Archive for January, 2010


Below is the entire article on fertilisation, to see more articles like this, in full for free please visit our main site – ! Thank you !


Fertilisation is an internal process in mammals, the gamete cells however are not fully mature when they leave the gonad (either testicle or ovary) and so continue a process of maturation right up to actual fertilisation, the ovum matures fully when it undergoes its second meiotic division, the process for sperm is as follows:

  • Sperm leaving the Sertoli cell are non-motile and their DNA (located in the ‘head’ of the sperm) is not condensed, sperm are not fertile in this state.
  • It normally takes 8-15 days for sperm to mature as they pass through the epididymis
  • Over this period, certain changes occur in the membrane and nucleus of the sperm. These changes are dependent on androgens.
  • The membranes of the sperm also develop zona pellucida constituent receptors (ZP3 protein) which is important for fertilisation


Upon ejaculation sperm are deposited either in the anterior vagina or directly into the uterus. Despite billions of sperm being deposited only a few (100-1,000) sperm are considered competent (able to reach the site of fertilisation – the infundibulum of the oviduct, around 8-10 hours after ejaculation). The majority of these sperm pass into the peritoneum.

Up to 95% of sperm are expelled out of the vagina to be destroyed by macrophages. Oestradiol increases uterine activity to help passage sperm through the cervix and along the uterus. Only a small amount of sperm makes it to the isthmus, which acts in some species as a reservoir for the sperm for 24-40 hours after coitus. The sperm reach the isthmus by combination of the uterine activity and their own motility, taking around 2-7 hours. Abnormal sperm are prevented from passing any further up the female reproductive tract.

Survival times for the gametes in the female reproductive tract:

Ionic constituents such as citric acid in the isthmus inhibit sperm. This makes the sperm less motile. However at ovulation waves of sperm are periodically released into the ampulla, this is thought to be under the influence of hormonal control. At this point sperm become hyperactivated; they show exaggerated movement as they move to meet the egg influenced by a possible chemoattractant.

The fimbria (finger like projections at the end of the fallopian tube) help to move the ovum down the oviduct. Exogenous steroids (such as prescribed drugs) can affect the passage of the oocyte that is the basis of the mechanisms for the morning after pill in humans and misalliance steroid treatment in bitches.

Sperm Capacitation

Capacitated spermatozoa are ones that have undergone changes in the female reproductive tract enabling them to fertilise the ovum, this occurs in the isthmus. This process is reversible and no morphological changes occur. These changes can also be induced by simple dilation in a solution.

Capacitation occurs when there are alterations made to the plasma membrane. These include changes in the charge and the removal of cholesterol that decreases the cholesterol: phospholipids ratio.

Capacitation is responsible for the hyperactivated motility pattern, which leads to the wider and stronger beats of the tail to enhance motility.

The Acrosome Reaction

The sperm must penetrate through two layers of the ovum to fertilise it, these include the cumulus cells with their extracellular matrix and the zona pellucida. Sperm motility is important here to allow them to wriggle through the cumulus layer to reach the zona pellucida. The zona layer consists of 3 glycoproteins – ZP1, ZP2 and ZP3. ZP1 is mainly structural but ZP3 is a Ligand for the attachment of sperm and is species specific. Sperm develop a receptor for ZP3 as they mature in the male seminiferous tubules. The attachment of the sperm ZP3 receptor to the zona Ligand is responsible for the triggering of the acrosome reaction (in capacitated sperm). It is possible for non-capacitated sperm to attach but the acrosome reaction will not be induced.

Stimulation of the acrosome reaction requires an increase in intracellular Ca2+ that is induced by an ionophore – promoting rapid transport of Ca across the plasma membrane into the cell. The acrosome of the sperm cell swells and the membrane fuses with the over-lying plasma membrane. Vesicles are formed, which is followed by the removal of the outer membrane. Intracellular Ca and cyclic AMP levels increase.

After the acrosome reaction, binding of ZP2 receptors on the now exposed inner acrosome layer is essential to hold the oocyte and sperm together. The sperm is then able to work its way through the zona layer, with the aid of a digestive enzyme acrosin as well as its motility.


