Search

An estimated 40% of dogs living as companion dogs are believed to exhibit some form of anxiety or stress-related behavior. Although this represents a significant welfare issue, our understanding of the origins of anxiety in dogs remains limited. Genetics, environment, and training methods have all been investigated, yet little attention has been paid to the care provided by the mother. Research conducted with altricial species, that rely heavily on maternal care for survival, suggests that early maternal care behaviors play an important role in the development of the infant and thus, behavior and temperament later in life. The most critical maternal behaviors include contact, nursing, licking (particularly anogenital licking which stimulates urination and defecation), punishment, thermoregulation, and movement. In domestic dogs, rapid neurological development occurs between postnatal days 3 and 16, yet investigations fail to measure or acknowledge the role that maternal care has during this critical window, or how the experience of puppies during this time influences behavior later in life, including response to stressful events. Evidence from the rodent literature indicates profound effects of maternal care on neurological and behavioral development. Although there may be differences in maternal behavior between rats and dogs, the underlying physiological mechanisms underpinning the programming of stress-related behavior are likely to be similar. For instance, the hypothalamic-pituitary-adrenal axis or stress responsiveness pathways are profoundly altered by maternal behaviors, and these changes are conserved throughout adult life. In this review, we examine the literature related to maternal care in canids alongside the literature related to maternal care in rodents and provide evidence that maternal care is critical to the healthy development of domestic dogs. Emphasis is placed on methodologies for quantifying maternal care and on the physiological mechanisms that might underpin behavioral changes induced by different amounts and types of maternal care. [ABSTRACT FROM AUTHOR]

Prenatal growth is sensitive to the direct and indirect effects of maternal dietary intake; manipulation can lead to behavioural and physiological changes of the offspring later in life. Here, we report on three aspects of how a high-salt diet during pregnancy (conception to parturition) may affect the offspring's response to high oral salt loads: (i) dietary preferences for salt; (ii) response to salt and water balance and aldosterone and arginine vasopressin (AVP) concentrations after an oral salt challenge; (iii) concentrations of insulin and leptin after an oral salt challenge. We used two groups of lambs born to ewes fed either a high-salt (13% NaCl) diet during pregnancy (S lambs; n=12) or control animals born to ewes fed a conventional (0.5% NaCl) diet during pregnancy (C lambs; n=12). Lambs were subjected to short- (5 min) and long-term (24 h) preference tests for a high-salt (13% NaCl) or control diet, and the response to an oral challenge with either water or 25% NaCl solution were also carried out. Weaned lambs born to ewes fed high salt during pregnancy did not differ in their preference for dietary salt, but they did differ in their physiological responses to an oral salt challenge. Results indicate that these differences reflect an alteration in the regulation of water and salt balance as the metabolic hormones, insulin and leptin, were not affected. During the first 2 h after a single salt dose, S lambs had a 25% lower water intake compared to the C lambs. S lambs had, on average, a 13% lower AVP concentration than the C lambs (P=0.014). The plasma concentration of aldosterone was higher in the S lambs than in the C lambs (P=0.013). Results suggest that lambs born to ewes that ingest high amounts of salt during pregnancy are programmed to have an altered thirst threshold, and blunted response in aldosterone to oral salt loads. [ABSTRACT FROM AUTHOR]

Crimp, a distinguishing feature of sheep fibres, significantly affects wool value, processing and final fabric attributes. Several explanations for fibre bending have been proposed. Most concentrate on relative differences in the physicochemical properties of the cortical cells, which comprise the bulk of the fibre. However, the associations between cortical properties and fibre crimp are not consistent and may not reflect the underlying causation of fibre curvature (FC). We have formulated a mechanistic model in which fibre shape is dictated primarily by the degree of asymmetry in cell supply from the follicle bulb, and the point at which keratinisation is completed within the follicle. If this hypothesis is correct, one would anticipate that most variations in fibre crimp would be accounted for by quantitative differences in both the degree of mitotic asymmetry in follicle bulbs and the distance from the bulb to the point at which keratinisation is completed. To test this hypothesis, we took skin biopsies from Merino sheep from sites producing wool differing widely in fibre crimp frequency and FC. Mitotic asymmetry in follicle bulbs was measured using a DNA-labelling technique and the site of final keratinisation was defined by picric acid staining of the fibre. The proportion of parato ortho-cortical cell area was determined in the cross-sections of fibres within biopsy samples. Mitotic asymmetry in the follicle bulb accounted for 0.64 ( P,0.0001) of the total variance in objectively measured FC, while the point of final keratinisation of the fibre accounted for an additional 0.05 ( P,0.05) of the variance. There was no association between ortho- to para-cortical cell ratio and FC. FC was positively associated with a subjective follicle curvature score ( P,0.01). We conclude that fibre crimp is caused predominantly by asymmetric cell division in follicles that are highly curved. Differential pressures exerted by the subsequent asymmetric cell supply and cell hardening in the lower follicle cause fibre bending. The extent of bending is then modulated by the point at which keratinisation is completed; later hardening means the fibre remains pliable for longer, thereby reducing the pressure differential and reducing fibre bending. This means that even highly asymmetric follicles may produce a straight fibre if keratinisation is sufficiently delayed, as is the case in deficiencies of zinc and copper, or when keratinisation is perturbed by transgenesis. The model presented here can account for the many variations in fibre shape found in mammals. [ABSTRACT FROM AUTHOR]