The logic, methodological and practical limitations in the current benefit concept in the harm-benefit-analysis : an investigation in the context of the EU directive 2010/63 on the protection of animals used for scientific purposes

It has been well-established that there is variation in the strength and direction of the relationship between circulating glucocorticoids (GCs) and fitness. When studies demonstrate such variation or the direction of the GC-fitness relationship is unexpected, the results are often attributed to context-dependency. However, descriptors of context can be vague (e.g., "environmental context") and few studies explicitly test how the optimal hypothalamic-pituitary-adrenal (HPA) axis response to stressors varies across specific contexts. Although existing hypotheses create a strong foundation for understanding GC-fitness relationships, many do not provide explicit predictions of how, when, and why the relationships will change. Here, we discuss three broad factors which we expect to shape the relationships between HPA axis activity and fitness metrics: (1) whether the HPA axis-mediated response matches the challenge, (2) the intensity and frequency of challenges, and (3) life history. We also make predictions for how these factors might affect GC-fitness relationships and discuss ways to test these predictions. Observational studies, experimental manipulations of context, and large-scale cross-species comparisons will be critical to understanding the observed variation in GC-fitness relationships.

/pdf/understanding-context-dependence-in-glucocorticoid-fitness-gy3lccxmix.pdf

Understanding Context Dependence in Glucocorticoid-Fitness Relationships: The Role of the Nature of the Challenge, the Intensity and Frequency of Stressors, and Life History.

Olfactory impairments and depressive behavior are commonly reported by individuals with Parkinson’s disease (PD) being observed before motor symptoms. The mechanisms underlying these clinical manifestations are not fully elucidated. However, the imbalance in dopaminergic neurotransmission seems to play an important role in this context. In patients and animal models of PD, an increase in the dopaminergic interneurons of the glomerular layer in olfactory bulb (OB-gl) is observed, which may contribute to the olfactory impairment. In addition, neuronal imbalance in OB is related to depressive symptoms, as demonstrated by chemical olfactory bulbectomy. In view of that, we hypothesized that a reduction in the number or density of dopaminergic neurons present in OB could promote an olfactory improvement and, in contrast, would accentuate the depressive-like behaviors in the 6-hydroxydopamine (6-OHDA) model of PD. Therefore, we performed single or double injections of 6-OHDA within the substantia nigra pars compacta (SNpc) and/or in the OB-gl. We observed that, after 7 days, the group with nigral lesion exhibited olfactory impairment, as well as the group with the lesion in the OB-gl. However, the combination of the lesions prevented the occurrence of hyposmia. In relation to depressive-like behaviors, we observed that the SNpc injury promoted depressive-like behavior, being accentuated after a double injury. Our results demonstrated the importance of the dopaminergic neurons of the OB-gl in different non-motor features of PD, since the selective reduction of these periglomerular neurons was able to induce olfactory impairment and depressive-like behaviors.

Dopaminergic Lesion in the Olfactory Bulb Restores Olfaction and Induces Depressive-Like Behaviors in a 6-OHDA Model of Parkinson’s Disease

Detection and discrimination of odorants by the olfactory system plays a pivotal role in animal survival. Olfactory-based behaviors must be adapted to an ever-changing environment. Part of these adaptations includes changes of odorant detection by olfactory sensory neurons localized in the olfactory epithelium. It is now well established that internal signals such as hormones, neurotransmitters, or paracrine signals directly affect the electric activity of olfactory neurons. Furthermore, recent data have shown that activity-dependent survival of olfactory neurons is important in the olfactory epithelium. Finally, as olfactory neurons are directly exposed to environmental toxicants and pathogens, the olfactory epithelium also interacts closely with the immune system leading to neuroimmune modulations. Here, we review how detection of odorants can be modulated in the vertebrate olfactory epithelium. We choose to focus on three cellular types of the olfactory epithelium (the olfactory sensory neuron, the sustentacular and microvillar cells) to present the diversity of modulation of the detection of odorant in the olfactory epithelium. We also present some of the growing literature on the importance of immune cells in the functioning of the olfactory epithelium, although their impact on odorant detection is only just beginning to be unravelled.

/pdf/modulation-of-olfactory-signal-detection-in-the-olfactory-1xz4smoh5u.pdf

Modulation of olfactory signal detection in the olfactory epithelium: focus on the internal and external environment, and the emerging role of the immune system.

Chronic stress leads to long-lasting deficits in olfactory-guided behaviors, and to neuroplastic changes in the nucleus of the lateral olfactory tract.

In search of stress odours across species: Behavioural responses of rats to faeces from chickens and rats subjected to various types of stressful events

The olfactory mucosa (OM) is the primary site of odorant detection, and its axonal projections relay information to brain structures for signal processing. We have previously observed that olfactory function can be affected during a prolonged stress challenge in Wistar rats. The stress response is a neuroendocrine retro-controlled loop allowing pleiotropic adaptive tissue alterations, which are partly mediated through the release of glucocorticoid hormones. We hypothesised that, as part of their wide-ranging pleiotropic effects, glucocorticoids might affect the first step of olfactory detection. To study this, we used a number of approaches ranging from the molecular detection and functional characterisation of glucocorticoid receptors (GRs) in OM cells, to the study of GR acute activation in vivo at the molecular, electrophysiological and behavioural levels. In contrast to previous reports, where GR was reported to be exclusive in olfactory sensory neurones, we located functional GR expression mostly in olfactory ensheathing cells. Dexamethasone (2 mg/kg) was injected intraperitoneally to activate GR in vivo, and this led to functional odorant electrophysiological response (electro-olfactogram) and OM gene expression changes. In a habituation/cross-habituation test of olfactory sensitivity, we observed that DEX-treated rats exhibited higher responsiveness to a complex odorant mixture. These findings support the idea that olfactory perception is altered in stressed animals, as glucocorticoids might enhance odour detection, starting at the first step of detection.

The olfactory mucosa, first actor of olfactory detection, is sensitive to glucocorticoid hormone

Chronic variable stress exposure in male Wistar rats affects the first step of olfactory detection.

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In search of stress odours across species: Behavioural responses of rats to faeces from chickens and rats subjected to various types of stressful events

The olfactory mucosa, first actor of olfactory detection, is sensitive to glucocorticoid hormone

Chronic variable stress exposure in male Wistar rats affects the first step of olfactory detection.