  • Sperm reaches oocyte and releases hyaluronidase to digest hyaluronic acid rich cumulus cells
  • The enzyme acrosin is able to digest zona layers and membranes of the oocyte
  • Sperm cell membrane fuses with the egg cell membrane
  • Contents of the acrosome head are released into the egg
  • ZP3 ligand on the ovum binds to ZP3 receptor on the sperm
  • Binding of the ZP3 components releases further enzymes which allow the sperm to fuse with the egg

Sperm and Egg Fusion

Once sperm have made it through the zona layers and into the peri-vitalline space, the sperm head aligns away from the oocyte DNA to avoid complications arising. Sperm movement ceases and microvilli on the surface of the ovum interact with the sperm. This results in a change in electrical charge on the vitalline membrane resulting in hyperpolarisation.

Zygote Activity

The next steps of fertilisation ensure a diploid nature of the forming embryo and the prevention of polyspermy or meiosis.

Immediately after sperm and egg fusion intracellular Ca levels rise dramatically. This causes cortical granules to release their contents into the peri-vitalline space that disrupts the ZP receptors and prevents further binding by any other sperm. The increased Ca also activates secondary oocyte meiotic division.

Sperm head proteins decondense and a few hours after fusion, membranes form around each set of gamete haploid DNA to form two pronuclei. The pronuclei approach each other, the nuclear envelopes disappear and the two chromosome sets aggregate in prophase – this completes the process of fertilisation as the zygote can now begin mitotic division.

The majority of zygote cytoplasm comes from the oocyte and so even after vesicle membrane breakdown oocyte DNA dominates. Successful fertilisation requires the correct formation of proteins from the oocyte, most of which would have formed when the oocyte was still in the follicle – correct follicular growth is therefore important for successful fertilisation.

Mitosis of the zygote continues – cell cleavage results in the formation of blastomeres that are large cells. When the zygote is 8-cells large, the embryonic genome becomes active and it begins to synthesise its own ribosomal RNA. It is believed that cell differentiation occurs at the 8 cell stage as well, because separation of the cells at the 4 cell stage will result in 4 identical offspring, however separation at the 8 cell stage only results in a maximum of 5 identical offspring.

The zygote arrives in the uterus in the morulla or blastocyst stage still in the zona.


This article is quite short, so I have decided to include it in its entirety on the blog – but remember, if you liked what you saw here and would like to view more articles in full like this for free – navigate to You will also find a host of other links, tools and aids there, so why not head over after reading this?


Oogenesis is the female version of gametogenesis and is therefore the female equivalent of spermatogenesis. This process follows the immature, primordial ova right through to its maturation as a fertile ovum (egg).

Two processes which are important in cell division and therefore the creation of gametes (gametogenesis) are meiosis and mitosis, a quick recap on those process are shown below:

  • Mitosis – Typical cell division where the diploid (2n) chromosome number is kept. Mitosis results in the production of identical cells.
  • Meiosis – This type of cell division is usually associated with the production of gametes, it involves a reduction in the diploid (2n) chromosome count to a haploid (1n) chromosome count. Due to the occurrence of homologous recombination during crossover of genes, non-identical daughter cells are produced. Fertilisation sees two haploid cells (1n) fuse, which results in the restoration of the chromosome number to 2n.

Primordial Germ Cells

During embryonic life, primordial germ cells (the early stage sperm or ova) originate in the yolk sac endoderm where they migrate to the gonadal ridges (ventral to the lateral somites). The next step in their development depends on whether the embryo is destined to be male or female, whether the gonads are destined to be testes or ovaries:

  • Testes – Primordial germ cells migrate to the medulla of the gonadal ridge and become surrounded by mesenchymal cells to form primitive sex cords (seminiferous tubule precursors)
  • Ovaries – Primordial germ cells migrate to the cortex of the gonadal ridge. The germs cells undergo mitotic division to increase their number prior to puberty.

Stages of Oogenesis

The primordial germ cells differentiate into oogonia (s. oogonium), where by different processes they develop into oocytes. These oocytes enter interphase, undergoing meiosis until prophase 1, it is at this point all meiosis is halted, development will continue at fertilisation. All ova cells typically reach this stage before birth.

