Abstract
Neonatal 6-hydroxydopamine (6-OH-DA) treatment is known to produce a marked change in the ontogeny of central noradrenaline (NA) neurons with i.a. a permanent denervation in the cerebral cortex and hyperinnervation in the cerebellum. This treatment led to a 40% increase in the β-adrenergic binding sites in the cerebral cortex without changing their affinity towards [ 3H]dihydroalprenolol ([ 3H]DHA) (used as a ligand for β-receptor assay in vitro). In the cerebellum there was a 20% decrease in binding sites. The results indicate that the β-receptors develop independent of the noradrenaline nerve terminals whereas changes in transmitter availability may regulate the number of postsynaptic β-adrenergic receptors. These alterations in β-receptor density may play a contributory role in phenomena described as denervation supersensitivity (increase of receptors) and receptor desensitization (decrease of receptors) respectively.
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