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The focus of this thesis is on the study of reproduction strategy in the context of evolutionary and social-evolutionary theory. Much of the hierarchical structure that is evident in the natural world is due to major evolutionary transitions where individual subunits that once reproduced individually now reproduce only as part of a larger unit. Modelling and understanding the processes behind the evolution of this hierarchy can have applications in both biology and computer science. I argue that to explain the major transitions it is necessary to understand why an individual would reduce its reproductive success to invest instead in a higher reproductive process (i.e., reproduce collectively with other individuals). To address this problem, a method for studying reproduction strategy was developed and is presented in this thesis. The method takes an abstract physiological approach to reproduction. It considers an individual as a quantity of resources and set of genes which define its reproduction strategy. I then investigate the advantages of different reproduction strategies and identify which strategies may dominate others. The strategies considered in my investigations include: an individual reproducing on its own; an individual gambling its total resources against those of multiple other individuals; or an individual sharing its reproductive effort with a partner or several other partners. Starting with individual reproduction, I simply study why an individual might reduce its reproductive rate when, on the face of it, it seems that maximum fecundity should be the best option. The model is also motivated in light of current literature on life history and microbial ecology in particular. The results show how it can be advantageous for an individual to hedge its bets and delay reproduction; waiting instead until it has accumulated more resources and is less vulnerable to harsh periods. The results make predictions that are experimentally verifiable. Given the model of individual reproduction, I reapply the growth equations to question whether there is any advantage to sharing reproductive effort through collective reproduction. This model also shows that it can pay to hedge one’s bets and invest in the less vulnerable, but slower, collective reproductive strategy. The results show that there is a mathematical relationship between the number of parents and the up-front cost of reproduction spent on creating a new offspring – depending on the extra cost per parent, two parents may be the best strategy or perhaps many parents. Looking in more detail at the transition from unicellular organisms to multicellular organisms, I model the macrocyst stage in the slime mould Dictyostelium. I consider how the macrocyst stage may be an early example of collective reproduction in protozoa. Here individuals aggregate to be ingested by a central cell which produces homogeneous offspring. I assume that each individual is gambling on being the central cell and the model presented reveals under what conditions this is likely to be a good strategy when compared to individual reproduction. Again, the results show that there is an advantage to hedging one’s bets and investing in the macrocyst rather than going it alone. Finally I consider the origin of sexual reproduction in more detail. The traditional approach argues that the slower growth rate of sexually reproducing organisms means that there is a paradox concerning the origins and maintenance of sexual reproduction, especially when one considers males which do not contribute to their offspring. Extending the previous model of collective reproduction, I consider how many resources selfish individuals may contribute to their offspring. The results show that there is a lower bound to the resources individuals may contribute and that when there is a high amplitude of resource fluctuation, the sexual strategy can dominate an asexual strategy. As well as the main body of work on the topic of individual reproduction, some further background work is also presented. The models use both mathematical and computer simulation models. These two approaches are compared and contrasted with reference to their value in generating good scientific explanations of the sorts of phenomena found in the types of systems I am studying.

The GnRH-II system is thought to regulate sexual behaviour through an action in the brain, and/or control gonadotrophin secretion in association with the classical GnRH-I system at the level of the gonadotroph. The aim of this study described in this thesis was to comprehensively investigate the GnRH-II receptor system in a well characterised sheep model. Four types of studies were performed. The first study sequenced the ovine GnRH-II receptor gene by long-distance PCR. The second study investigated GnRH-II receptor gene expression in ovine tissues. The third study investigated evidence for GnRH-II receptor on gonadotrophs. A fourth study used two selective GnRH-I receptor antagonists to test whether administered GnRH-II acts through the GnRH-I receptor to elicit gonadotrophin secretion. In conclusion the presence of a premature stop codon in the ovine GnRH-II receptor, and a major deletion mean it is unlikely that a full 7 transmembrane domain G-protein coupled receptor is expressed in the sheep. RNA transcripts for part of the receptor were detected in testis, ovary and hindbrain, indicating that a partial GnRH-II receptor protein may be produced in a tissue-specific manner. The lack of a Pit-1 binding site in the 5’ flanking sequence of the ovine GnRH-II gene, the lack of RNA transcripts specifically in gonadotrophs and the <i>in vivo</i> evidence collectively suggest that GnRH-II does not function to regulate gonadotrophin secretion in the sheep. Overall these data complement recent published data for the marmoset, African green monkey, rhesus macaque and man, and are consistent with the generalised hypothesis that there has been redundancy in the multiple GnRH receptor systems during vertebrate evolution.

No description available.

No description available.

