The Ebola Virus: What is it actually?

The Ebola Virus has been getting a lot of news coverage recently with a massive outbreak in West Africa. As of March this year the death toll is the highest of any Ebola outbreak ever recorded. The exact number is still increasing, but over one thousand individuals have been exposed with causalities now around 800 (Sender, 2014). Obviously this virus is deadly and scary, but what exactly is it? My family and I were discussing these outbreaks over dinner, and I thought that a great way to learn about it is to do some research.


Firstly, the Ebola virus causes Ebola virus disease (EVD) or Ebola haemorrhagic fever (EHF) in humans. It is part of Genus Ebolavirus and the Filoviridae family. The Genus Ebolavirus consists of five distinct species:

  1. Zaire ebolavirus (EBOV)
  2. Bundibugyo ebolavirus (BDBV)
  3. Reston ebolavirus (RESTV)
  4. Taï Forest ebolavirus (TAFV)
  5. Sudan ebolavirus (SUDV)

Not all of these species are dangerous to humans. However, BDBV, EBOV and SUDV are all associated with mass outbreaks of EVD in Africa. Out of these three, EBOV is the most deadly. According to the World Health Organisation (World Health Organization, 2014) the RESTV species can infect humans, but they do not cause severe illness or death as is the case with the other three. Since 1994, EBOV and the TAFV species has infected chimpanzees and gorillas (WHO, 2014). Outbreaks of severe EVD have also been found in macaque monkeys in the Philippines in 1989, 1990 and 1996. Not only do outbreaks in non-human primates cause concern for them, but it also creates concern that one day EVD in humans can be brought on by the TAFV species.

EVD in humans first appear in 1976 in Western Africa. The virus occurred in two simultaneous outbreaks in two different villages, in Nzara, Sudan and Yambuku, Democratic Republic of Congo. The outbreak in the DRC fell along the Ebola River, hence the name.


As mentioned above, the Ebola virus is a virological taxon part of Genus Ebolavirus. The Ebola virus, as an acellular virus, replicates through a host cell. The virus attaches itself to the host cell’s receptors through glycoproteins. Then it fuses its own viral membrane with the cell’s membrane. This fusion process allows the virus to release its nucleocapsid (which contains the virus’ genetic material) into the cytoplasm of the host cell. Using the cellular machinery of its host, the virus creates viral proteins and then as the protein levels rise, new nucleocapsids are also created (Noda et al. 2006). As the new genetic material rises in number, budding occurs. Budding is where the virus, creates an “envelope” using the host’s cell membrane. Essentially, creating a new virus from the host itself (ibid). Eventually, as more and more viruses are created from the host, the host will be destroyed.

Ultimately, the number of viruses in the body begins to wreak havoc. In humans and other primates, the virus eventually causes extreme haemorrhagic fever and in most cases, death.


Ebola is transmitted to humans through contact with infected bodily fluids (ie. blood, secretions). Contact can be direct through broken skin or mucous membranes or indirectly with environments contaminated with the fluids.The incubation period (2 to 21 days) means that people can get infected by a person that does not even know they are ill. It is natural that family and friends want to mourn their recently deceased loved ones; however, the mourning process can become a high risk activity. Often, the burial ceremonies involve direct contact with the deceased person before the virus has died. In other words, healthy individuals are being infected by their infected, deceased loved one (WHO, 2014). Other common ways Ebola is transmitted is through recovered individuals and working in the healthcare field. Any one that has sex with a man recovered from Ebola can become infected from their semen. The semen carries the Ebola virus up to seven weeks after recovery, hence the man will feel healthy, engage in sexual activity and unknowingly, infect others (WHO, 2014). Healthcare professions are at high risk when the proper sanitary precautions are not enforced or possible. Lastly, people that work with infected primates or pigs can also become infected with the disease; however, the likelihood lesser than contact with a diseased human. As stated above, not all viruses that have infected animals are capable of causing EVD in humans.

