Brain Catecholamine Systems in Stress

Abstract

Publisher Summary In the study discussed in this chapter, immunohistochemical, in situ hybridization histochemistry, tract-tracing, and in vivo microdialysis techniques have been used to investigate the participation of the central catecholaminergic (CA) systems in the organization of responses to an acute neurogenic (pain) stress: subcutaneous injection of 0.5 ml of 4% formalin into the hind paw of rats. This single injection produces a local pain that develops immediately after injection and results in four- to fivefold increase in corticosterone and adrenocorticotropic hormone (ACTH) levels in the plasma and a similar increase in norepinephrine levels in the paraventricular nucleus (PVN). Formalin also induced a rapid expression of c-fos and corticotropin-releasing hormones (CRHs) mRNA in the PVN. The possible crossover of the nociceptive spinal afferents to the medullary CA neurons and the crossover of the ascending CA neurons to the PVN were investigated after spinal and medullary surgical hemisections. Hemisection between the spinal cord and the medulla oblongata did not influence formalin-induced elevation of plasma corticosterone and ACTH levels, and strong c-fos immunoreactivity was observed in the medullary CA cell groups and in the PVN bilaterally, as in the sham-operated animals. Hemisection between the medullary CA cell groups and the PVN (unilateral knife cut at the pons-medulla oblongata border) decreased CRH immunoreactivity and CRH gene expression in the PVN ipsilateral to the transection but remained unchanged contralateral to the knife cut. Although, unilateral pontomedullary hemisection reduce TH and CRH immunoreactivity and CRH gene expression in the PVN, it does not influence the high plasma corticosterone and ACTH levels in response to formalin stress. However, acute immobilization stress in hemisected animals is able to induce CRH expression. These findings suggest that in brain stem-hemisected animals, the remaining intact ascending pathways are sufficient to allow normal, or almost normal, activation of the hypothalamopituitary-adrenal axis during stress.