  • Oogonia (2n) undergo mitosis (oocytogenesis) forming primary oocytes
  • Primary oocytes (2n) undergo meiosis 1 (ootidogenesis) forming secondary oocytes, the primary oocytes are halted in prophase 1 of meiosis until ovulation
  • Secondary oocytes (1n) undergo meiosis 2 (ootidogenesis), remaining in metaphase 2 until fertilised

Development of Follicles

Mesenchymal cells begin to surround the oocytes, which forms the primordial follicles. These surrounding cells eventually become cuboidal to form the granulosa cells. The follicle grows as the layers of granulosa cells increases; growth of the oocyte also contributes.

Gonadotrophins such as LH and FSH stimulate further follicular growth causing a cohort of follicles to emerge as a follicular wave (from which one will become dominant and be ovulated).  Fluid spaces develop in the granulosa cell mass (antrum formation) making the structure an antral follicle. The oocyte within the follicle remains attached to one edge of the internal follicle wall surrounded by cells of the cumulus (cumulus oophorus).

At regular intervals, from the cohort of follicles that initially emerge in the follicular waves some are selected to develop – they develop larger antral spaces. From the smaller group of selected larger follicles, typically only one becomes dominant – the others undergo atresia (the process of degeneration of follicles that are not ovulated in menstrual or oestrous cycle).

The oocyte within the follicle is still at the primary oocyte stage – it is still halted at prophase 1 of meiosis. However under the influence of a gonadotrophin surge associated with the process of ovulation, the process of meiosis resumes within the oocyte. The oocyte undergoes a meiotic division to form two differently sized cells, a large secondary oocyte and the first polar body. It is at this point ovulation takes place, meiosis again halted (until fertilisation).

Upon fertilisation by a spermatozoon, meiosis resumes, the secondary oocyte undergoes a second meiotic division to again produce two differently sized cells, a large zygote (a diploid [2n] cell resulting from the fusion of two haploid [1n] cells) and a smaller second polar body. The secondary oocyte, after being ovulated, has only a short period in which it can be fertilised – resulting in the development of the embryo.

Adverse Immune Reactions

Below is the introduction and summary to this article, the full article includes information about the types of hypersensitivity (types I-IV) you can view and download it now for free at


The immune system has become adapted to ensure that ‘self’ cells are not subject to an immune attack. The body is able to do this because tolerance is developed towards self-cells, should this tolerance be broken down by some means, the host becomes subject to autoimmune attacks which can be potentially damaging.


Autoimmunity occurs when the body fails to recognise self-cells from non-self, this results in immune responses and damage to the tissue of the host. The variety of autoimmune responses can be split generally in to two groups; organ specific and non-organ specific. In autoimmune responses it is thought that either over reactive T-helper cells or deficient T suppressor cells are the cause. Autoimmunity can also be induced by reactions to a foreign antigen that then reacts with a self-antigen to invoke a response, for example infection with a minor bacteria (streptococcus) can lead to antibodies being produced against an antigen displayed on heart valves that would lead to cardiac problems. Autoimmunity is diagnosed by autoantibodies and the deliberate induction of autoimmunity has been used to control fertility and tumours (immunotherapy).


  • Autoimmunity – Inappropriate immune response to self antigens
  • Hypersensitivity – Overactive immune response to foreign and self antigens
  • Immunodeficiency – Ineffective immune response
  • Type I hypersensitivity – (IgE mediated, initiated in 2-30 minutes) Antigen induces cross-linking of IgE bound to mast cells with release of vasoactive mediators.
  • Type II hypersensitivity – (Antibody-mediated cytotoxic, 5-8 hours) Antibody directed against cell-surface antigens mediates cell destruction via ADCC or complement.
  • Type III hypersensitivity – (Immune complex mediated, 2-8 hours) Antigen-Antibody complexes deposited at various sites induces mast cell degranulation, neutrophil degranulation damages tissue.
  • Type IV hypersensitivity – (Delayed cell-mediated, 24-72 hours) Memory TH1 cells release cytokines that recruit and activate macrophages.