Currently there is debate that fruit bats, in particular genera Hypsignathus monstrosus, Epomops franqueti and Myonycteris torquata are natural hosts for Ebola. This hypothesis is based on an overlap between the EVD outbreaks and the geographic distribution of fruit bats in Africa.

Symptoms and Diagnostics

A major concern when treating Ebola is that it carries symptoms similar to many other diseases. According to the World Health Organisation (2014) “malaria, typhoid fever, shigellosis, cholera, leptospirosis, plague, rickettsiosis, relapsing fever, meningitis, hepatitis and other viral haemorrhagic fevers” all need to be ruled out. Of course with equipment available in the Western world, this process is quite simple. Ebola can be precisely diagnosed by running a variety of diagnostic tests including but not limited to electron microscopy, antigen detection tests and virus isolation by cell culture (WHO, 2014). These diagnostic tools can rule out other disorders by checking for low white blood cell and platelet counts plus elevated liver enzymes (WHO, 2014).

In Africa, however, these diagnostic tools are not always available. Therefore, it is important that the symptoms are clearly laid out and understood. EVD causes “severe acute viral illness” with symptoms including headache, muscle pain, weakness, fever and sore throat. These initial symptoms then progress into vomiting, rash, diarrhoea, reduced kidney and liver function and sometimes internal and/or external bleeding.

Treatment and Prevention 

Currently there is no vaccine for EVD despite many being tested. Those infected with EVD are being treated with various drug therapies, which are always being improved and remedied. Until a vaccine or a truly efficient treatment has been discovered, patients with EVD are being treated in intensive care where they are holistically cared for, keeping them hydrated through IV with an electrolyte solution.

As the mortality rate for Ebola is so high (as high as 90%) the best way to treat Ebola is to prevent it from happening in the first place (BMC, 2014). In other words, the best way to handle Ebola is to prevent it. For the general public this means educating them on how the disease is transmitted, teaching them proper sanitation procedures and providing them with ways to keep clean and safe such as making condoms and cleaning products readily available.

For more information do your own research or check out some of the websites in my bibliography.

Thank you for reading!





Assembly and Budding of Ebolavirus. (n.d.). Retrieved August 6, 2014, from

Ebola virus. (2014, May 8). Retrieved August 6, 2014, from

Ebola Virus. (2014, August 4). Retrieved August 6, 2014, from

Ebola Virus. (2014, June 17). Retrieved August 6, 2014, from

Ebola virus disease. (2014, April 8). Retrieved August 6, 2014, from

Ebola virus disease. (2014, April 1). Retrieved August 1, 2014, from

Ebola virus disease. (2014, January 1). Retrieved August 6, 2014, from

Noda, T., Ebihara, H., Muramoto, Y., Fujii, K., Takada, A., Sagara, H., … Kawaoka, Y. (2006, September 29). Assembly and Budding of Ebolavirus. Retrieved August 6, 2014, from Noda, T., Ebihara, H., Muramoto, Y., Fujii, K., Takada, A., Sagara, H., … Kawaoka, Y. (n.d.). Assembly and Budding of Ebolavirus. Retrieved August 6, 2014.

Sender, H. (2014, July 31). Where Is The Ebola Virus? Outbreak Map Shows Virus Deaths In West Africa. Retrieved August 6, 2014, from

Depression: Symptoms, Aetiology and Treatment Options


Depression is a serious affective disorder that affects millions of people in the world, approximately 5% of the population. In the United States alone approximately 33 million people will suffer from depression at some point in their life (Bear, 2007). In addition, the disorder is the leading cause of suicide. Despite its high prevalence, however, stigma still also remains high. A primary reason for the stigma surrounding any mental disorder is a misunderstanding of the symptoms and causes.


