W2A-030 Bovine reproduction-0.txt
Puberty

Puberty, the process by which animals become capable of producing offspring, is often given a very restricted definition. According to Short (1984), 'we generally refer to puberty as that moment at which the female first comes into oestrus and ovulates, or the male first produces spermatozoa in his ejaculate'." The trouble with this widely-held perception of puberty is that it concentrates exclusively on the apparent endpoint of a protracted and complex physiological process and suggests that puberty is a discrete event that can be assigned to a particular day (or moment!). There is the additional problem that the apparent end-point (first release of the gametes) is not necessarily conclusive evidence that the animal has now reached the stage at which it can reproduce itself; for instance, it is clear that many heifers may not be capable of doing so until well after first ovulation (see review by Moran et al., 1989).

In fact, the onset of puberty is a gradual process that is in train for several months during which there are significant morphological, physiological and behavioural responses to the progressive expression of both the steroidogenic and gametogenic activities of the gonads. The essential feature of the process is the maturation of the brain-hypothalamic-pituitary-gonadal axis, which culminates in the adult pattern of reproductive activity. The components of the hypothalamic-pituitary-gonadal axis are present before birth and, even at that stage, each component is capable of responding to appropriate hormonal signals. During gestation, steroid hormones released from the placenta have an inhibitory effect on the fetal hypothalamus that suppresses the activities of the axis. After birth the axis becomes an independent regulatory system that secretes increased amounts of gonadotrophins and gonadal steroids. However, the system is restricted to a relatively low level of activity (juvenile level); for instance, in the female the level of activity is well below that required for ovulation or cyclic ovarian activity. The restraint is due partly to the fine sensitivity of the GnRH pulse generator to negative feedback by gonadal steroids and partly to inhibitory inputs from the neural circuits that control the hypothalamus.

The transition to sexual maturity is brought about by progressive changes in the neuroendocrine activities of the axis in response to a variety of internal and environmental factors. The 'gonadostat' hypothesis postulates that the essential change during the transition to sexual maturity is a progressive decrease in sensitivity of the hypothalamus to the negative feedback effects of gonadal steroids (Fig. 30.13) so that the frequency of GnRH pulses is increased progressively. This leads to an increase in the sensitivity of the pituitary gonadotropes to GnRH and to an increase in the responsiveness of the gonads to the gonadotrophins (Fig. 30.14). Greater quantities of gonadotrophins are released from the pituitary gland and, in turn, greater quantities of steroids are released by the gonads. For instance, in the female the sensitivity of the hypothalamus to the negative feedback effect of oestrogen declines progressively and, as it does so, the increasing quantities of oestrogen from the ovaries can no longer hold the axis within the juvenile pattern of activity. There is a gradual movement of the regulatory system towards the adult pattern (Figs 30.13 and 30.14). Eventually, the ovaries produce a surge of oestrogen that exerts a positive feedback effect on the surge generator in the hypothalamus (Fig. 30.14) and this induces a surge of LH that leads to ovulation.

As our knowledge of these changes expands, there is increasing evidence that sexual maturity is regulated to a considerable extent by changing patterns of neural control over the hypothalamus. These alterations in intrinsic neural activity do not appear to be dependent on gonadal hormones; however, they play a crucial role in that they gradually release the GnRH pulse generator from the restraints exercised by the central nervous system during the juvenile period, thus enabling it to respond to the gonadal steroids in the adult manner. It is evident that the classical 'gonodostat' hypothesis does not furnish an entirely satisfactory explanation of the onset of puberty in all its details. Nevertheless, it does provide a conceptual framework that is adequate for the purposes of this text.

The first ovulation is likely to be silent; it appears that the hormonal requirements for the expression of oestrus are small quantities of progesterone from a regressing corpus luteum followed by a surge of oestrogen from the preovulatory follicle - a sequence that is absent at the time of first ovulation. Thus, the first oestrus observed by the stockperson indicated that the process of puberty is well advanced but it does not provide a precise date for the 'moment' of puberty.

The earliest possible maturation of the individual components of the reproductive axis (and, therefore, of the axis itself) is determined by genes, i.e. there are inherent breed variations in the onset of puberty. However, in all breeds this process is subject to delays caused by a variety of endogenous and exogenous influences, some of which can be manipulated by the stockperson to ensure that the heifer is ready for breeding at the desired time. The principal environmental factors that influence the onset of puberty are: season of birth, level of nutrition, growth rate, photoperiod, high ambient temperatures, intercurrent diseases, and presence of the male.

Specific reference to these factors will be made in the clinical segment of the text. For the moment, suffice it to say that, as a general guideline, the stockperson should devise a management strategy in the knowledge that the onset of puberty is a labile process that is conditioned by competition between the reproductive system and the other body systems of the growing animal for energy and specific nutrients. Reproduction, particularly in the female where it involves pregnancy followed by lactation, is an energy-consuming process to which Nature assigns a relatively low priority for the prepubertal animal. Evidence is accumulating from work on a number of species that inadequate intake of energy or nutrients can depress or abolish the activities of the GnRH pulse generator in the juvenile animal. This has been attributed, variously, to deficiencies in body weight, in rate of growth, in fat content or in fat:lean ratio. There is no agreement on the particular cue(s) that inhibit(s) the pulse generator but there is general acceptance of the thesis that the function of the generator is closely coupled with energy balance and that it is allowed to progress from the juvenile to the adult level of activity in the female only when the energetic status appears to be adequate to sustain pregnancy and lactation.

