&Adrenergic 1251-Pindolol Binding Sites in the lnterpeduncular Nucleus of the Rat: Normal Distribution and the Effects of Deafferentation

The plasticity of the &and &adrenergic receptor subtypes was examined in the interpeduncular nucleus (IPN) of the adult rat. The B-adrenergic receptor antagonist i251-pindolol (1261-PIN) was used in conjunction with the selective subtype antagonists ICI 118,551 and ICI 89,408 to determine the subnuclear distribution of /I,and &-adrenergic receptors in this nucleus and to correlate the receptor distribution with the distribution of both noradrenergic afferents from the locus coeruieus (LC) and non-noradrenergic afferents from the fasiculus retroflexus (FR). The density of these binding sites was examined following lesions that decreased (LC lesions) or increased (FR lesions) the density of the noradrenergic projection in the IPN. Quantitative radioautography indicated that &labeled binding sites account for the larger percentage of binding sites in the IPN. The B,-binding sites are densest in the those subnuclei that receive a noradrenergic projection from the LC: the central, rostral, and intermediate subnuclei. &binding sites are algo homogeneously distributed throughout the lateral subnuclei, where there is no detectable noradrenergic innervation. &-binding sites have a more restricted distribution. They are concentrated in the ventral half of the lateral subnuclei, where they account for 70% of total ‘251-PIN binding sites. &-binding sites are also present along the ventral border of the IPN. Some of this labeling extends into the central and intermediate subnuclei. Bilateral lesions of the LC, which selectively remove noradrenergic innervation to the IPN, result in an increase in the @,-binding sites. Bilateral lesions of the FR, which remove the major cholinergic and peptidergic input from the IPN, elicit an increase in noradrenergic projections and a decrease in p,-binding sites. @,-binding sites thus exhibit both up-regulation and down-regulation which is correlated with the density of the noradrenergic projection. Our results suggest, therefore, that the density of &-binding sites is regulated by noradrenergic input. &binding sites increase in density in response to both