Implications of coping characteristics and social status for welfare and production of paired growing gilts

This paper considers the question whether knowledge on individual coping characteristics of growing pigs may be used to improve welfare and production after mixing. Gilts with either reactive or proactive coping characteristics were identified according to behavioural resistance in a backtest, respectively, being low (LR) and high resistant (HR) in this test. At 7 weeks of age, several pairs of unfamiliar gilts were formed, and pairs and dominance relationships were studied over a 3-week period. The following pairs (combinations) were established: two LR gilts (LR/LR; n = 12), two HR gilts (FIRM; n = 12), one LR and one HR gilt (LR gilt dominant: LR(d)/HR; n = 11), and one LR and one HR gilt (HR gilt dominant: LR/HR(d); n = 12). Results showed that on the day of mixing, aggression subsided less quickly and increases in body temperature were higher in LR/ HR(d) and HR/HR pairs. Also, during the first week post-mixing, feed efficiency was lower and skin damage was higher in LR/HR(d) and HR/HR pairs. Mixing of two HR gilts caused highest levels of stress, indicated by greater catecholamine concentrations in urine following the day of mixing, and higher baseline levels of plasma ACTH at I week post-mixing. The lower tendency of fearfulness. In contrast to gilts within HR/HR pairs to contact a novel object may present higher those of LR/HR(d) pairs, responses of LR(d)/HR pairs revealed much lower levels of stress, which emphasised the importance of dominance relationships, being independent of coping characteristics of individual gilts. We speculate that in LR/HR pairs, dominant LR gilts were able to suppress aggressiveness of HR subordinates. HR or proactive gilts, however, may become aggressive when being dominant. General effects of social status, independent of combination, were also found. Compared to dominants, subordinates showed higher acute cortisol, body temperature and vocal responses to mixing. In the longer term, they showed a higher vocal and parasympathetic responsitivity towards the novel object, and their body growth was impaired. Measures not influenced by combination and social status included those of leucocyte subsets, prolactin, and average heart rates during novelty tests. To conclude, aggressive conditions in newly formed groups. and consequently welfare and production, may largely depend on coping characteristics of individual pigs, but also on dominance relationships. Accordingly, the practical value of the backtest is being discussed. (C) 2002 Elsevier Science B.V. All rights reserved

The motivational drive to natural rewards is modulated by prenatal glucocorticoid exposure

Exposure to elevated levels of glucocorticoids (GCs) during neurodevelopment has been identified as a triggering factor for the development of reward-associated disorders in adulthood. Disturbances in the neural networks responsible for the complex processes that assign value to rewards and associated stimuli are critical for disorders such as depression, obsessive–compulsive disorders, obesity and addiction. Essential in the understanding on how cues influence behavior is the Pavlovian–instrumental transfer (PIT), a phenomenon that refers to the capacity of a Pavlovian stimulus that predicts a reward to elicit instrumental responses for that same reward. Here, we demonstrate that in utero exposure to GCs (iuGC) impairs both general and selective versions of the PIT paradigm, suggestive of deficits in motivational drive. The iuGC animals presented impaired neuronal activation pattern upon PIT performance in cortical and limbic regions, as well as morphometric changes and reduced levels of dopamine in prefrontal and orbitofrontal cortices, key regions involved in the integration of Pavlovian and instrumental stimuli. Normalization of dopamine levels rescued this behavior, a process that relied on D2/D3, but not D1, dopamine receptor activation. In summary, iuGC exposure programs the mesocorticolimbic dopaminergic circuitry, leading to a reduction in the attribution of the incentive salience to cues, in a dopamine-D2/D3-dependent manner. Ultimately, these results are important to understand how GCs bias incentive processes, a fact that is particularly relevant for disorders where differential attribution of incentive salience is critical.We thank Pedro Morgado for discussions and help in the technical aspects of PIT procedure. This project was supported by a grant of Institute for the Study of Affective Neuroscience (ISAN) and by Janssen Neuroscience Prize. CS-C, SB, MMC and AJR are recipients of Fundacao para a Ciencia e Tecnologia (FCT) fellowships (CS-C: SFRH/BD/51992/2012; SB: SFRH/BD/89936/2012; MMC: SRFH/BD/51061/2010; AJR: SFRH/BPD/33611/2009)

Ventral and dorsal striatal dopamine efflux and behavior in rats with simple vs. co-morbid histories of cocaine sensitization and neonatal ventral hippocampal lesions

xposing animal models of mental illness to addictive drugs provides an approach to understanding the neural etiology of dual diagnosis disorders. Previous studies have shown that neonatal ventral hippocampal lesions (NVHL) in rats produce features of both schizophrenia and addiction vulnerability. Objective This study investigated ventral and dorsal striatal dopamine (DA) efflux in NVHL rats combined with behavioral sensitization to cocaine. Methods Adult NVHL vs. SHAM-operated rats underwent a 5-day injection series of cocaine (15 mg/kg/day) vs. saline. One week later, rats were cannulated in nucleus accumbens SHELL, CORE, or caudate–putamen. Another week later, in vivo microdialysis sampled DA during locomotor testing in which a single cocaine injection (15 mg/kg) was delivered. Results NVHLs and cocaine history significantly increased behavioral activation approximately 2-fold over SHAM-saline history rats. DA efflux curves corresponded time dependently with the cocaine injection and locomotor curves and varied significantly by striatal region: Baseline DA levels increased 5-fold while cocaine-stimulated DA efflux decreased by half across a ventral to dorsal striatal gradient. However, NVHLs, prior cocaine history, and individual differences in behavior were not underpinned by differential DA efflux overall or within any striatal region.Conclusion Differences in ventral/dorsal striatal DA efflux are not present in and are not required for producing differential levels of acute cocaine-induced behavioral activation in NVHLs with and without a behaviorally sensitizing cocaine history. These findings suggest other neurotransmitter systems, and alterations in striatal network function post-synaptic to DA transmission are more important to understanding the interactive effects of addictive drugs and mental illness

Genomic Analysis of Individual Differences in Ethanol Drinking: Evidence for Non-Genetic Factors in C57BL/6 Mice

Genetic analysis of factors affecting risk to develop excessive ethanol drinking has been extensively studied in humans and animal models for over 20 years. However, little progress has been made in determining molecular mechanisms underlying environmental or non-genetic events contributing to variation in ethanol drinking. Here, we identify persistent and substantial variation in ethanol drinking behavior within an inbred mouse strain and utilize this model to identify gene networks influencing such “non-genetic” variation in ethanol intake. C57BL/6NCrl mice showed persistent inter-individual variation of ethanol intake in a two-bottle choice paradigm over a three-week period, ranging from less than 1 g/kg to over 14 g/kg ethanol in an 18 h interval. Differences in sweet or bitter taste susceptibility or litter effects did not appreciably correlate with ethanol intake variation. Whole genome microarray expression analysis in nucleus accumbens, prefrontal cortex and ventral midbrain region of individual animals identified gene expression patterns correlated with ethanol intake. Results included several gene networks previously implicated in ethanol behaviors, such as glutamate signaling, BDNF and genes involved in synaptic vesicle function. Additionally, genes functioning in epigenetic chromatin or DNA modifications such as acetylation and/or methylation also had expression patterns correlated with ethanol intake. In verification for the significance of the expression findings, we found that a histone deacetylase inhibitor, trichostatin A, caused an increase in 2-bottle ethanol intake. Our results thus implicate specific brain regional gene networks, including chromatin modification factors, as potentially important mechanisms underlying individual variation in ethanol intake