Management characteristics, lameness, and body injuries of dairy cattle housed in high-performance dairy herds in Wisconsin.

The objective of this study was to benchmark the prevalence of lameness, hock and knee injuries, and neck and back injuries among high-performance, freestall-housed dairy herds in Wisconsin. A random selection of 66 herds with 200 or more cows was derived from herds that clustered with high performance in year 2011 Dairy Herd Improvement records for milk production, udder health, reproduction, and other health parameters. Herds were surveyed to collect information about management, facilities, and well-being. Well-being measures were obtained through direct observation of the high-producing mature cow group, surveying 9,690 cows in total. Total herd size averaged (mean ± standard deviation) 851±717 cows, ranging 203 to 2,966 cows, with an energy-corrected milk production of 40.1±4.4kg/cow per day. Prevalence of clinical lameness (5-point scale, locomotion score ≥3) and severe lameness (locomotion score ≥4) averaged 13.2±7.3 and 2.5±2.7%, respectively. The prevalence of all hock and knee injuries, including hair loss, swelling, and ulceration, was similar at 50.3±28.3 and 53.0±24.0%, respectively. Severe (swelling and ulceration) hock and knee injury prevalence were 12.2±15.3 and 6.2±5.5%, respectively. The prevalence of all neck injuries (including hair loss, swelling and ulceration) was 8.6±16.3%; whereas the prevalence of swollen or abraded necks was low, averaging 2.0±4.1%. Back injuries (proportion of cows with missing or abraded spinous processes, hooks, or pins) followed a similar trend with a low mean prevalence of 3.6±3.4%. Overall, physical well-being characteristics of this selection of high-producing, freestall-housed dairy herds provide evidence that lameness and injury are not inevitable consequences of the confinement housing of large numbers of dairy cattle. In particular, lameness prevalence rivals that of lower-production grazing systems. However, hock and other injury risk remains a concern that can be addressed through a choice in stall surface type. Use of deep, loose bedding yielded significant advantages over a mat or mattress type surface in terms of lameness, hock and knee injury, and proportion of cows with dirty udders (distinct demarcated to confluent plaques of manure). The performance benchmarks achieved by these herds may be used to set standards by which similarly managed herds may be judged using welfare audit tools.

Survey of facility and management characteristics of large, Upper Midwest dairy herds clustered by Dairy Herd Improvement records.

A survey of management practices was conducted to investigate potential associations with groupings of herds formed by cluster analysis (CA) of Dairy Herd Improvement (DHI) data of 557 Upper Midwest herds of 200 cows or greater. Differences in herd management practices were identified between the groups, despite underlying similarities; for example, freestall housing and milking in a parlor. Group 6 comprised larger herds with a high proportion of primiparous cows and most frequently utilized practices promoting increased production [e.g., 84.4% used recombinant bovine somatotropin (rbST)], decreased lameness (e.g., 96.9% used routine hoof trimming for cows), and improved efficiency in reproduction [e.g., 93.8% synchronized the first breeding in cows (SYNCH)] and labor (e.g., mean ± SD, 67 ± 19 cows per 50-h per week full-time equivalent worker). Group 1 had the best mean DHI performances and followed most closely group 6 for the rate of adoption of intensive management practices while tending to outperform group 6 despite a generally smaller mean herd size (e.g., 42.3 ± 3.6 kg vs. 39.9 ± 3.6 kg of energy-corrected milk production; 608 ± 352 cows vs. 1,716 ± 1,405 cows). Group 2 were smaller herds with relatively high levels of performance that used less intensive management (e.g., 100% milked twice daily) and less technology (33.3 vs. 73.0% of group 1 used rbST). Group 4 were smaller but poorer-performing herds with low turnover and least frequently used intensive management practices (e.g., 39.1% SYNCH; 30.4% allowed mature, high-producing cows access to pasture). Group 5 used modern technologies and practices associated with improved production, yet had the least desirable mean DHI performance of all 6 groups. This group had the lowest proportion of deep loose-bedded stalls (only 52.2% used sand bedding) and the highest proportion (34.8%) of herds not using routine hoof trimming. The survey of group 3 herds did not reveal strong trends in management. The differences identified between herd groupings confirm significant variation in management practices linked to variation in overall herd performance measured by DHI variables. This approach provides an opportunity for consultants and outreach educators to better tailor efforts toward a certain type of dairy management philosophy, rather than taking a blanket approach to applying recommendations to farms simply because of their larger herd size.

17beta-estradiol: effect on CA1 hippocampal synaptic plasticity.

An understanding of synaptic plasticity in the mammalian brain has been one of R. F. Thompson's major pursuits throughout his illustrious career. A current series of experiments of significant interest to R. F. Thompson is an examination of the interactions between sex hormones, synaptic plasticity, aging, and stress. This research is contained within a broader project whose aim is to investigate animal models that evaluate estrogen interactions with Alzheimer's disease. This paper reviews the recent results that have led to a better understanding of how the sex hormone estrogen influences synaptic plasticity in an important structure within the mammalian brain responsible for learning and memory: the hippocampus. In this review, a number of experiments have been highlighted that investigate the molecular mechanisms that underlie estrogen's effect on two specific forms of synaptic plasticity commonly studied in neurophysiology and the behavioral neurosciences: long-term potentiation and long-term depression.