Selective culling is an integral part of efficient management of the dairy herd. It can be practised successfully only when the stockperson has available an adequate number of high-quality heifers due to calve down at the appropriate time. This requires careful management of the prepubertal animal to ensure that the reactivation of the hypothalamic pulse generator is not delayed unduly by environmental influences, principally nutritional factors and subclinical diseases.

Similarly, young bulls intended for breeding purposes require careful management during the juvenile period because the onset of puberty in the male is also influenced by a variety of factors (including breed, season of birth, energy intake and liveweight gain) that affect the reactivation of the hypothalamic GnRH pulse generator.

Male physiology

In the male, puberty is associated with changes in the pattern of LH secretion, a gradual increase in the concentration of testosterone in the blood, rapid growth of the testes and the initiation of spermatogenesis. In essence, the adult pattern of GnRH release is attained and the testes proceed to fulfil two primary functions: the synthesis and release of androgens (steriodogenesis) and the production of spermatozoa (gametogenesis). In most male mammals, these functions are performed best at temperatures somewhat lower than body core temperature.

In the bull the testes are located in the pendulous scrotum, where they are attuned to function at 3-4 below core temperature. The three principal mechanisms by which the scrotal temperature is reduced are as follows. 1 Precooling of the arterial blood supply as it passes through the vascular cone in the spermatic cord. The vascular cone consists of a coiled segment of the spermatic artery that is surrounded by the pampiniform plexus of the spermatic vein. Because of this anatomical arrangement the arterial blood and the venous blood are flowing in parallel but in opposite directions; this allows for an efficient countercurrent exchange of heat between the two vessels. The net result is that the arterial blood delivered to the testes is several degrees below body core temperature. 2 Sweating from the many sweat glands in the scrotal skin. 3 Physical contact with cold ground or other cold objects.

In very cold weather, the temperature at the base of the scrotum may be up to 7 below core values but the bull can attempt to curtail the drop in temperature by drawing the scrotum closer to the (relatively) warm body wall by contracting the cremaster and dartos muscles.

The gametogenic function of the testes is much more heat sensitive that the steroidogenic function; for instance, a retained testicle in a cryptorchid animal ('rig') may secrete androgens but the seminiferous tubules will remain infantile in structure and they will not produce spermatozoa. The retained testicle has a propensity to develop neoplasms.

Morphology of the testis

The testis is surrounded by a thick fibrous capsule, the tunica albuginea, form which septa project inwards to divide the substance of the testes into lobules (Fig. 30.15). Each lobule contains one to four highly convoluted seminiferous tubules and interstitial tissue that fills the spaces between the convolutions.

The interstitial tissue contains blood vessels, lymphatic vessels, nerves and the steroid-secreting Leydig cells.

The seminiferous tubules are about 200 pm in diameter and they may be up to 70 cm long; they open at both ends into the rete testis (Fig. 30.15). The tubules contain two populations of cells: (i) a fixed population of non-proliferating somatic cells, the Sertoli cells, and (ii) a migratory population of proliferating, differentiating germ cells (Fig. 30.16).

SERTOLI CELLS

The Sertoli cells have been described as the 'backbone' of the tubule. They are columnar cells that rest on the basement membrane and extend the full depth of the epithelial layer; they envelop the developing germ cells in deep recesses in their lateral walls and, ultimately, in their luminal surfaces. The Sertoli cells continually alter shape to accommodate the morphological changes in the germ cells during their migration from the base to the luminal surface. The plasma membranes of adjacent Sertoli cells form specialized interepithelial tight junctions that extend entirely around the circumference of each cell (Fig. 30.17). These junctions constitute the epithelial component of the blood-testis barrier that precludes the passage of many substances form the blood or interstitial fluid into the lumen of the seminiferous tubule. They also divide the intercellular spaces into two compartments: the basal compartment that contains the undifferentiated germ cells and the adluminal compartment that provides the appropriate microenvironment of the more differentiated germ cells (see below).

The basal surface of the Sertoli cell has specific receptors for FSH. The cells respond to the gonadotrophin by secreting (i) a nutrient fluid that sustains the germ cells in the intercellular spaces, (ii) androgen-binding protein that binds and transports testosterone to the epididymis, and (iii) inhibin that modulates the secretion of FSH by negative feedback at the pituitary gland (Fig. 30.18). Sertoli cells also have receptors for androgens; it is known that testosterone can maintain the functional integrity of the Sertoli cell when FSH is withdrawn.

Sertoli cells are resistant to relatively high levels of heat, ionizing radiation and many toxins, e.g. cadmium, nitrofurans, cytotoxins, that destroy differentiating germ cells.

GERM CELLS

A detailed description of the process of spermatogenesis (see Table 30.1) is beyond the scope of this text. Suffice it to say that the spermatogonia are the stem cells and that they begin the process by undergoing a number of mitotic divisions in the basal compartment. These divisions produce a pool of cells that are joined to each other by intercellular bridges (Fig. 30.19).
