[Stress. Neurophysiologic studies]

The hypothalamic-pituitary-adrenocortical (HPA) axis knowingly plays a key role in the physiological response to various stressing situations, owing to its gluconeogenetic function, and also, possibly, to its large range of modulating effects on a series of more specific defense mechanisms including the immune system, the latter effect serving to protect the organism against overactive defense reactions. It has long been accepted that under most aggressive conditions the CNS is an essential part of the mechanism controlling the subsequent acute stimulation of the HPA axis. In this line of research, the HPA axis reacts within a few minutes after a standard ether-stress, with a 6 fold increase over the baseline of CRH41 secretion, and at the periphery with 20-fold and 14-fold increases, respectively, in plasma concentrations of ACTH and corticosterone in unanesthetized free-moving rats. From a series of additional experiments a few selected brain structures emerged as basic components of the CNS control involved in the HPA axis stress responses: 1) The catecholamine (CA) producing neurons of the medulla oblongata (A1/C1 and A2/C2 nuclei) which directly innervate the CRH41-secreting neurons in the paraventricular nuclei (PVN) via the ventral noradrenergic bundle (VNAB), yield the major stimulatory pathway to the stress-induced CRH-ACTH surge. Not only was this surge dramatically obliterated by a neurotoxic deletion of the VNAB, with a local microinfusion of 6-hydroxydopamine (6-OHDA) but it was restored by intra-cerebroventricular (icv) microinfusions of adrenaline (AD) or noradrenaline (NA).(ABSTRACT TRUNCATED AT 250 WORDS)