Cyclic changes in estradiol regulate synaptic plasticity through the MAP kinase pathway.

Hippocampal synaptic structure and function exhibit marked variations during the estrus cycle of female rats. Estradiol activates the mitogen-activated protein (MAP) kinase pathway in numerous cell types, and MAP kinase has been shown to play a critical role in the mechanisms underlying synaptic plasticity. Here, we report that endogenous estrogen produces a tonic phosphorylation/activation of extracellular signal-regulated kinase 2 (ERK2)/MAP kinase throughout the female rat brain and an increase in tyrosine phosphorylation of NR2 subunits of N-methyl-D-aspartate (NMDA) receptors. Moreover, cyclic changes in estrogen levels during the estrus cycle of female rats are associated with corresponding changes in the levels of activation of ERK2, the state of tyrosine phosphorylation of NR2 subunits of NMDA receptors, and the magnitude of long-term potentiation in hippocampus. Thus, cyclic changes in female sexual hormones result in marked variations in the state of activation of a major cellular signaling pathway critical for learning and memory and in a cellular model of learning and memory.

The tyrosine kinase and mitogen-activated protein kinase pathways mediate multiple effects of estrogen in hippocampus.

Estrogen replacement therapy in women is associated with improvement of cognitive deficits and reduced incidence of Alzheimer's disease. The present study indicates that estrogen is neuroprotective against N-methyl-d-aspartate (NMDA)- and kainate-mediated neurotoxicity, an effect mediated by tyrosine kinase/mitogen-activated protein kinase (MAPK) pathways. Estrogen also stimulates tyrosine phosphorylation of NMDA receptors via an src tyrosine kinase/MAPK pathway. Finally, estrogen-mediated enhancement of long-term potentiation in hippocampal slices is mediated by activation of an src tyrosine kinase pathway. Thus, estrogen, by activating an src tyrosine kinase and the extracellular signal-related protein kinase/MAPK signaling pathway, both enhances NMDA receptor function and long-term potentiation and retains neuroprotective properties against excitotoxicity. These findings warrant further evaluation of the usefulness of estrogenic compounds for the treatment of Alzheimer's disease and other neurodegenerative diseases.

17beta-estradiol suppresses expression of long-term depression in aged rats.

It has been recently reported that the female steroid hormone 17beta-estradiol enhances synaptic transmission and the magnitude of long-term potentiation (LTP) in adult rodent hippocampus. Moreover, 17beta-estradiol ameliorates cognitive and memory function in postmenopausal women. Since aging is associated with an alteration of synaptic plasticity (e.g., higher susceptibility to long-term depression [LTD]), we examined whether 17beta-estradiol alters the expression of LTD in aged rats. We now report that the induction of LTD recorded from CA1 hippocampal neurons of aged rats is suppressed by 17beta-estradiol treatment, which produced only a minimal effect in suppressing LTD in adult rats. These results suggest that estrogen may act to improve memory by suppressing forgetfulness via a synaptic mechanism, such as LTD.

17beta-estradiol enhances NMDA receptor-mediated EPSPs and long-term potentiation.

Gonadal steroid hormones influence CNS functioning through a variety of different mechanisms. To test the hypothesis that estrogen modulates synaptic plasticity in the hippocampus, in vitro hippocampal slices from 2-mo-old Sprague-Dawley male rats were used to determine the effect of 17beta-estradiol on both N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potentials (EPSPs) through intracellular recordings and long-term potentiation (LTP) through extracellular recordings. Intracellular EPSPs and extracellular field EPSPs (fEPSPs) were recorded from CA1 pyramidal cells by stimulating Schaffer collateral fibers. In intracellular experiments, slices were perfused with medium containing bicuculline (5 microM) and low Mg2+ (0.1 mM) to enhance the NMDA receptor-mediated currents and 6, 7-dinitroquinoxaline-2,3-dione (DNQX) (10 microM) to block the alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprianate (AMPA) receptor-mediated component. The effects of 17beta-estradiol on NMDA receptor-mediated activity were excitatory; concentrations >10 nM induced seizure activity, and lower concentrations (1 nM) markedly increased the amplitude of NMDA-mediated EPSPs (both the first and second responses increased during paired pulse stimulation by 180 and 197%, respectively). In extracellular experiments, slices perfused with 17beta-estradiol (100 pM) exhibited a pronounced, persisting, and significant enhancement of LTP of both the fEPSP slope (192%) and fEPSP amplitude (177%) compared with control slices (fEPSP slope = 155%; fEPSP amplitude = 156%) 30 min after high-frequency stimulation. These data demonstrate that estrogen enhances NMDA receptor-mediated currents and promotes an enhancement of LTP magnitude.

Behavioral stress modifies hippocampal plasticity through N-methyl-D-aspartate receptor activation.