Even though depression strikes people differently, the cardinal symptoms are lowered mood and feelings of dejection, a lack of pleasure or interest rather than sadness. Accompanying symptoms include changes in appetite, fatigue, insomnia or hypersomnia, diminished concentration, feelings of worthlessness and/or guilt and recurrent thoughts of death and/or suicide (Bear, 2007). Depression can be one half of bipolar disorder but also occur on its own and in varying degrees of severity. Usually, for a diagnosis of major depression, the cardinal symptoms of depression must be present every day for approximately 2 weeks. Importantly, the cause of depression cannot be linked to a bereavement. This clear distinction is what separates depression from sadness.

Types of depression include chronic depression of dysthymia, major or clinical depression, atypical depression and manic depression. Chronic depression or dysthymia is usually less severe than major or clinical depression; however, it can be more disabling in that the symptoms are long-term (2 years+) or recurrent throughout a lifetime. Major or clinical depression is more severe; however, the symptoms do not last longer than 2 years and is not typically recurrent. Approximately 17% of sufferers have chronic symptoms.  It is important to note, however, that when depression is left untreated, recurrence is far more likely. Manic depression is found in bipolar disorder, to find out more click here. Finally, atypical depression is when a person suffers from the accompanying symptoms rather than the cardinal symptoms.

Aetiology and Treatment Options 

Biological basis 

Affective or mood disorders such as depression alter the typical function of the brain. Many different parts of the brain are usually affected at the same time, but the major system involved is the hypothalamic-pituitary-adrenal system (HPA). Exaggerated activity in the HPA system is common in people with anxiety and affective disorders. Specific to depression, blood cortisol levels are heightened as is the concentration of corticotropin-releasing hormones (CRH) in the cerebrospinal fluid.

Monoamine hypothesis

The monoamine hypothesis of depression states that a deficit in monoamines causes mood disorders. Monoamines include serotonin and catecholamines (inc. dopamine, noradrenaline, norepinephrine).  Current anti-depressants focus on this theory of depression. Anti-depressants inhibit the re-uptake of of monoamines, increasing the concentration of them in the synaptic cleft. The great benefit of anti-depressants is that they promote long-term, adaptive changes in the brain reducing the possibility of another depressive episode. Unfortunately, not all depressed people find anti-depressants effective. This can mean that either the treatment does not work for them at all or they require a greater dosage. Furthermore, it can takes week for depressants to take affect. Lastly, anti-depressants can raise levels of norepinephrine, which makes anti-depressants less effective. As anti-depressants are not always effective,  patients with prolonged depressive episodes may seek alternative treatment. Electroconvulsive therapy (ECT) and therapy are both options. ECT is mainly used in extreme cases because it can offer immediate relief. However, ECT is controversial due to the danger of memory loss. This is not surprising considering ECT is a localised seizure controlled by keeping the patient under anaesthesia. It is unknown exactly how ECT works; however, the hippocampus has been implicated. The hippocampus is involved in regulating CRH levels and the HPA system.

Types of anti-depressants include: selective serotonin re-uptake inhibitors, serotonin-noradrenaline re-uptake inhibitors, tricyclic anti-depressants and monoamine oxidase inhibitors. For people with bipolar disorder, lithium is also used to stabilise mood primarily the mania but has been shown stabilise mood overall.

Diathesis-Stress hypothesis 

The diathesis-stress hypothesis proposes that mental disorders have a genetic component that predisposes us to mental illness. Certain life stressors then makes us susceptible to mental illness actually presenting themselves. As such, traumatic childhoods full of abuse and/or neglect can leave a child at high risk for developing mental disorders. Tragically, children whose poor treatment is due to mentally ill caregivers, this cycle becomes hard to break. However, according to the diathesis-stress model, a trigger is not enough to bring forth mental illness without a genetic foundation. This genetic foundation goes hand in hand with the HPA system. Of course this does not mean that only traumatised children will suffer from mental health disorders. Individuals that have experienced a highly stressful life even such as divorce, moving away from home, changing schools, becoming ill, etc. will also be at risk are they predisposed to mental health issues.

