The response of the natriuretic peptide system to water deprivation in the desert rodent, Notomys alexis

Natriuretic peptides (NPs) are regulatory molecules that cause cGMP-mediated diuresis and natriuresis in mammals. Accordingly, it is interesting to consider their role in desert-adapted animals in which water is often limited. This study investigated the response of the natriuretic peptide (NP) system to varying periods of water deprivation (WD) in the Australian desert rodent species, Notomys alexis. It was hypothesised that the expression of the NP system will be down-regulated in water-deprived N. alexis compared to water-replete animals. The plasma levels of ANP were significantly reduced after 3 days of WD, but were unaffected by 7, 14 and 28 days of WD. Water deprivation for 3, 7, 14 days had a variable effect on the mRNA expression of ANP, CNP, NPR-A, NPR-B, and NPR-C, and a uniform down-regulation was not observed. However, after 28 days of WD, mRNA expression was similar to water-replete animals, except for NPR-A. Surprisingly, 7 and 14 days of WD caused an up-regulation in the ability of ANP to stimulate cGMP; this also occurred at 14 days for CNP. Taken together, the mRNA expression and peptide mediated guanylyl cyclase activity data after WD were in the opposite direction to what was predicted. Interestingly, after 28 days of WD, most parameters were similar to those of water-replete animals, which indicates that a down-regulation of the NP system is not part of the physiological response to an absence of free water in N. alexis.

Habitat manipulation and rodent damage control: reducing rodent damage in Australian macadamia orchards

This paper examines the relationship between adjacent non-crop vegetation and rodent (Rattus rattus) damage in Australian macadamia (Macadamia integrifolia) orchard systems. Orchards adjacent to structurally diverse, non-crop vegetation dominated by woody weeds exhibited significantly higher damage when compared to orchards adjacent to managed grasslands. This relationship formed the basis for a rodent damage reduction strategy utilising habitat manipulation. Structurally diverse, non-crop habitats were modified to grasslands leading to a reduction in rodent damage of 65%. This strategy was cost-effective and has the potential to be long-term with minimal effort needed to maintain sites in a modified state. Habitat manipulation is a process whereby the resource load in a system is reduced and hence rodent densities cannot reach levels where they cause significant crop damage. This paper provides empirical evidence to support habitat manipulation as a practical, cost-effective control strategy for rodent pests.

Size matters : extraordinary rodent abundance on an Australian tropical floodplain

Published estimates of the total biomass of natural populations of mammalian herbivores generally have ignored small-bodied taxa (especially, rodents). Including such taxa may dramatically change our understanding of total biomass and energy flow in such systems. Dusky rats (Rattus colletti) are small (up to 210 g) native Australian mammals, and our 5-year mark-recapture study on a tropical flood plain (Adelaide River, Northern Territory) revealed that rat biomass can reach extraordinary levels (up to 4.7 t km⁻²). Because their small body size results in high mass-specific metabolic rates, a given biomass of rodents has a several-fold higher total energy requirement than the same mass of large-bodied herbivores. Accordingly, during some years dusky rat biomass can be double that estimated for large herbivores on the world's most productive savannas in eastern and southern Africa. The huge rodent biomass strongly suggests that the Adelaide River flood plain must be an incredibly productive habitat. Considering the immense biological importance of these productive ecosystems, flood plain conservation must be placed high on the priority list of habitats that require immediate protection.

Developmental changes in the expression of creatine synthesizing enzymes and creatine transporter in a precocial rodent, the spiny mouse

Background : Creatine synthesis takes place predominately in the kidney and liver via a two-step process involving AGAT (L-arginine:glycine amidinotransferase) and GAMT (guanidinoacetate methyltransferase). Creatine is taken into cells via the creatine transporter (CrT), where it plays an essential role in energy homeostasis, particularly for tissues with high and fluctuating energy demands. Very little is known of the fetal requirement for creatine and how this may change with advancing pregnancy and into the early neonatal period. Using the spiny mouse as a model of human perinatal development, the purpose of the present study was to comprehensively examine the development of the creatine synthesis and transport systems.

Results : The estimated amount of total creatine in the placenta and brain significantly increased in the second half of pregnancy, coinciding with a significant increase in expression of CrT mRNA. In the fetal brain, mRNA expression of AGAT increased steadily across the second half of pregnancy, although GAMT mRNA expression was relatively low until 34 days gestation (term is 38–39 days). In the fetal kidney and liver, AGAT and GAMT mRNA and protein expression were also relatively low until 34–37 days gestation. Between mid-gestation and term, neither AGAT or GAMT mRNA or protein could be detected in the placenta.