Behavioral stress has detrimental effects on subsequent cognitive performance in many species, including humans. For example, humans exposed to stressful situations typically exhibit marked deficits in various learning and memory tasks. However, the underlying neural mechanisms by which stress exerts its effects on learning and memory are unknown. We now report that in adult male rats, stress (i.e., restraint plus tailshock) impairs long-term potentiation (LTP) but enhances long-term depression (LTD) in the CA1 area of the hippocampus, a structure implicated in learning and memory processes. These effects on LTP and LTD are prevented when the animals were given CGP39551 (the carboxyethylester of CGP 37849; DL-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist, before experiencing stress. In contrast, the anxiolytic drug diazepam did not block the stress effects on hippocampal plasticity. Thus, the effects of stress on subsequent LTP and LTD appear to be mediated through the activation of the NMDA subtype of glutamate receptors. Such modifications in hippocampal plasticity may contribute to learning and memory impairments associated with stress.

Unpredictable and uncontrollable stress impairs neuronal plasticity in the rat hippocampus.

Almost by definition, learning and the effect of stress on learning represent modifications of existing neuronal circuitry. Under some circumstances, this modification can be measured electrophysiologically. One such measure of plasticity is long-term potentiation (LTP), a long-lasting increase in synaptic efficacy following brief exposure to tetanic stimulation. In 1987, Foy et al. reported that hippocampal LTP was impaired by exposure to inescapable shock. We have recent evidence that the impairment in LTP can be prevented by allowing the animal to learn to escape the shock (Shors et al., 1989), indicating that the stress effect is to some extent mediated by "psychological" variables. Regardless of LTP's putative role in learning and memory processes, such a stress-induced decrease in neuronal plasticity is likely to have profound effects on the behaving organism.

Behavioral stress impairs long-term potentiation in rodent hippocampus.

A number of hormones secreted from the pituitary-adrenal system during stress affect learning and memory processes. The phenomenon of hippocampal long-term potentiation (LTP) is viewed by many as a putative mechanism of memory storage and has proved a most valuable model for study of neuronal plasticity at the cellular level. The present study was conducted to investigate the possibility that stressful events which occur prior (in vivo) to the preparation of brain slices may influence the electrophysiology of the in vitro hippocampal explant when tested for LTP. Adult male rats (Long-Evans male X Sprague-Dawley female) were pair-housed 1 week prior to testing. One animal in each pair was either placed in a restraining tube for 30 min and received no tail shocks (Restraint) or placed in a restraining tube and received tail shocks (1 microA, 1 s) every minute for 30 min (Restraint + Shock). The other animal in each pair was taken directly from the home cage and received no restraint or tail shock (Control). In vitro hippocampal slices were then prepared immediately from these animals according to standard methods. Our results demonstrate a marked impairment of LTP in hippocampal explants taken from rats exposed to stress. The significance of this result with respect to cellular mechanisms underlying the relationship between stress, cognition, and learning is discussed.

Reversal of hippocampal sexual dimorphism by gonadal steroid manipulation.

Hippocampal slices display a sexually dimorphic pattern of physiological neuromodulation to gonadal steroid administration. To determine if this is the result of organizational or activational hormone action, plasma steroid levels of adult male rats were manipulated. The results support an activational mechanism since steroid levels can be manipulated to abolish, reverse, or maintain the functional dimorphism. The results suggest a role for gonadal steroid action in rapid neuromodulation of brain function.

17-alpha-Estradiol and 17-beta-estradiol in hippocampus.

Electrophysiological field potentials recorded from in vitro hippocampal slice preparations show responses to exogenous gonadal steroids added to the incubation medium. The peak effect of the addition of 17-beta-estradiol occurred at a 100 pmol concentration; the CA1 field potential was increased by an average of 148 percent. 17-alpha-estradiol, often used as a negative control in experiments demonstrating estrogen specificity of receptor binding sites and biological responses, had no effect on field potentials following addition of drug to the incubation medium. The addition of a 100 pmol concentration of 17-beta-estradiol to the same slices which had been pretreated with 17-alpha-estradiol, blocked the facilitatory response elicited by the 17-beta-estradiol administered alone. Since no enhancement of the field potential is observed with 17-beta-estradiol following pretreatment of 17-alpha-estradiol, this would support the hypothesis that hippocampal modulation by gonadal steroid hormones may be due to involvement of an estrogen receptor mediated phenomena.

delta 9-THC and 17-beta-estradiol in hippocampus.

Electrophysiological field potentials recorded from in vitro hippocampal slice preparations show dose-dependent differences in response to 17-beta-estradiol (E2) and delta-9-tetrahydrocannabinol (THC) added to the incubation medium. Using a wide range of doses (1 pM-10 nM), it was found that mid-range concentrations of estradiol (100 pM) and THC (10 pM) tended to increase field potentials in CA1 of rodents. Higher dose levels of each agent were found to depress neuronal activity. In the context of prior findings, these results suggest that the two compounds share a common mechanism of action in the hippocampus.