In a healthy individual, cortisol activates hippocampal glucocorticoid receptors, which inhibit the the HPA system. However, in a depressed individual there is a flaw in the feedback system. On a molecular level there is a diminished hippocampal response to cortisol due to reduced number of  glucocorticoid receptors. Here the genetic component of depression comes into play; glucocorticoid receptors are the product of gene expression. Hence, an individual with few glucocorticoid receptors is more susceptible. Fittingly, the amount of glucocorticoid receptors are epigentically influenced, early sensory experience can alter the number as well. This means that a childhood where we are well looked after, loved, cared for, kept safe and happy can protect us from developing depression even if we disposed to at birth. This illustrates how important the interaction of nature and nurture is. Think Voldemort vs Harry Potter. Despite the traumatic death of his parents, the one year of unconditional love and Lily’s sacrifice protected him not just magically but neurologically. Interestingly, in an interview with Oprah Winfrey, JK Rowling discuss this exact point.



Antidepressants . (n.d.). Antidepressants. Retrieved July 18, 2014, from

Bear, M. F., Connors, B. W., & Paradiso, M. A. (Eds.). (2007). Neuroscience(Vol. 2). Lippincott Williams & Wilkins.

Pinel, J. P. (2010). Biopsychology (8th ed., International ed.). Harlow: Pearson Education.

What the Heck is an HPA Axis & What Does it Have to do with Stress?. (n.d.). Fibromyalgia & Chronic Fatigue. Retrieved July 18, 2014, from


Basic Nutrition: Essential Nutrients and Biosynthesis  

Our bodies rely on food for energy but also for biosynthesis. Biosynthesis is the production of complex molecules within living organisms or cells; a process necessary for self-maintenance. For example, the synthesis of protein from neuropeptides. Two necessary precursors for biosynthesis are organic carbon (such as from sugar) and organic nitrogen (such as from amino acids). For a diet to be sufficient, therefore, it must supply chemical energy, organic molecules and finally essential nutrients.

For energy, animals ingest and digest nutrients such as carbohydrates, proteins and lipids to get enough ATP necessary for cellular respiration and energy storage. Essential nutrients are ingested as precursors to complex molecules and as minerals and vitamins. Unlike complex molecules, essential nutrients cannot be synthesised from raw materials. Thus, they must be ingested.

Amino Acids and Fatty Acids

Four types of essential nutrients exist: amino acids, fatty acids, vitamins and minerals. Approximately, half of the 20 amino acids are required for humans including: methionine, valine, threonine, phenylaline, leucine, isoleucine, tryptophan, lysine and histidine. Meat, fish, poultry, dairy products are considered complete proteins because they contain all essential amino acids. However, vegans and vegetarians or even meat-eaters can get all their essential amino acids by eating a full diet consisting of beans, legumes, nuts, seeds and vegetables. Insufficient amounts of amino acids causes protein deficiency, which can be severely detrimental to healthy development. Therefore, if you stop eating meat, it is important to make sure you are eating a diet that contains all your essential amino acids.

Essential fatty acids are also required. Only two are known to be essential for human survival: alpha-linoleic acid and linoleic acid. Alpha-linoleic acid is a long-chain omega-3 fatty acid and is high in food such as salmon, tofu, shrimp, flax seeds and walnuts (fish, seeds, grains and vegetables). Linoleic acid is a long-chain omega-6 fatty acid and is found nuts, grains, cereals and poultry. Insufficient amounts of omega-3 and omega-6 contributes to impaired cellular functioning and heart disease.

Vitamins and Minerals 

The final two essential nutrients are vitamins and minerals. Vitamins come in two, organic forms: soluble and water-soluble. Fat-soluble vitamins are found in fatty foods such as animal products, vegetable oils, etc. They include vitamin A, D, E and K and are stored in our liver and fatty tissue. Deficiency in certain vitamins cause different issues (a future post will discuss this in more detail). Water-soluble vitamins, on the other hand, are not stored in the body and so need to be consumed more frequently. These means that when we urinate, these vitamins leave our body. Fortunately, that means it is hard to consume too many water-soluble vitamins. Too many fat-soluble vitamins can cause toxicity. Water-soluble vitamins include vitamin C, B and folic acid and can be found in foods such as fruit, vegetables (especially greens) and grains. As water-soluble vitamins are sensitive to heat and air, boiling can destroy the vitamins. Foods high in fat-soluble vitamins are far more durable.

