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Feather pecking (FP) in laying hens remains an important economic and welfare issue. This paper reviews the literature on causes of FP in laying hens. With the ban on conventional cages in the EU from 2012 and the expected future ban on beak trimming in many European countries, addressing this welfare issue has become more pressing than ever. The aim of this review paper is to provide a detailed overview of underlying principles of FP. FP is affected by many different factors and any approach to prevent or reduce FP in commercial flocks should acknowledge that fact and use a multifactorial approach to address this issue. Two forms of FP can be distinguished: gentle FP and severe FP. Severe FP causes the most welfare issues in commercial flocks. Severe FP is clearly related to feeding and foraging behaviour and its development seems to be enhanced in conditions where birds have difficulty in coping with environmental stressors. Stimulating feeding and foraging behaviour by providing high-fibre diets and suitable litter from an early age onwards, and controlling fear and stress levels through genetic selection, reducing maternal stress and improving the stockmanship skills of the farmer, together offer the best prospect for preventing or controlling FP.

An association study between SNP markers and feather condition score on the back, rump and belly of laying hens was performed. Feather condition score is a measure of feather damage, which has been shown to be closely related to feather pecking behaviour in hens housed in groups. A population of 662 hens was genotyped for 1536 SNPs of which 1022 could be used for the association study. The analysis was conducted across 9 different lines of White Leghorn and Rhode Island Red origin. Across lines linkage disequilibrium is conserved at shorter distances than within lines; therefore, SNPs significantly associated with feather condition score across lines are expected to be closer to the functional mutations. The SNPs that had a significant across-line effect but did not show significant SNP-by-line interaction were identified, to test that the association was consistent across lines. Both the direct effect of the individual’s genotype on its plumage condition, and the associative effect of the genotype of the cage mates on the individual’s plumage condition were analysed. The direct genetic effect can be considered as the susceptibility to be pecked at, whereas the associative genetic effect can be interpreted as the propensity to perform feather pecking. Finally, 11 significant associations between SNPs and behavioural traits were detected in the direct model, and 81 in the associative model. A role of the gene for the serotonin receptor 2C (HTR2C) on chromosome 4 was found. This supports existing evidence of a prominent involvement of the serotonergic system in the modulation of this behavioural disorder in laying hens. The genes for IL9, IL4, CCL4 and NFKB were found to be associated to plumage condition, revealing relationships between the immune system and behaviour.

The objective of the current study was to estimate genetic and phenotypic correlations among feather pecking (FP) behavior and stress response, immune response, and egg quality parameters. These traits have been measured in an F-2 cross, coming from a cross between a high and a low FP line of laying hens. Heritabilities (h 2) of stress response (32 wk), primary immune response to keyhole limpet hemocyanin (KLH) (36 wk) and Mycobacterium butyricum (39 wk), and egg quality parameters (35, 44, and 50 wk of age) were calculated. The h 2 was 0.05 +/- 0.05 (SE) for stress response, 0.15 +/- 0.07 for antibody response to KLH, and 0.08 +/- 0.06 for antibody response to M. butyricum. The h 2 for egg quality traits were in the range of 0.12 to 0.30. Significant phenotypic correlations were found between gentle FP in adult hens and stress response, egg weight at 44 and 50 wk, and egg deformation at 50 wk. Significant additive genetic correlations were found between severe FP in adult hens and antibody response to KLH (0.79 +/- 0.35), and between ground pecking in adult hens and egg deformation at 50 wk (0.63 +/- 0.26), and between ground pecking and eggshell strength at 35, 44, and 50 wk of age (-0.86 +/- 0.29, -0.81 +/- 0.20, -0.76 +/- 0.24, respectively).