Conclusion : Our results suggest that in the spiny mouse, a species where, like the human, considerable organogenesis occurs before birth, there appears to be a limited capacity for endogenous creatine synthesis until approximately 0.9 of pregnancy. This implies that a maternal source of creatine, transferred across the placenta, may be essential until the creatine synthesis and transport system matures in preparation for birth. If these results also apply to the human, premature birth may increase the risk of creatine deficiency.

A new rodent model to assess blood stage immunity to the plasmodium falciparum antigen merozoite surface protein 119 reveals a protective role for invasion inhibitory antibodies

Antibodies capable of inhibiting the invasion of Plasmodium merozoites into erythrocytes are present in individuals that are clinically immune to the malaria parasite. Those targeting the 19-kD COOH-terminal domain of the major merozoite surface protein (MSP)-119 are a major component of this inhibitory activity. However, it has been difficult to assess the overall relevance of such antibodies to antiparasite immunity. Here we use an allelic replacement approach to generate a rodent malaria parasite (Plasmodium berghei) that expresses a human malaria (Plasmodium falciparum) form of MSP-119. We show that mice made semi-immune to this parasite line generate high levels of merozoite inhibitory antibodies that are specific for P. falciparum MSP-119. Importantly, protection from homologous blood stage challenge in these mice correlated with levels of P. falciparum MSP-119–specific inhibitory antibodies, but not with titres of total MSP-119–specific immunoglobulins. We conclude that merozoite inhibitory antibodies generated in response to infection can play a significant role in suppressing parasitemia in vivo. This study provides a strong impetus for the development of blood stage vaccines designed to generate invasion inhibitory antibodies and offers a new animal model to trial P. falciparum MSP-119 vaccines.

Foraging behaviour of two rodent species inhabiting a kopje (rocky outcrop) in Tsavo West National Park, Kenya

We employed patch use theory to evaluate how several environmental factors influence the foraging behaviour of two rodent species: Grammomys dolichurus and Acomys cahirinus. Foraging efficiency was determined by measuring the remaining food in artificial food patches (giving-up densities: GUDs) from two experiments. In the first experiment, we placed patches in different microhabitat types (cover vs open) and at varying distances from cover. This experiment was conducted during three moon stages (waxing, full, waning). We found that the rodents had higher GUDs (lower foraging efficiency) in the open microhabitat. The distance from nearest shelter had a marginally significant positive effect on GUDs. GUDs were higher in both microhabitat types during the waxing and full phases, but decreased sharply once the moon began to rise after sunset. These results are likely due to higher predation risk away from cover and in more illuminated environments. In the second experiment, we examined mouse responses to seeds impregnated with plant toxins. Seeds impregnated with oxalic acid were avoided by the rodents, while seeds soaked in tannic acid did not differ significantly from control seeds. Our results highlight important ecological factors affecting the foraging behaviour of these rodents.

The energetic and oxidative costs of reproduction in a free-ranging rodent

1. As understanding of the energetic costs of reproduction in birds and mammals continues to improve, oxidative stress is an increasingly cited example of a non-energetic cost of reproduction that may serve as a proximal physiological link underlying life-history trade-offs.

2. Here, we provide the first study to measure daily energy expenditure (DEE) and oxidative damage in a wild population. We measured both traits on eastern chipmunks (Tamias striatus) and assessed their relationships with age, reproductive status, litter size and environmental conditions.

3. We found that both physiological traits were correlated with environmental characteristics (e.g. temperature, seasons). DEE tended to increase with decreasing temperature, while oxidative damage was lower in spring, after a winter of torpor expression, than in autumn. We also found that DEE decreased with age, while oxidative damage was elevated in young individuals, reduced in animals of intermediate age and tended to increase at older age.

4. After controlling for age and environmental variables, we found that both female DEE and oxidative damage increased with litter size, although the latter increased weakly.

5. Our results corroborate findings from laboratory studies but highlight the importance of considering environmental conditions, age and reproductive status in broader analyses of the causes and consequences of physiological costs of reproduction in wild animals.