Minerals on the other hand are inorganic and include calcium, iron, phosphorus, magnesium, sulphur, sodium, potassium and chloride. Minerals also come in two forms: macro or major minerals and trace elements. Macrominerals include electrolytes and the body stores about 5 grams of each one on hand. In order to stay healthy, a person to consume about 100mg a day to maintain the 5 gram store and equalise the loss. Trace elements are found in much smaller quantities, hence their name and include iron, zinc, iodine, selenium, copper, manganese, fluoride, chromium and molybdenum. Minerals are essential because they serve as reinforcers for bone growth, strong teeth, maintaining homeostasis and synthesising energy from food. A great source of minerals is from plants such as fruits, vegetables and nuts as they get minerals directly from the soil they grow in. Grains, meats, cereals, dairy, etc. also contain minerals but in a diluted amount due to processing or because they have already been used by the animal itself.

All in all, a proper diet needs to incorporate all essential nutrients for proper health and functioning.


Campbell, N. A., & Reece, J. B. (2008). Animal Nutrition . Biology (8th ed., ). San Francisco: Pearson, Benjamin Cummings.

Rinzler, C. A. (2006). Nutrition for Dummies (4th ed.). Indianapolis, IN: Wiley Pub.

Vitamins and minerals . (2012, November 26). . Retrieved June 24, 2014, from

Basic Cellular Anatomy

All cell functions are limited by their size as they must house the organelles essential for life: DNA, protein molecules and internal structures. Even these smallest cells must also have enough surface area to respirate, obtain nutrients and dispose of waste materials. 

Prokaryotic cells evolved far earlier than eukaryotic cells, and as such present day prokaryotes have a different cellular anatomy. The most common type of prokaryotes are Bacteria and Archaea, and their key features are as follows:

  1. Organelles in the cytosol are not membrane-bound. 
  2. Chromosomes are grouped in the nucleoid with no nuclear membrane. 
  3. Prokaryotes are much smaller cells. 

Eukaryotes including animals, fungi, plants and protists also have defining characteristics. 

  1. All organelles are membrane-bound. 
  2. Chromosomes are found in a membrane-bound nucleus. 

Regardless of which category a cell falls into, all their organelles are organised into four basic functional groups: support, hydrolysis, energy and manufacturing. 



The plasma membrane (PM) forms the boundary for the cell. In animal cells, the plasma membrane is the second outermost player; however, in plant cells, this membrane is reinforced by the cell wall. The most important characteristics of the PM is its selective permeability. Composed of a phospholipids, proteins and carbohydrates, the PM regulates transportation across the cell. Non-polar substances such as oxygen gas and carbon dioxide can easily permeate the thin layer. Other substances require more active transportation involving the embedded proteins. 

The cytoplasm contains cytosol and suspends all the organelles. In addition, it gives the cell its shape. 

The cytoskeleton reinforces the shape of the cell and helps move the cell. It consists of a network of fibres that run through the cytoplasm. The three fibres that make up the cytoskeleton include microfilaments, intermediate filaments and microtubules. 

  1. Microfilaments: composed of actin; the smallest; when paired with myosin, is involved in movement
  2. Intermediate filaments: medium sized; permanent cellular fixtures; help maintain the shape of the cell and the placement of organelles 
  3. Microtubules: largest; made of tubulin; shape and support the cell; serve as tracks for the movement of molecules in the cell; separate chromosomes during cellular division 

Mircovilli are tiny projections that help increase the cells surface area. 

The extracellular matrix (ECM) of animal cells wraps around the plasma membrane, and is composed of glycoproteins (like collagen) secreted by the cell. The ECM helps strengthen tissues and transmit external stimuli into the cell that tun genes on and off to modify activity. 

