Abstract
The environment contributes to production diseases that in turn badly affect cow performance, fertility and culling. Oestrus intensity is lower in lame cows, and in all cows 26% potential oestrus events are not expressed (to avoid getting pregnant). To understand these trade-offs, we need to know how animals react to their environment and how the environment influences hypothalamus-pituitary-adrenal axis (HPA) interactions with the hypothalamus-pituitary-ovarian axis (HPO). Neurotransmitters control secretion of GnRH into hypophyseal portal blood. GnRH/LH pulse amplitude and frequency drive oestradiol production, culminating in oestrus behaviour and a precisely-timed GnRH/LH surge, all of which are disrupted by poor environments. Responses to peripheral neuronal agents give clues about mechanisms, but do these drugs alter perception of stimuli, or suppress consequent responses? In vitro studies confirm some neuronal interactions between the HPA and HPO; and immuno-histochemistry clarifies the location and sequence of inter-neurone activity within the brain. In both species, exogenous corticoids, ACTH and/or CRH act at the pituitary (reduce LH release by GnRH), and hypothalamus (lower GnRH pulse frequency and delay surge release). This requires inter-neurones as GnRH cells do not have receptors for HPA compounds. There are two (simultaneous, therefore fail-safe?) pathways for CRH suppression of GnRH release via CRH-Receptors: one being the regulation of kisspeptin/dynorphin and other cell types in the hypothalamus, and the other being the direct contact between CRH and GnRH cell terminals in the median eminence. When we domesticate animals, we must provide the best possible environment otherwise animals trade-off with lower production, less intense oestrus behaviour, and impaired fertility. Avoiding life-time peri-parturient problems by managing persistent lactations in cows may be a worthy trade-off on both welfare and economic terms – better than the camouflage use of drugs/hormones/feed additives/intricate technologies? In the long term, getting animals and environment in a more harmonious balance is the ultimate strategy.
Highlights
The environment contributes to production diseases that in turn badly affect cow performance, fertility and culling
luteinising hormone (LH) secretion is provoked by repeated low dose gonadotrophin releasing hormone (GnRH) injections, and, responses are reduced by 50%, a lowered self-priming effect is still evident indicating inhibitory effects occur at both hypothalamic and pituitary level (Ozturk et al, 1998)
Each step in hypothalamus-pituitary-adrenal axis (HPA) axis activation can be mimicked by administering exogenous components: corticotrophin releasing hormone (CRH) infusion into ewe hypothalamus portal blood increases peripheral adreno-corticotrophin hormone (ACTH) and cortisol (Naylor et al, 1990); ACTH i.v. injections increase cortisol; whereas 10-day treatment of cows with betamethasone suppresses plasma cortisol for up to 26 days and delays luteolysis probably by blocking prostaglandin F2-alpha release that is usually stimulated by follicular oestradiol (Dobson et al, 1987)
Summary
Stopping the low dose LH injections after 4 days results in an immediate decrease in LH concentrations with a consequent decline in oestradiol secretion but large non-functional follicle structures remain (Figure 4; Dobson et al, 1997). Each step in HPA axis activation can be mimicked by administering exogenous components: CRH infusion into ewe hypothalamus portal blood increases peripheral ACTH and cortisol (Naylor et al, 1990); ACTH i.v. injections increase cortisol (cows: Alam et al, 1986; ewes: Phogat et al, 1999a); whereas 10-day treatment of cows with betamethasone (a synthetic corticoid) suppresses plasma cortisol for up to 26 days and delays luteolysis probably by blocking prostaglandin F2-alpha release that is usually stimulated by follicular oestradiol (Dobson et al, 1987).
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