No abstract

Newborn rats were subjected to undernutrition and 6-hydroxydopamine (6-OHDA) treatment. Body and brain weight were affected more deeply during development in malnourished animals than in the 6-OHDA-treated ones. An increase in 5-hydroxytryptamine (5-HT) concentration in the anterior and posterior brain was observed at the age of 21 days in the malnourished group, suggesting changes in amine metabolism during nerve terminal maturation in the brain. In the 6-OHDA-treated group the 5-HT brain content was unchanged at the ages studied, which does not exclude the possibility of 5-HT metabolic modifications in the absence of noradrenergic pathways during postnatal development of the rat brain.

In brain of adult and developing rats the Na⁺-K⁺-adenosine triphosphatase (Na⁺-K⁺-ATPase) system seems to react to serotonin (5-MT) changes induced pharmacologically. A 5-HT agonist (quipazine) elicits a response of the enzyme activity in the cerebral cortex in vivo, which is neutralized with a 5-HT antagonist (methysergide). This effect was observed from day 21 to adulthood. Also in a state of 5-HT receptor hypersensitivity (rats treated early with 5,6-dihydroxytryptamine), the response of Na⁺-K⁺-ATPase to the 5-HT agonist was higher than without neurotoxic lesion of 5-HT paths. These data suggest involvement of the Na⁺-K⁺-ATPase system in 5-HT receptor sensitivity in the rat brain.

The postnatal development of ³H-5-HT specific binding sites has been studied in rat brain. Experimental conditions allowed the characterization of the class of sites corresponding to the synaptosomal receptor for 5-HT. The related affinity constant and maximal binding were measured at various ages after birth. During the second week after birth, the serotonin receptor system developed explosively, the maximal number of sites increasing from a nonsignificant value to that observed in adult rats. Lesion of the presynaptic neurons using 5,6-DHT led to a significant increase of the number of sites.

No abstract