The importance of tissue protein reserves to lactating females attempting to sustain milk output under conditions of severe dietary protein restriction was investigated using rats. Four experiments were carried out to study the effect of variation in repletion of tissue protein reserves on lactational performance, rates of body protein mobilisation and changes in tissue protein metabolism involved in promoting protein mobilisation. The extent to which body protein reserves were capable of maintaining milk quantity and quality under such conditions was also considered. The lactation performance of multiparous, female Sprague-Dawley rats, offered isoenergetic diets (21 MJ GE/kg DM), was assessed from growth of a standardised litter of 12 pups. Variation in repletion of protein reserves at parturition was achieved by applying a period of protein restriction during the latter half of gestation. Changes in body composition were estimated from carcass analysis and rates of protein mobilisation were derived from serial slaughter experiments. Tissue protein synthesis was estimated <i>in vivo</i> using a flooding dose of [<SUP>3</SUP>H] phenylalanine and tissue Na<SUP></SUP>+ , K<SUP></SUP>+ -ATPase activity was measured polarographically <i>in vitro</i>. Milk samples were obtained following injection of oxytocin. Females offered a high protein diet (215 gCP/kg DM) during lactation exhibited an increase in both feed intake and lactational performance while not utilising their body protein stores. However, in rats offered imbalanced feeds (low protein/high energy) such an increase in intake was not apparent and dams were forced to draw upon their endogenous protein reserves in an attempt to sustain milk production. Between 15 and 22% of body protein was lost by dams assumed to be 'Fully' protein replete at parturition. When dietary protein was limiting, reductions in the size of the protein reserve had a significant inpact on a female's ability to sustain milk production, and dams which were initially 'Fully' replete supported greater (P< 0.05) litter growth during early lactation, due to a greater endogenous protein supply and feed intake (P< 0.05), than their 'Depleted' contemporaries.

The growth of sheep fed forage brassica crops is lower than would be predicted from the chemical composition of the crops, which are generally highly digestible and contain moderate concentrations of carbohydrate and protein. The problem has been attributed to low voluntary food intake (VFI) and among potential reasons for this is the presence, in the herbage, of secondary plant metabolites. The fate and physiological effects of two groups of compounds, the glucosinolates and S-methyl cysteine sulphoxide (SMCO) were studied in a series of in vivo and in vitro experiments. The glucosinolate breakdown products allyl cyanide (ACN) and allyl isothiocyanate (AITC) were continuously infused for 21 days into the rumen of sheep fed either fresh forage rape or dried grass pellets. The VFI of forage rape by ACN-infused sheep (2.4 mmol/d) was reduced, although not significantly, while AITC (2.4 mmol/d) caused no VFI reduction. Neither compound affected VFI when infused (4.8 mmol/d) into sheep fed the dried grass pellet diet. Thyroid hormone concentrations were unaffected by treatment on the dried grass diet but plasma T3 concentrations were reduced by AITC on the forage rape diet. In a further experiment, 3 levels of ACN (0, 4.8 and 9.6 mmol/d) were infused intra-ruminally into dried grass-fed sheep for 63 days. Voluntary food intake was again reduced by treatment and liver damage was indicated by elevated plasma gamma glutamyl transpeptidase (GGTP) concentrations. Clinical indicators of kidney function (plasma creatinine, plasma urea) indicated no renal effects. Hepatic cytochrome oxidase activity was significantly depressed at the highest rate of ACN infusion at the end of the treatment period indicating chronic cyanide toxicity. Rumen degradation of glucosinolate breakdown products was examined by measuring the stability of ACN and AITC in rumen fluid in vitro. ACN was degraded by rumen fluid from cabbage-adapted sheep but not when the donor had been offered dried grass pellets. In a further experiment, rumen fluid samples taken at intervals from sheep consuming cabbage for 30 days had variable ACN-degrading activity with little evidence for a cumulative increase in activity over time.

