Adrenalectomy-Produced Facilitation of Pavlovian Conditioned Cardiodecelerations in Immobilized Rats

Previous evidence has suggested that both hormonal and behavioral aspects of adrenal stress activation may contribute to heart rate (HR) conditioning during physical/pharmacological immobilization. Accordingly, four studies were conducted to determine if bilateral adrenalectomy facilitates stimulus-control over Pavlovian conditioned cardiodecelerations in rats immobilized either through physical restraint or neuromuscular paralysis. Plasma corticosterone assays were used as an index of the effectiveness of adrenal removal. The results showed that adrenalectomy facilitated both simple and discriminated Pavlovian conditioned cardiodecelerations in rats paralyzed with d-tubocurarine chloride (dTC) without significantly altering the characteristics of EMG recovery from paralysis. Similarly, adrenalectomy facilitated simple Pavlovian HR conditioning in physically restrained rats. The results suggest that adrenal activation may disrupt the parasympathetically-mediated Pavlovian conditioned cardiodeceleration in the physically-and dTC-immobilized rat. However, the specific nature of neuroendocrine mechanisms underlying cardiovascular conditioning during immobilization remains problematical.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75069/1/j.1469-8986.1977.tb03371.x.pd

Relevance of Stress and Female Sex Hormones for Emotion and Cognition

There are clear sex differences in incidence and onset of stress-related and other psychiatric disorders in humans. Yet, rodent models for psychiatric disorders are predominantly based on male animals. The strongest argument for not using female rodents is their estrous cycle and the fluctuating sex hormones per phase which multiplies the number of animals to be tested. Here, we will discuss studies focused on sex differences in emotionality and cognitive abilities in experimental conditions with and without stress. First, female sex hormones such as estrogens and progesterone affect emotions and cognition, contributing to sex differences in behavior. Second, females respond differently to stress than males which might be related to the phase of the estrous cycle. For example, female rats and mice express less anxiety than males in a novel environment. Proestrus females are less anxious than females in the other estrous phases. Third, males perform in spatial tasks superior to females. However, while stress impairs spatial memory in males, females improve their spatial abilities, depending on the task and kind of stressor. We conclude that the differences in emotion, cognition and responses to stress between males and females over the different phases of the estrous cycle should be used in animal models for stress-related psychiatric disorders

A rise in NAD precursor nicotinamide mononucleotide (NMN) after injury promotes axon degeneration.

NAD metabolism regulates diverse biological processes, including ageing, circadian rhythm and axon survival. Axons depend on the activity of the central enzyme in NAD biosynthesis, nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2), for their maintenance and degenerate rapidly when this activity is lost. However, whether axon survival is regulated by the supply of NAD or by another action of this enzyme remains unclear. Here we show that the nucleotide precursor of NAD, nicotinamide mononucleotide (NMN), accumulates after nerve injury and promotes axon degeneration. Inhibitors of NMN-synthesising enzyme NAMPT confer robust morphological and functional protection of injured axons and synapses despite lowering NAD. Exogenous NMN abolishes this protection, suggesting that NMN accumulation within axons after NMNAT2 degradation could promote degeneration. Ectopic expression of NMN deamidase, a bacterial NMN-scavenging enzyme, prolongs survival of injured axons, providing genetic evidence to support such a mechanism. NMN rises prior to degeneration and both the NAMPT inhibitor FK866 and the axon protective protein Wld(S) prevent this rise. These data indicate that the mechanism by which NMNAT and the related Wld(S) protein promote axon survival is by limiting NMN accumulation. They indicate a novel physiological function for NMN in mammals and reveal an unexpected link between new strategies for cancer chemotherapy and the treatment of axonopathies