Catecholamine metabolism in neonatal rat brain during asphyxia and recovery

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Abstract
Infant rats were subjected to various degrees of asphyxia — 1‐day‐old rats were exposed to 100% N2for 20 min and 4‐day‐old rats were exposed to 94%N2‐6%O2for 30 min. The activity of tyrosine hydroxylase, the first and rate limiting enzyme in the catecholamine (CA) synthesis, was studied in vivo in whole brain and in various brain parts by measuring the accumulation of dihydroxyphenylalanine (DOPA) after inhibition of aromatic L‐aminoacid decarboxylase with NSD 1015. Measurements of the endogenous levels of tyrosine, dopamine (DA) and noradrenaline (NA) were also made during asphyxia and recovery. During asphyxia there was a decrease in DOPA accumulation in the whole brain of the 1‐day‐old animals and in the striatum, midbrain and brainstem regions of the 4‐day‐old rats. In the recovery phase both tyrosine and DOPA levels in the whole brain of the 1‐day‐old animals increased approximately 2‐fold 30 min after anoxia. In the regional brain study, a significant increase compared to controls was only noted in the striatum region. After 2 h, tyrosine and DOPA accumulation had reached normal or subnormal levels. In the 1‐day‐old rats there were no changes in whole brain DA or NA levels during anoxia and recovery except for an increase in DA levels noted after 6 h in the recovery phase. The disappearance rate of DA but not NA during hypoxia was retarded in the whole brain of the 4‐day‐old animals after H 44/68 (α‐methyltyrosine), indicating a reduced nerve impulse activity in central dopaminergic but not noradrenergic nerves. The catecholamine neurotransmitters DA and NA are ascribed a lot of important functions in the mature brain. As hypoxia or anoxia cause profound changes in the metabolism of these transmitters during the neonatal period, this might be relevant as a factor underlying early childhood behavioural or neurological disorders.

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