and striatal dopamine (DA)
and metabolites were seen, while 5-hydroxyindoleacetic acid (5-HIAA)
was increased in cortex and cerebellum. At P7, NA increased in cerebel
lum, while serotonin (5-HT) and 5-HIAA decreased in cortex and cerebel
lum. At P21, increased hippocampal NA and striatal homovanillic acid (
HVA) were found, while striatal 5-HT decreased and 5-HIAA increased in
striatum and hippocampus. At P60, striatal 3,4-dihydroxyphenylacetic
acid (DOPAC) and 5-HIAA levels were found to be enhanced. No effects w
ere seen on 5-HT, tyrosine hydroxylase, or DARPP-32 immunostaining in
cortex, hippocampus, and striatum. Thus, the neonatal anoxia induced b
oth acute and persistent neurochemical abnormalities in monoamine syst
ems that were not accompanied by morphological changes detectable with
the methods used. The monoamine alterations found could be critically
connected to the behavioral disturbances observed in rats after neona
tal anoxia. The findings may also be of relevance to dysfunctions seen
in humans after perinatal oxygen deficiency, e.g., the attention defi
cit hyperactivity disorder syndrome.