In the near future EU-legislation will ban the use of conventional battery cages, while national legislation in some countries in Western Europe will ban beak trimming as well. The ban on battery cages and beak trimming causes an increased risk of feather pecking and cannibalism in laying hens. Many factors influence feather pecking behaviour, but this paper focuses on nutritional factors. Nutritional factors can have positive and negative effects on feather pecking behaviour in laying hens. Severe feather pecking has been demonstrated in birds that were fed a too low mineral level in the diet, a too low protein level or a too low amino acid level (methionine, arginine). Sometimes somewhat more feather pecking was found when layers were fed diets with mainly vegetable protein sources as compared with diets with protein from animal origin. Also more feather pecking may occur when the diets were fed restrictedly, fed coarsely ground, or fed as pellets. Feeding high-fibre diets, low energy diets, or roughages reduced feather pecking. Providing additional grain or straw in the litter during rearing could result in lower levels of feather pecking behaviour in adult stages. Some of these positive effects on feather pecking seem to be related to the time birds spend on feed intake and foraging. This paper gives an overview of the relationships between the occurrence of feather pecking behaviour and nutritional factors, such as diet composition and feeding strategies in laying hens.

Background Sepsis-associated encephalopathy (SAE) is characterized by diffuse brain dysfunction, long-term cognitive impairment, and increased morbidity and mortality. The current treatment for SAE is mainly symptomatic; the lack of specific treatment options and a poor understanding of the underlying mechanism of disease are responsible for poor patient outcomes. Fgr is a member of the Src family of tyrosine kinases and is involved in the innate immune response, hematologic cancer, diet-induced obesity, and hemorrhage-induced thalamic pain. This study investigated the protection provided by an Fgr kinase inhibitor in SAE and the underlying mechanism(s) of action. Methods A cecal ligation and puncture (CLP)-induced mouse sepsis model was established. Mice were treated with or without an Fgr inhibitor and a PGC-1α inhibitor/activator. An open field test, a novel object recognition test, and an elevated plus maze were used to assess neurobehavioral changes in the mice. Western blotting and immunofluorescence were used to measure protein expression, and mRNA levels were measured using quantitative PCR (qPCR). An enzyme-linked immunosorbent assay was performed to quantify inflammatory cytokines. Mitochondrial membrane potential and morphology were measured by JC-1, electron microscopy, and the MitoTracker Deep Red probe. Oxidative stress and mitochondrial dysfunction were analyzed. In addition, the regulatory effect of Fgr on sirtuin 1 (SIRT1) was assessed. Results CLP-induced sepsis increased the expression of Fgr in the hippocampal neurons. Pharmacological inhibition of Fgr attenuated CLP-induced neuroinflammation, the survival rate, cognitive and emotional dysfunction, oxidative stress, and mitochondrial dysfunction. Moreover, Fgr interacted with SIRT1 and reduced its activity and expression. In addition, activation of SIRT1/PGC-1α promoted the protective effects of the Fgr inhibitor on CLP-induced brain dysfunction, while inactivation of SIRT1/PGC-1α counteracted the benefits of the Fgr inhibitor. Conclusions To our knowledge, this is the first report of Fgr kinase inhibition markedly ameliorating SAE through activation of the SIRT1/PGC-1α pathway, and this may be a promising therapeutic target for SAE. Graphical Abstract

