Using a multitrait animal model BLUP, selection was conducted over seven generations for growth rate (ADG), real-time ultrasound LM area (LMA), backfat thickness (BF), and intramuscular fat content (IMF) to develop a new line of purebred Duroc pigs with enhanced meat production and meat quality. This selection experiment examined 543 slaughtered pigs (394 barrows and 153 gilts) from the first to the seventh generation for meat quality traits. Further, electric impedance and collagen content of loin meat were measured from the fourth to sixth generation. The present study was intended to estimate genetic parameters of the correlated traits of tenderness (TEND), meat color (pork color standard: PCS; lightness = L*), drip loss (DL), cooking loss (CL), pH (PH), electric impedance (IMP), and collagen (COL) of the LM, and the genetic trends of these traits. Respective heritability estimates for IMF, TEND, DL, CL, PCS, L*, PH, IMP, and COL were 0.39, 0.45, 0.14, 0.09, 0.18, 0.16, 0.07, 0.22, and 0.23. Genetic correlations of IMF with ADG and BF were low and positive, but low and negative with LMA. Tenderness was correlated negatively with ADG (-0.44) and BF (-0.59), but positively correlated with LMA (0.32). The genetic correlation between LMA and DL was positive and high (0.64). The genetic correlations of TEND with IMF and COL were low (-0.09 and 0.26, respectively), but a moderate genetic correlation (0.43) between COL and IMF was estimated, suggesting related increases of IMF and connective tissue. Genetic correlations among meat quality traits suggested that when IMF increases, the water holding capacity improves. Genetic trends of meat quality traits showed increased IMF and lighter meat color.

Here we report that the lifespan of mice cloned from somatic cells is significantly shorter than that of genotype- and sex-matched controls, most likely due to severe pneumonia and hepatic failure. This finding demonstrates the possibility of long-term deleterious effects of somatic-cell cloning, even after normal birth.

In the present study, we established and characterized an animal model of vulnerability to repeated stress. We found that control Sprague-Dawley (SD) rats showed a gradual decrease in the HPA axis response following 14 days of repeated restraint stress, whereas Fischer 344 (F344) rats did not show such HPA axis habituation. Similar habituation was observed in the expression of c-fos mRNA, corticotropin-releasing hormone hnRNA, and phospho-CREB and phospho-ERK proteins in the hypothalamic paraventricular nucleus (PVN) of SD rats, but not in the F344 rats. In addition, repeatedly restrained F344 rats exhibited decreased cell proliferation in the dentate gyrus of the hippocampus and increased anxiety-related behaviours, while repeatedly restrained SD rats exhibited a selective enhancement of hippocampal cell proliferation in the ventral area. Moreover, we found a lower expression of glucocorticoid receptor (GR) protein, but not mRNA, in the PVN of F344 rats compared to SD rats. We also identified that microRNA (miR)-18a inhibited translation of GR mRNA in cultured neuronal cells and that increased expression of miR-18a in the PVN was observed in F344 rats compared with SD rats. These strain differences in GR protein levels were not found in the hippocampus and prefrontal cortex, and the expression of miR-18a was much lower in these brain regions than in the PVN. Our results suggest that F344 rats could be a useful animal model for studying vulnerability to repeated stress, and that miR-18a-mediated down-regulation of GR translation may be an important factor to be considered in susceptibility to stress-related disorders.

No abstract

Modulation of neurotrophic factors to protect neurons from damage is proposed as a novel mechanism for the action of antidepressants. However, the effect of antidepressants on modulation of glial cell line-derived neurotrophic factor (GDNF), which has potent and widespread effects, remains unknown. Here, we demonstrated that long-term use of antidepressant treatment signi®cantly increased GDNF mRNA expression and GDNF release in time-and concentrationdependent manners in rat C6 glioblastoma cells. Amitriptyline treatment also increased GDNF mRNA expression in rat astrocytes. GDNF release continued for 24 h following withdrawal of amitriptyline. Furthermore, following treatment with antidepressants belonging to several different classes (amitriptyline, clomipramine, mianserin,¯uoxetine and paroxetine) signi®cantly increased GDNF release, but which did not occur after treatment with non-antidepressant psychotropic drugs (haloperidol, diazepam and diphenhydramine).Amitriptyline-induced GDNF release was inhibited by U0126 (10 mM), a mitogen-activated protein kinase (MAPK)-extracellular signal-related kinase (ERK) kinase (MEK) inhibitor, but was not inhibited by H-89 (1 mM), a protein kinase A inhibitor, calphostin C (100 nM), a protein kinase C inhibitor and PD 169316 (10 mM), a p38 mitogen-activated protein kinase inhibitor. These results suggested that amitriptylineinduced GDNF synthesis and release occurred at the transcriptional level, and may be regulated by MEK/MAPK signalling. The enhanced and prolonged induction of GDNF by antidepressants could promote neuronal survival, and protect neurons from the damaging effects of stress. This may contribute to explain therapeutic action of antidepressants and suggest new strategies of pharmacological intervention.