Female Reproductive Anatomy Questions

If you need to know about the female reproductive tract, specifically in domestic animals, then it may be worth your while taking a look at these questions. They are in .csv format meaning you can view them in excel, however if you have flashcard software such as mentalcase or gFlash+ then if you leave a comment below I shall send you the link to download them in a better format for your flashcard software!

Hope they help – 127 questions on the female from the ovary to the vestibule as well as including a summary of parturition times and lengths.

Here is the link: (Remember to right click and click Save Target As… if you want to open it in excel!)

Immunity To Tumours

The second article of the day, the introduction is to this four page article is below. If this is what you were looking for please view the full article for free at The full article includes treatments, specific cell responses and the immune mechanisms.


A tumour is a swelling of part of the body caused by abnormal cell growth, this occurs when the normal cell division process becomes unregulated and cells proliferate uncontrolled. This results in cloned cells of the original defective cell, leading to a neoplasm – a new growth of tissue in the body that is abnormal. A tumour at a single site is known as a benign tumour, it becomes malignant (very virulent or infections and prone to reoccurrence after removal) when the tumour cells spreads to further sites within the body and begins to proliferate at these sites. Secondary malignant growths distant from the primary growth are known as metastases.

Not all tumours are cancerous, cancerous cells are damaged cells of the patients body that do not undergo apoptosis (programmed cell death), this means that their growth is no longer controlled and metabolism of the cells are altered.

Malignant tumours are named according to the tissue of origin:

  • Carcinoma – Arising in the epithelial tissue of skin or internal organs
  • Sarcoma – Arising in connective tissue or other non-epithelial tissue (mesenchymal cells)
  • Leukaemia – Arising in haematopoietic cells or blood forming organs such as bone marrow to produce abnormal leukocytes, these also suppress the production of normal blood cells
  • Germ Cell Tumours – Arising in reproductive tissues
  • Blastoma – Arising in embryonic tissues
  • Lymphoma – Arising in the lymph nodes

An early stage malignant tumour is called a premalignant tumour; premalignant tumours and benign tumours can often be treated with surgery alone. With malignant tumours this become much more difficult and other methods must be used in conjunction.



Luteolysis is the degradation of the corpus luteum (as opposed to luteinisation – the formation of the corpus luteum). Luteolysis occurs in the absence of pregnancy, at the end of the luteal phase. The process of luteolysis is initiated by oxytocin (secreted by the corpus luteum) and prostaglandin F2a in domestic animals.


Progesterone is produced by the corpus luteum, which inhibits the hypothalamus (the hypothalamus secretes GnRH, therefore progesterone inhibits GnRH secretion). The corpus luteum also secretes oxytocin.

Initially the oxytocin appears to have no effect, however after a short period of time (e.g. 12-15 days in the cow) oxytocin receptors begin to form. When these oxytocin receptors are stimulated by the oxytocin secreted by the corpus luteum, prostaglandin F2a synthesis and secretion by the endometrium is stimulated.

Prostaglandin inhibits the production of progesterone (which is inhibiting the GnRH secretion and thus preventing the emergence of new dominant follicles). If progesterone production is inhibited then the oestrous cycle is able to begin again.

Prostaglandin also stimulates further oxytocin release, stimulating more oxytocin receptors that cause further prostaglandin F2a release. This is known as a positive cascade system and is used to quickly progress a biological situation, here the situation would be the prevention of inhibition of progesterone (which is inhibiting GnRH secretion).

The reduction of plasma progesterone concentration means follicular growth can now continue and dominant follicles can now emerge. In pregnancy, there is no corpus luteum formation (luteinisation) so there is no luteolysis – therefore progesterone levels remain high.


  1. Corpus luteum produces progesterone and oxytocin – progesterone is inhibiting GnRH secretion
  2. Oxytocin receptors form
  3. Stimulated receptors cause prostaglandin F2a by endometrium
  4. Prostaglandin inhibits the secretion of progesterone and stimulates further oxytocin release
  5. Positive cascade system rapidly increases plasma prostaglandin concentration
  6. Progesterone levels are low again and GnRH secretion resumes
  7. Follicular development begins again, ready to repeat the oestrous cycle