Metformin counters the insulin-induced suppression of fatty acid oxidation and stimulation of triacylglycerol storage in rodent skeletal muscle

The present study examined the acute effects of metformin on fatty acid (FA) metabolism in oxidative soleus (SOL) and glycolytic epitrochlearis (EPT) rodent muscle. SOL and EPT were incubated for either 30 or 180 min in the absence or presence of 2 mM metformin and with or without insulin (10 mU/ml). Metformin did not alter basal FA metabolism but countered the effects of insulin on FA oxidation and incorporation into triacylglyerol (TAG). Specifically, metformin prevented the insulin-induced suppression of FA oxidation in SOL but did not alter FA incorporation into lipid pools. In contrast, in EPT metformin blunted the incorporation of FA into TAG when insulin was present but did not alter FA oxidation. In SOL, metformin resulted in a 50% increase in AMP-activated protein kinase α2 activity and prevented the insulin-induced increase in malonyl-CoA content. In both fiber types, basal and insulin-stimulated glucose oxidation were not significantly altered by metformin. All effects were similar regardless of whether they were measured after 30 or 180 min. Because increased muscle lipid storage and impaired FA oxidation have been associated with insulin resistance in this tissue, the ability of metformin to reverse these abnormalities in muscle FA metabolism may be a part of the mechanism by which metformin improves glucose clearance and insulin sensitivity. The present data also suggest that increased glucose clearance is not due to its enhanced subsequent oxidation. Additional studies are warranted to determine whether chronic metformin treatment has similar effects on muscle FA metabolism.

The control of rodent damage in Australian macadamia orchards by manipulation of adjacent non-crop habitats

 Habitat manipulation was used as a management strategy for the control of rodent (Rattus rattus) damage in Australian macadamia orchard systems. Large, temporally stable non-crop habitats were converted to highly modified grasslands. These sites were manipulated by removing all non-crop vegetation over 10 cm in height to a distance of approximately 20 m from the orchard. Regrowth was controlled by the application of herbicide. The total cost of the habitat manipulation was $AUD 292 per site. Manipulation resulted in a reduction in damage of 65% within the associated orchards. This reduction in rodent damage resulted in a saving of $AUD 980 per site. Therefore habitat manipulation was cost-effective and is a viable startegy for the control of rodent damage in Australian macadamia orchard systems.

CD8+ T cells from a novel T cell receptor transgenic mouse induce liver-stage immunity that can be boosted by blood-stage infection in rodent malaria

To follow the fate of CD8+ T cells responsive to Plasmodium berghei ANKA (PbA) infection, we generated an MHC I-restricted TCR transgenic mouse line against this pathogen. T cells from this line, termed PbT-I T cells, were able to respond to blood-stage infection by PbA and two other rodent malaria species, P. yoelii XNL and P. chabaudi AS. These PbT-I T cells were also able to respond to sporozoites and to protect mice from liver-stage infection. Examination of the requirements for priming after intravenous administration of irradiated sporozoites, an effective vaccination approach, showed that the spleen rather than the liver was the main site of priming and that responses depended on CD8α+ dendritic cells. Importantly, sequential exposure to irradiated sporozoites followed two days later by blood-stage infection led to augmented PbT-I T cell expansion. These findings indicate that PbT-I T cells are a highly versatile tool for studying multiple stages and species of rodent malaria and suggest that cross-stage reactive CD8+ T cells may be utilized in liver-stage vaccine design to enable boosting by blood-stage infections.

Effects of stress on reproduction in non-rodent mammals : the role of glucocorticoids and sex differences

The means by which stress influences reproduction is not clearly understood, but may involve a number of endocrine, paracrine and neural systems. Stress impacts on the reproductive axis at the hypothalamus (to affect GnRH secretion) and the pituitary gland (to affect gonadotrophin secretion), with direct effects on the gonads being of less importance. Different stressors have different effects and there are differences in response to short- and long-term stress. Many short-term stresses fail to affect reproduction and there are reports of stimulatory effects of some 'stressors'. There are species differences in the way that specific stressors affect reproduction. Sex differences in the effects of a particular stressor have been delineated and these may relate to effects of stress at different levels of the hypothalamo-pituitary axis. The significance of stress-induced secretion of cortisol varies with species. In some instances, there appears to be little impact of short-term increases in cortisol concentrations and protracted increases in plasma concentration seem to be required before any deleterious effect on reproduction is apparent. Issues of sex, sex steroid status, type of stressor and duration of stress need to be considered to improve understanding of this issue.