RESUMO
Failure of transfer of passive immunity (FTPI) due to inadequate ingestion of colostral immunoglobulins by calves is associated with increased mortality and morbidity risks. Feeding calves a sufficient amount of quality-tested colostrum within the first hours of life is essential for successfully transferring passive immunity. Many farms have implemented a second meal of colostrum to maximize the opportunities for passive immunity transfer. However, excellent passive immunity can be achieved with a single feeding of sufficient quality-tested colostrum. Moreover, there is currently no evidence demonstrating the impact of a second colostrum feeding within 24 h of life in calves receiving adequate volumes of quality-tested colostrum in an initial feeding. Hence, the objective of this retrospective cohort study was to compare the risks of FPTI, pre-weaning morbidity and mortality, and growth and performance between dairy calves that received one or two feedings of colostrum. For this, the health and production records of a large dairy herd were analyzed. At this farm, newborn calves receive 3 L of quality-tested colostrum soon after birth, followed by another 2 L 5-6 h later. However, at times of shortages of colostrum, calves only receive the initial 3 L meal. The records of 2064 male and 2272 female calves were analyzed, where 4156 and 180 calves received 2 and 1 colostrum meals, respectively. Data from both sexes were included in the analysis of the risks of FTPI, morbidity, and mortality; however, only data from heifer calves were utilized for growth and performance analysis. Survival analysis, and logistic and linear regression models were used to investigate the impact of receiving two feedings of colostrum on calf FTPI status, morbidity, mortality, reproductive indices, pre-weaning average daily gain (ADG), and first lactation 305-d Mature Equivalent milk production (305ME). Calves that received two feedings of colostrum had lower odds of FTPI, a lower probability of being treated for respiratory disease, diarrhea, or any disease, and a greater pre-weaning ADG. However, there was no association between the number of colostrum feedings and pre-weaning mortality, and the probabilities of first insemination and first calving, although heifers receiving two colostrum feedings tended to receive fewer inseminations and to have a greater first lactation 305ME. Collectively, our results suggest that feeding calves a second feeding of colostrum 5-6 h after the initial feeding soon after birth could be an effective strategy to decrease FTPI and morbidity and optimize ADG in dairy calves pre-weaning.
RESUMO
Neurons can respond to decreased network activity with a homeostatic increase in the amplitudes of miniature EPSCs (mEPSCs). The prevailing view is that mEPSC amplitudes are uniformly multiplied by a single factor, termed "synaptic scaling." Deviations from purely multiplicative scaling have been attributed to biological differences, or to a distortion imposed by a detection threshold limit. Here, we demonstrate in neurons dissociated from cortices of male and female mice that the shift in mEPSC amplitudes observed in the experimental data cannot be reproduced by simulation of uniform multiplicative scaling, with or without the distortion caused by applying a detection threshold. Furthermore, we demonstrate explicitly that the scaling factor is not uniform but is close to 1 for small mEPSCs, and increases with increasing mEPSC amplitude across a substantial portion of the data. This pattern was also observed for previously published data from dissociated mouse hippocampal neurons and dissociated rat cortical neurons. The finding of "divergent scaling" shifts the current view of homeostatic plasticity as a process that alters all synapses on a neuron equally to one that must accommodate the differential effect observed for small versus large mEPSCs. Divergent scaling still accomplishes the essential homeostatic task of modifying synaptic strengths in the opposite direction of the activity change, but the consequences are greatest for those synapses which individually are more likely to bring a neuron to threshold.SIGNIFICANCE STATEMENT In homeostatic plasticity, the responses to chronic increases or decreases in network activity act in the opposite direction to restore normal activity levels. Homeostatic plasticity is likely to play a role in diseases associated with long-term changes in brain function, such as epilepsy and neuropsychiatric illnesses. One homeostatic response is the increase in synaptic strength following a chronic block of activity. Research is focused on finding a globally expressed signaling pathway, because it has been proposed that the plasticity is uniformly expressed across all synapses. Here, we show that the plasticity is not uniform. Our work suggests that homeostatic signaling molecules are likely to be differentially expressed across synapses.
