Interaction between noradrenergic and glucocorticoid brain systems: Probable involvement in the development of depression

Abstract

Electrophysiological and biochemical experiments on slices of the rat dorsal hippocampus demonstrated that dexamethasone (100 nM) augmented and prolonged the depressive effect of noradrenaline on synaptic transmission in the СА1 zone; this effect is related to weakening of the uptake of noradrenaline by neurons. The effect of dexamethasone is mediated by glucocorticoid receptors. Inhibitors of presynaptic translocase of noradrenaline, cocaine and imipramine, increased, similarly to dexamethasone, the effects of noradrenaline; an additive synergism was observed upon combined applications of dexamethasone and cocaine. The effect of dexamethasone decreased with an increase in the extracellular concentration of glucose, but increased upon application of the Nа/K-ATPase inhibitor strophantin. The potentiating influence of dexamethasone on the effects of noradrenaline was weaker in slices obtained from rats with behavioral depression induced by social isolation or chronic introduction of dexamethasone. We hypothesize that glucocorticoids stabilize noradrenergic neurotransmission in the brain under the action of stressogenic influences. The role of glucocorticoid mechanisms in the development of depression is discussed.

The Role of Glucocorticoid Receptor and Oxytocin Receptor in the Septic Heart in a Clinically Relevant, Resuscitated Porcine Model With Underlying Atherosclerosis

“…Even though OT can reportedly affect endogenous catecholamine release and -responsiveness (47,48), nothing is known about the effects of exogenous high-level noradrenaline administration on OT/OTR signaling in the heart. Glucocorticoid signaling can potentiate noradrenaline signaling in various brain regions (49,50), but there are no reports in the literature about their relationship in the heart.…”