Background Huntington disease (HD) is a neurodegenerative disorder with complex motor and behavioural manifestations. The Q175 knock-in mouse model of HD has gained recent popularity as a genetically accurate model of the human disease. However, behavioural phenotypes are often subtle and progress slowly in this model. Here, we have implemented machine-learning algorithms to investigate behaviour in the Q175 model and compare differences between sexes and disease stages. We explore distinct behavioural patterns and motor functions in open field, rotarod, water T-maze, and home cage lever-pulling tasks. Results In the open field, we observed habituation deficits in two versions of the Q175 model (zQ175dn and Q175FDN, on two different background strains), and using B-SOiD, an advanced machine learning approach, we found altered performance of rearing in male manifest zQ175dn mice. Notably, we found that weight had a considerable effect on performance of accelerating rotarod and water T-maze tasks and controlled for this by normalizing for weight. Manifest zQ175dn mice displayed a deficit in accelerating rotarod (after weight normalization), as well as changes to paw kinematics specific to males. Our water T-maze experiments revealed response learning deficits in manifest zQ175dn mice and reversal learning deficits in premanifest male zQ175dn mice; further analysis using PyMouseTracks software allowed us to characterize new behavioural features in this task, including time at decision point and number of accelerations. In a home cage-based lever-pulling assessment, we found significant learning deficits in male manifest zQ175dn mice. A subset of mice also underwent electrophysiology slice experiments, revealing a reduced spontaneous excitatory event frequency in male manifest zQ175dn mice. Conclusions Our study uncovered several behavioural changes in Q175 mice that differed by sex, age, and strain. Our results highlight the impact of weight and experimental protocol on behavioural results, and the utility of machine learning tools to examine behaviour in more detailed ways than was previously possible. Specifically, this work provides the field with an updated overview of behavioural impairments in this model of HD, as well as novel techniques for dissecting behaviour in the open field, accelerating rotarod, and T-maze tasks.

Background. Fluoxetine (FLU) is the first-line and widely used medication for depression; however, FLU treatment is almost ineffective in 30%-40% of patients with depression. In addition, there are some problems in FLU treatment, such as delayed efficacy, large side effects, and poor tolerance. Chaihu Shugan San (CSS) is a classic and effective antidepressant Chinese herbal medicine that has been used in China for thousands of years. CSS or coadministration of CSS and FLU has become one of the most recommended methods in the treatment of depression in China. However, the specific pathways of CSS and coadministration of CSS and FLU for antidepressant are still unclear. Objective. This study was designed to evaluate the antidepressant effects of CSS and coadministration of CSS and FLU. Methods. The chronic unpredictable mild stress (CUMS) rat model was used to simulate depression. 120 healthy adult male Sprague-Dawley (SD) rats were randomly divided into seven groups: the control group, CUMS group, low-dose CSS group, high-dose CSS group, FLU group, coadministration of low-dose CSS and FLU group, and coadministration of high-dose CSS and FLU group. The rats in different groups were given different interventions. Then, the depression-like behavior and cognitive function were evaluated by the sucrose preference test (SPT), forced swimming test (FST), open field test (OFT), and Y-maze test. What is more, the antidepressant mechanism of CSS and coadministration of CSS and FLU were studied through BDNF mRNA, ERK mRNA, CREB mRNA, BDNF, p-ERK/ERK, and p-CREB/CREB levels in the hippocampus and frontal cortex by Western blot and RT-PCR. Results. Compared with the CUMS group, CSS and coadministration of CSS and FLU could alleviate the depressive symptoms and improve cognitive function in CUMS rats (p<0.05); CSS and coadministration of CSS and FLU could increase the expression of BDNF, p-CREB/CREB, p-ERK/ERK, and BDNF mRNA, CREB mRNA, and ERK mRNA in the hippocampus and frontal cortex (p<0.05). Besides, the high-dose CSS combined with the fluoxetine group was significantly better than the fluoxetine group and CSS group (p<0.05). Discussion and Conclusion. Finally, we found that both CSS and coadministration of CSS and FLU play an antidepressant role, which may be due to the regulation of the BDNF/ERK/CREB signaling pathway in the hippocampus and frontal cortex. Among them, the coadministration of CSS and FLU can enhance the antidepressant effect of CSS or FLU alone, and the underlying mechanism needs further investigation.

