Stress during first gestation of ewes impairs memory and learning of male offspring.

This study aimed to investigate the influence of gestational stress induced by lipopolysaccharide (LPS, Escherichia coli) on the physiological changes of ewes, as well as on the subsequent behavioral interaction between ewes and lambs and on the memory and learning of 30-day-old offspring in a T-maze. Thirty-six nulliparous pregnant crossbred Santa Ines ewes with an initial live weight of 45 ± 6 kg, age of 12 ± 2 months, and body condition score between 3 and 3.5 (on a scale of 1 to 5) were divided into two treatments: LPS treatment (E. coli; 0.8 µg.kg-1) and Control (placebo/saline) administered in late pregnancy (day 120). Blood samples were collected before (0 h at 5:00 h) and 1 h, 2 h, 4 h, 8 h, 12 h, 24 h after the administration of LPS or placebo to determine the cortisol release curve. Rectal temperature was measured at the same time points. After birth, male lambs (N = 19) were used to evaluate the maternal-offspring behavioral interaction, weight, and cognitive ability in a T-maze. Blood cortisol and rectal temperature of ewes increased after LPS administration and returned to baseline levels after 24 h. The activities facilitating and stimulating suckling were higher on LPS group (P < 0.05). Lambs whose mothers were challenged with LPS during late pregnancy showed greater learning and memory disabilities including fear behavior and the inability to make decisions at 30 days of age in the T-maze. In sheep, the immunological stress induced by LPS in late pregnancy promotes an inflammatory response characterized by specific rectal temperature and cortisol release profiles, improving maternal care that can increase offspring survival; however, the exposure of sheep fetuses to maternal inflammation causes cognitive impairment in lambs at 30 days of age, which could not be reduced by the behavioral interaction between the mother and offspring.

Heat stress affects the expression of key genes in the placenta, placental characteristics, and efficiency of Saanen goats and the survival and growth of their kids.

Heat stress is detrimental during gestation; however, the effects of heat stress on goat placental characteristics and kid survival remain unclear. The objective of this study was to evaluate the effects of heat stress at final gestation on cortisol concentration, placenta characteristics, and the expression of genes related to placenta. Forty-six primiparous and multiparous Saanen goats were subjected to control (CT; under a thermoneutral environment: air temperature between 12°C and 25°C and the relative humidity from 45 to 73%, n = 23) or heat stress (HS; under a climatic chamber: air temperature at 37°C and the relative humidity at 60 to 70% from 0800 to 1600 h, n = 23) from the last 60 d of pregnancy until the first colostrum suckling. The heat challenge imposed on HS goats during the prepartum period increased their rectal temperature, respiratory frequency, and cortisol levels in plasma and amniotic fluid versus CT goats. In the placenta, HS treatment also increased the expression of the HSPA1A gene. Heat-stressed goats also showed significantly lower expression of HSD11B2 and greater expression of MC2R and NR3C1 than CT goats, suggesting that heat stress decreased the effectiveness by which the HSD11B2 enzyme converts cortisol to cortisone and increased placental responsiveness to cortisol. The HS goats took longer to release the placenta with lighter placental cotyledons, and HS goats had a lower ratio between the kid's weight at birth and placenta weight than CT goats. There was no treatment effect on the kids' survival or weights at birth, but the kids from goats subjected to HS presented lesser cortisol concentration and greater mortality rates at weaning than kids from CT goats. Finally, the overexpression of HSPA1A by HS goats suggests a protective response of placenta. However, the heat stress negatively affected the placenta's expulsion length, placental cotyledons number, weight and area, the ratio between kid's weight and placenta weight, and cortisol signaling. Indeed, the upregulation of MC2R and NR3C1 and downregulation of HSD11B2 on placenta caused by heat stress were associated with greater cortisol concentrations in the amniotic fluid of HS goats. Although HS and CT kids had adequate weights and survival rate during the first weeks of life, the heat stress increased the mortality at weaning of HS kids versus CT kids, suggesting that the heat stress effect persists and can change the ability of kids to respond to weaning challenge.

Effect of heat stress in late gestation on subsequent lactation performance and mammary cell gene expression of Saanen goats.

Little is known about the effects of heat stress during the late gestation period on lactation in dairy goats. For this reason, 32 Saanen goats were randomly assigned to 1 of 2 groups, control (CT; n = 16) or heat stress (HS; n = 16), during late gestation. The HS goats were housed in a climatic chamber before parturition and subjected to heat stress for the last 45 d. After parturition, the HS goats were housed in the same conditions as the CT group. Mammary gland biopsies were performed on 7 goats per treatment at -30, -15, 15, and 30 d relative to parturition, so that the expression levels of several genes could be determined. The HS goats produced less milk than the CT goats did during the first half of lactation, but not during the rest of lactation. Before parturition, apoptosis-related transcripts (TP53 and BAX) were higher in the mammary glands of the HS goats than in those of the CT goats. The HS goats also had higher levels of HSPB1 gene expression during gestation and lactation. However, expression of the prolactin receptor gene was lower after parturition in the mammary glands of HS, suggesting downregulation of prolactin signaling. In summary, heat stress during final gestation reduces milk yield in the subsequent lactation. Although the upregulation of apoptosis signaling in the HS goats suggests that heat stress affects mammary cell number, the loss of the effect on milk production is more compatible with an effect on cell activity, which could be due to a downregulation of prolactin signaling.