The activity of the brain stem catecholaminergic (CA) cell groups of the ventrolateral (A1C1) and dorsomedial (A2C2) medulla that are known to contain primarily noradrenergic neurones (A1 and A2) and a smaller proportion of adrenergic cells (C1 and C2) as well as the noradrenergic group locus ceruleus (LC) in the dorsal pons was determined at various times up to 16 days following surgical adrenalectomy. The activity of the CA cell groups was estimated by the rate of tyrosine hydroxylation in vivo that was assessed by measuring the 3, 4-dihydroxyphenylalanine (DOPA) accumulated 20 min following administration of DOPA decarboxylase inhibitor NSD 1015. In the medullary nuclei noradrenaline content was found around 40- up to 70-fold the adrenaline content. This result was taken as evidence that the noradrenergic cells are likely to provide the main contribution to the tyrosine hydroxylation rate that we measured. Endogenous DOPA content represented between 2 and 10% of the noradrenaline content. NSD 1015 induced an accumulation of DOPA that was linear for at least 20 min and reached at this time more than 10-fold the endogenous level. While no modification of the in vivo tyrosine hydroxylation rate was observed in the LC, a significant increase was found in both medullary groups following adrenalectomy. In the A1C1 group it was detected 8 days after surgery and was then maintained with a maximum that represented up to a 60% increase over the basal value. In the A2C2 group the activation was slightly delayed and less marked. Increase in ACTH level occurred much earlier: it was about 70% of the maximal level already 4 days following adrenalectomy. The tyrosine hydroxylase activity measured in vitro with saturating concentrations of substrate and cofactors, was not affected by adrenalectomy. Daily injection of dexamethasone prevented the increase in plasma ACTH as well as the increase of the in vivo tyrosine hydroxylation rate in the medullary CA groups triggered by adrenalectomy. This activation is thus likely to be mediated by type II glucoreceptors and does not seem to involve an increase of the tyrosine hydroxylase content but rather other regulatory processes of the hydroxylation step in vivo. While the brain stem CA neurons are known to participate in the control of the hypothalamo-pituitary axis, their delayed activation following adrenalectomy suggests that they are not directly involved in the early increase in plasma ACTH level triggered by the lack of circulating corticosteroids.