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~tivity.~ 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,

Corticotropin-Releasing Hormone Microinfusion in the Central Amygdala Enhances Active Behaviour Responses in the Conditioned Defensive Burying Paradigm

“…Hence, this CRH system in the CeA may play a role in selecting the appropriate behavioural coping style in response to environmental challenges (Korte et al, 1994). This interpretation is supported by peptidergic manipulations of the CeA in normal male rats (Roozendaal et al, 1992a) and in two strains of rats known to adopt an active versus a passive coping style, respectively (Roozendaal er al., 1992b). Thus, the CRH-induced increase in active behaviour after infusion into the CeA, could be a result of a shift in the balance of the different coping styles towards a more active coping style.…”

Postweaning, forebrain-specific perturbation of the oxytocin system impairs fear conditioning

“…Administration of exogenous Oxt and Avp has effects on many forms of memory and anxiety (Caldwell et al 2008; Landgraf & Neumann 2004; Lee et al 2009; Neumann 2008; Ross & Young 2009). Intra‐amygdalar administrations of Oxt and Avp have opposite effects on freezing and heart rate (Roozendaal et al 1992). Similarly, subcutaneous injections of Oxt C‐terminal fragments decrease freezing while Avp fragments increase freezing following footshock (Stoehr et al 1992).…”

Brain Oxytocin in Social Fear Conditioning and Its Extinction: Involvement of the Lateral Septum

“…In detail, the CeA coordinates the behavioral and physiological correlates of fear expression (LeDoux et al, 1988;Kalin et al, 1998). Both local infusion (Roozendaal et al, 1992;Viviani et al, 2011) and evoked axonal release (Knobloch et al, 2012) of OXT attenuated the fear response in rodents. Interestingly, SAD patients show hyperactivity of the amygdala in response to threatening faces, which can be attenuated by intranasal OXT (Kirsch et al, 2005;Labuschagne et al, 2010).…”