STRESS-INDUCED NOREPINEPHRINE RELEASE IN THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND PITUITARY-ADRENOCORTICAL AND SYMPATHOADRENAL ACTIVITY- IN-VIVO MICRODIALYSIS STUDIES

The hypothalamic-pituitary-adrenocortical (HPA) axis and the autonomic nervous system are major effector systems that serve to maintain home ostasis during exposure to stressors. In the past decade, interest in neurochemical regulation and in pathways controlling activation of the HPA axis has focused on catecholamines, which are present in high con centrations in specific brain areas-especially in the hypothalamus. Th e work described in this review has concentrated on the application of in vivo microdialysis in rat brain regions such as the paraventricula r nucleus (PVN) of the hypothalamus, the central nucleus of the amygda la (ACE), the bed nucleus of the stria terminalis (BNST), and the post erolateral hypothalamus in order to examine aspects of catecholaminerg ic function and relationships between altered catecholaminergic functi on and the HPA axis and sympathoadrenal system activation in stress. E xposure of animals to immobilization (IMMO) markedly and rapidly incre ases rates of synthesis, release, and metabolism of norepinephrine (NE ) in all the brain areas mentioned above and supports previous suggest ions that in the PVN NE stimulates release of corticotropin-releasing hormone (CRH). The role of NE in the ACE and the BNST and most other a reas possessing noradrenergic innervation remains unclear. Studies inv olving lower brainstem hemisections show that noradrenergic terminals in the PVN are derived mainly from medullary catecholaminergic groups rather than from the locus ceruleus, which is the main source of NE in the brain. Moreover, the medullary catecholaminergic groups contribut e substantially to IMMO-induced noradrenergic activation in the PVN. D ata obtained from adrenalectomized rats, with or without glucocorticoi d replacement, and from hypercortisolemic rats suggest that glucocorti coids feedback to inhibit CRH release in the PVN, via attenuation of n oradrenergic activation. Results from rats exposed to different stress ors have indicated substantial differences among stressors in elicitin g PVN noradrenergic responses as well as of responses of the HPA, symp athoneural, and adrenomedullary systems. Finally, involvement of other areas that participate in the regulation of the HPA axis such as the ACE, the BNST, and the hippocampus and the importance of stress-induce d changes in expression of immediate early genes such as c-fos are dis cussed.