Background Human genetic association studies point to immune response and lipid metabolism, in addition to amyloid-beta (Aβ) and tau, as major pathways in Alzheimer’s disease (AD) etiology. Accumulating evidence suggests that chronic neuroinflammation, mainly mediated by microglia and astrocytes, plays a causative role in neurodegeneration in AD. Our group and others have reported early and dramatic losses of brain sulfatide in AD cases and animal models that are mediated by ApoE in an isoform-dependent manner and accelerated by Aβ accumulation. To date, it remains unclear if changes in specific brain lipids are sufficient to drive AD-related pathology. Methods To study the consequences of CNS sulfatide deficiency and gain insights into the underlying mechanisms, we developed a novel mouse model of adult-onset myelin sulfatide deficiency, i.e., tamoxifen-inducible myelinating glia-specific cerebroside sulfotransferase (CST) conditional knockout mice (CST fl/fl /Plp1-CreERT), took advantage of constitutive CST knockout mice (CST −/− ), and generated CST/ApoE double knockout mice (CST −/− /ApoE −/− ), and assessed these mice using a broad range of methodologies including lipidomics, RNA profiling, behavioral testing, PLX3397-mediated microglia depletion, mass spectrometry (MS) imaging, immunofluorescence, electron microscopy, and Western blot. Results We found that mild central nervous system (CNS) sulfatide losses within myelinating cells are sufficient to activate disease-associated microglia and astrocytes, and to increase the expression of AD risk genes (e.g., Apoe, Trem2, Cd33, and Mmp12 ), as well as previously established causal regulators of the immune/microglia network in late-onset AD (e.g., Tyrobp, Dock, and Fcerg1 ), leading to chronic AD-like neuroinflammation and mild cognitive impairment. Notably, neuroinflammation and mild cognitive impairment showed gender differences, being more pronounced in females than males. Subsequent mechanistic studies demonstrated that although CNS sulfatide losses led to ApoE upregulation, genetically-induced myelin sulfatide deficiency led to neuroinflammation independently of ApoE. These results, together with our previous studies (sulfatide deficiency in the context of AD is mediated by ApoE and accelerated by Aβ accumulation) placed both Aβ and ApoE upstream of sulfatide deficiency-induced neuroinflammation, and suggested a positive feedback loop where sulfatide losses may be amplified by increased ApoE expression. We also demonstrated that CNS sulfatide deficiency-induced astrogliosis and ApoE upregulation are not secondary to microgliosis, and that astrogliosis and microgliosis seem to be driven by activation of STAT3 and PU.1/Spi1 transcription factors, respectively. Conclusion Our results strongly suggest that sulfatide deficiency is an important contributor and driver of neuroinflammation and mild cognitive impairment in AD pathology.

The medial prefrontal cortex (mPFC) is critical to cognitive and emotional function and underlies many neuropsychiatric disorders, including mood, fear and anxiety disorders. In rodents, disruption of mPFC activity affects anxiety- and depression-like behavior, with specialized contributions from its subdivisions. The rodent mPFC is divided into the dorsomedial prefrontal cortex (dmPFC), spanning the anterior cingulate cortex (ACC) and dorsal prelimbic cortex (PL), and the ventromedial prefrontal cortex (vmPFC), which includes the ventral PL, infralimbic cortex (IL), and in some studies the dorsal peduncular cortex (DP) and dorsal tenia tecta (DTT). The DP/DTT have recently been implicated in the regulation of stress-induced sympathetic responses via projections to the hypothalamus. While many studies implicate the PL and IL in anxiety-, depression-like and fear behavior, the contribution of the DP/DTT to affective and emotional behavior remains unknown. Here, we used chemogenetics and optogenetics to bidirectionally modulate DP/DTT activity and examine its effects on affective behaviors, fear and stress responses in C57BL/6J mice. Acute chemogenetic activation of DP/DTT significantly increased anxiety-like behavior in the open field and elevated plus maze tests, as well as passive coping in the tail suspension test. DP/DTT activation also led to an increase in serum corticosterone levels and facilitated auditory fear extinction learning and retrieval. Activation of DP/DTT projections to the dorsomedial hypothalamus (DMH) acutely decreased freezing at baseline and during extinction learning, but did not alter affective behavior. These findings point to the DP/DTT as a new regulator of affective behavior and fear extinction in mice.