Stereotaxic deletion of selected areas of the ventral noradrenergic ascending bundle (VNAB-X) by discrete bilateral injections of 6-hydroxydopamine (6-OHDA; 4 µg in 0.2 µl saline) was used to explore the role of brain catechol-amines (CA) and their interaction with corticosteroid feedback in stress responses of the ACTH-corticosterone (CORT) axis. The stereotaxic coordinates used for 6-OHDA lesions and the optimization of postlesion delays were determined by (a) radioautographic labeling of the VNAB axons after tracer injections into the dorsal A2/C2, or the ventral Al/Cl medullary areas, (b) histofiuorescence and immunocytochemical location of interrupted CA pathways versus the postlesional scar, and (c) postlesional noradrenaline and adrenaline concentrations in whole hypothalami and paraventricular nuclei (PVN) punch samples. Two sites of 6-OHDA lesions were selected; both led to striking falls in PVN concentrations of both CA. The more dorsal lesion (dVNAB-X) was the same as that of our earlier studies and interrupted pathways originating predominantly in the A2/C2 area; the second more ventral lesion (vVNAB-X) interrupted axons stemming preferentially from the A1/C1 area. Both VNAB lesions inhibited the ether stress-induced ACTH and CORT surges in rats with intact adrenals. But the blockade (overall poststress release, amplitude and swiftness of hormonal responses) by dVNAB-X was greater than by vVNAB-X. The basal ACTH level in adrenalectomized rats (ADX) was elevated 20-fold and ether stress induced a 4-fold ACTH surge. As in sham-ADX rats, vVNAB-X in ADX rats induced only moderate inhibition of the ACTH response versus ADX + sham-vVNAB-X controls. On the other hand ADX + dVNAB-X rats showed a greatly amplified ACTH stress response over the ADX-sham dVNAB-X controls. This amplification was reversed by oral CORT supplementation. The data suggest that the CA pathways of the VNAB participating, directly or indirectly, in the poststress corticotropic activation may include subsets of CA axons of different origins, whose functional roles in stress are modulated in opposite directions by the plasma corticosteroid level.

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