Opposite effects of central amygdaloid vasopressin and oxytocin on the regulation of conditioned stress responses in male rats.

Abstract

The central nucleus of the amygdala (CEA) seems to be selectively involved in the passive component of the behavioral (immobility) and the accompanying parasympathetic response (bradycardia) during conditioned environmental challenges,' leaving conditioned sympathetic, adreno-medullary, and adreno-cortical responses unaffected (Roozendaal et al., in preparation). Robust monosynaptic, .peptidergic connections to the vagal complex and periaqueductal gray may be mediating these effects. Intracerebroventricularly administered arginine-8-vasopressin (AVP) potentiates these stress-induced bradycardiac and immobility responses.* AVP may exert these effects via AVP and/or oxytocin (OT) receptive systems in the CEA.' Microinfusion of AVP (dissolved in 1 p1 artificial CSF) into the CEA of conscious male Wistar rats under resting conditions, leads to a dose-dependent change in heart rate and behavior: A high dose of AVP (2 ng), but not lower ones (20 and 200 pg), causes a transient increase in heart rate and behavioral a~t iv i ty .~ Moreover, in a part of the animals, the low dose of AVP even causes an opposite effect, that is, bradycardia. OT administration (2 ng) induces responses similar to those induced with the high dose of AVP. Neither plasma norepinephrine nor epinephrine is influenced after AVP infusion, suggesting that the tachycardia is due to reduced parasympathetic control, rather than a stimulation of the sympathetic outflow. The effects of AVP and OT during conditioned stress were studied in male Roman high-avoidance (RHA) and Roman low-avoidance. (RLA) rats, selected genetically for shuttle-box acquisition behavior. In RLA rats the cardiac and behavioral responses to the emotional stressor are bradycardia and immobility,