| Abstract: | Neonatal rats were exposed to 20 or 30 min of total or partial oxygen deprivation. During asphyxia and subsequent recovery the endogenous levels of tryptophan and 5-hydroxytryptamine (5-HT, serotonin) were measured. The activity of tryptophan hydroxylase, the first and rate limiting enzyme in the 5-HT synthesis pathway, was studied in vivo by measuring the accumulation of 5-hydroxytryptophan (5-HTP) after inhibition of aromatic L-amino acid decarboxylase with NSD 1015. During asphyxia there was a decrease in tryptophan hydroxylase activity in the whole brain and various brain regions studied. The levels of tryptophan, 5-HTP and 5-HT all increased after 30 min of recovery from asphyxia. In the whole brain, 5-HTP and 5-HT levels were normal 2 h after anoxia while tryptophan levels normalized more slowly to reach control values after 6 h. In the regional brain study, the 5-HTP levels returned quickly to control levels after asphyxia in the striatum and midbrain but not in the brainstem and hemispheres regions. The whole brain 5-HTP and 5-HT levels did not differ from controls 24 and 48 h after the asphyxia. Although the neonatal nervous system exhibits a great resistance to asphyxia, the metabolism of the neurotransmitter 5-HT is affected already during a short period of asphyxia and subsequent recovery. As 5-HT is ascribed important neurotransmitter functions, this might be relevant to the neurological sequelae of human asphyxia neonatorum. |