ACS, ACLS and PLA<SUB>2</SUB> activities were detected in guinea-pig endometrium on both 7 (day of low PGF<SUB>2α</SUB> output) and day 15 (day of high PGF<SUB>2α</SUB> output) of the oestrous cycle and in the endometrium of ovariectomizd guinea-pigs treated with oestradiol and/or progesterone. Treatment with aristolochic acid (ARA) and quinacrine (QUIN) (PLA<SUB>2</SUB> inhibitors) significantly (P ¸0.05) reduced PG<SUB>2α</SUB> output from both day 7 and day 15 endometrium cultured for 24 h, demonstrating the crucial role that PLA<SUB>2</SUB> plays in the regulation of AA release for PGF<SUB>2α</SUB> synthesis in the guinea-pig. Unexpectedly, treatment with p-hydroxymercuribenzoic acid (HMB0 and thimerosal (THM) (ACS and ACLS inhibitors) also significantly (P < 0.05) decreased PGF<SUB>2α</SUB> output. However, during long term inhibition of ACS and ACLS, since the rate of uptake of AA into lysophospholipids will be reduced, the amount of AA appropriately placed in the <I>sn</I>-2 position of appropriate phospholipids for the action of PLA<SUB>2</SUB> will also be reduced. Therefore, PLA<SUB>2</SUB> may be indirectly inhibited by a lack of substrate. ACS, ACLS and PLA<SUB>2</SUB> activities were detected in the endometrium and conceptus of early pregnant (day 15) guinea-pigs. All three enzymes were also detected in the endometrium, chorio-allantoic placenta, chorion and amnion of day 29 and 36 pregnant guinea-pigs. Treatment with THM and ARA of day 22, 29 and 36 pregnant guinea-pig endometrial and fetal tissues during 24 h culture suggested that the control of AA uptake is important in the maternal placenta, fetal placenta, chorion and amnion, and that PLA<SUB>2</SUB> appears to have an essential role in the control of PG synthesis from the endometrium, chorion and amnion of pregnant guinea-pigs. ACS, ACLS and PLA<SUB>2</SUB> may have a role in the control of arachidonic acid turnover, and therefore PG production, in guinea-pig uterine and fetal tissues. The stimulus responsible for increased PLA<SUB>2</SUB> activity towards the end of the cycle, and the mechanism of the anti-luteolytic factor provided by the guinea-pig conceptus, remains obscure. The control of AA uptake in the placenta and fetal membranes seems to have a role in the delicate regulation of PG synthesis during pregnancy.

The aim of this study was to investigate the corticostriatal pathways in a highly organised and topographically arranged cortical area using an intracellular <I>in vivo</I> method of the recording, filling and tracing of single corticostriatal neurons. In order to do so a successful intracellular recording protocol had to be developed (from an existing extracellular method) to ensure maximum neuronal filling. This process was an ongoing one and the various stages of development are highlighted. Alongside this a suitable biocyin method had to be developed for the visualisation of terminal fields arising from single neuronal fills. The various stages in the development of this method are also described. This study has resulted in recordings from all four types of layer V pyramidal projection neurons described <I>in vitro</I>. Whilst the morphology was identical to that observed <I>in vitro</I> for the IB and RS neurons the physiological responses to whisker deflection were more complex, especially in IB neuronal firing patterns. In general there was a lot more background synaptic activity observed in all the cellular records. The IB neurons tended to show more complex firing patterns, firing either as mainly single action potentials with occassional burst or predominantly bursts with occassional action potentials. Only rarely did they fire the typical burst firing observed <I>in vitro</I>. It was apparent from this study that the RS2 and IB1 neurons were very similar in both their physiology and morphology and were more difficult to classify.

The importance of dietary protein and energy intake to the development and activity of the mammary gland was investigated in lactating rats. Four rat trails were undertaken. The first examined the influence of protein undernutrition and re-alimentation on mammary gland size and secretory cell activity. The results showed that rats offered a protein restricted diet during lactation suffer mammary underdevelopment, but this may be rapidly reversed by re-alimentation with a diet of high protein concentration. However, lactating rats offered a lower protein concentration diet significantly reduce voluntary food intake, which poses a dilemma of interpretation as it is not possible to definitively ascribe the mammary underdevelopment to a protein or energy deficiency. The reduction in food intake shown by these rats also led to a significant loss of body weight due to mobilisation of body tissue. It has previously been proposed that mobilisation of muscle carnosine and haemoglobin, both of which contain relatively high levels of histidine, resulted in elevated levels of plasma histidine. This is converted in the brain to the neurotransmitter histamine which acts on the hypothalamus suppressing food intake. The second trial investigated the role of the histamine receptor antagonist, cyproheptadine on the voluntary food intake of low protein concentration diets offered to both lactating or young, growing rats. This work indicated that lactating rats offered a protein deficient diet increased their voluntary food intake and also lactational ability until day 8 of lactation, when injected intraperitoneally with cyproheptadine, after which intake dropped. However, the drug had no significant effect on the variables measured in the growing animals. Since cyproheptadine was only effective in lactating rats over the short term, trial 3 was designed to investigate whether the mammary gland's response to protein re-alimentation, seen in trial 1 was due to an increase in the intake of dietary protein, energy or both. This experiment aimed to differentiate the effects of dietary protein and energy intake on mammary development and milk composition by rationing dietary protein and energy allowances separately.