title: Noradrenergic regulation of type-I and type-II corticosteroid receptors in amygdala and hypothalamus.
abstract: The effects of glucocorticoids on various brain functions including the negative feedback control of HPA axis are mediated by two types of receptor (type I or mineralocorticoid and type II or glucocorticoid) in the central nervous system. Furthermore, noradrenergic systems have been showed to stimulate the activity of hypothalamo-pituitary-adrenal (HPA) axis. The neural and receptor controls of HPA axis activity are generally thought to be independent. Although receptor numbers, especially type-II receptors, are thought to be regulated by circulating levels of corticosterone, they may also be under direct neural control. Thus, it may be suggested that these two types of control are functionally related and that noradrenergic systems may affect HPA axis activity either directly or indirectly via change in receptor characteristics. A major problem in the interpretation of studies examining neurotransmitter regulation of corticosteroid receptors is that the effects of drugs or brain lesions on receptors levels may be secondary to their effects on adrenocortical function. In order to demonstrate a neuronal control on corticosteroid receptors, we tested the effect of 6-hydroxydopamine lesion of noradrenergic systems in the pedunculus cerebellaris superior in adrenalectomized animals whose corticosterone levels were maintained within normal limits by corticosterone replacement implants. Both types of receptor were assayed in hypothalamus and amygdala. We show that: (1) corticosteroid receptors are influenced by noradrenergic systems; (2) this effect depends on the brain region and the receptor type. After the noradrenergic lesion type-I receptors were reduced in hypothalamus and amygdala, whereas type-II receptor were only increased in hypothalamus while receptor affinities were unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Laboratoire de Psychobiologie des Comportements Adaptatifs, INSERM U259, Université de Bordeaux II, France.
authors.forename: S
authors.initials: S
authors.lastname: Maccari
authors.forename: P V
authors.initials: PV
authors.lastname: Piazza
authors.forename: F
authors.initials: F
authors.lastname: Rouge-Pont
authors.forename: L
authors.initials: L
authors.lastname: Angelucci
authors.forename: H
authors.initials: H
authors.lastname: Simon
authors.forename: M
authors.initials: M
authors.lastname: le Moal
mesh_terms: D000315:Adrenalectomy; D000679:Amygdala / Q000502:physiology*; D000818:Animals; D003345:Corticosterone / Q000494:pharmacology; D007031:Hypothalamus / Q000502:physiology*; D008297:Male; D009638:Norepinephrine / Q000502:physiology*; D016627:Oxidopamine; D051381:Rats; D011919:Rats, Inbred Strains; D011965:Receptors, Glucocorticoid / Q000502:physiology*; D013563:Sympathectomy, Chemical
chemical_list: D011965:Receptors, Glucocorticoid; D016627:Oxidopamine; D003345:Corticosterone; D009638:Norepinephrine