Centrosomes are regions in the cell where microtubules initiate. In animal cells, the centrosomes contain a pair of centrioles. 

Found only in plant cells, the cell wall forms the outermost layer. Made up of polysaccharides (including cellulose) and proteins, it is much tougher and less pliable than the plasma membrane. However, it helps plants stand upright in the correct shape. 

Also only found in plant cells, plasmodesmata are channels that run through the cell wall. They help connect the cytoplasms of adjacent cells. 

Flagellum and cilia are locomotive organelles found in some animal cells. They are hair-like projections composed of membrane inclosed microtubules. Examples of animal cells with flagella and cilia: sperm (flagella), cells in the digestive tract (cilia), cells in the trachea (cilia). 



Lysosomes are digestive organelles that hydrolyse (breakdown with water) macromolecules like proteins, carbohydrates and nucleic acids. Hydrolysis breaks down these macromolecules into monomers that are then released and recycled. A cell is threatened by a burst lysosome as they are very acidic. 

Vacuoles are only found in plant cells and take up a large deal of space in the cell. Their prominent role is storage and breakdown of waste products and hydrolysis of macromolecules. Older cells will contain larger vacuoles, suggesting that vacuoles play an important role in plant growth. Some plant cells can be 80% vacuole. Tonoplasts encompass the vacuoles. 

Peroxisomes are organelles with a variety of metabolic functions including hydrolysis of macromolecules (mainly large fatty acid chains). The broken down fatty acids fuel mitochondria. Another role of peroxisomes is to detoxify alcohol. A waste product produced here is hydrogen peroxide, which is toxic to the body. Fortunately, peroxisomes also contain catalase, which breaks down the acid into water or another neutral compound. 



Mitochondria are the cite of cellular respiration and generation of ATP. Mitochondria are unique that they have a double-membrane called with infolds called cristea and also because they have their own DNA called mDNA. Almost mDNA is exclusively inherited through our mother because male mDNA is usually destroyed during conception. In addition to its own DNA, mitochondria also contain enzymes and ribosomes. All of these additional components are found in the matrix and catalyse respiration reactions to produce ATP. 

Chloroplasts, found only in plants and algae, are the site of photosynthesis. 



The nucleus contains the majority of the cell’s DNA, and is the cite of messenger RNA (mRNA) synthesis. mRNA contains the code for protein synthesis outside of the nucleus. Surrounding the nucleus is the nuclear envelope, which contains nuclear pores that allows mRNA to leave the nucleus. The complex of DNA is called chromatin. Whenever a cell prepares for cell division, fibres of chromatin coil up into chromosomes. 

Ribosomes are the final location for mRNA and the site of protein synthesis. Ribosomes come in various sizes and locations. They can be free floating in the cytoplasm or attached to the rough endoplasmic reticulum (ER). Free floating ribosomes are responsible for synthesising proteins that are used in the cell. Ribosomes attached to the rough ER synthesise proteins for export or use in the cell. 


The endoplasmic reticulum comes in two forms: smooth and rough. The ER makes up the largest component of the cell and consists of a network of membranes and sacs. The inner portion of the ER is called the cisternal space. The smooth ER synthesises lipids, metabolises carbohydrates and detoxifies drugs and poisons. As proteins are synthesised by the ribosomes attached to the rough ER, the polypeptide chains travel across the membrane and into the cisternal space. Here, the polypeptides are concentrated to be packaged into transport vesicles and shipped to the Golgi apparatus. 

The Golgi apparatus modifies incoming transport vesicles and then repackages them and ships them out again. The Golgi apparatus has polarity, a cis and trans faces. The cis face receives and the trans face ships. 



Tight junctions are sites were two neighbouring animal cells are fused so tightly that they are water-tight. 

Desmosomes fasted animal cells together with intermediate filaments. This anchoring also gives them the name anchoring junctions. These types of IC junctions are common in tissues subject to stress such as muscles and skin. 

Finally, gap junctions provide channels between animal cells for the movement of ions, sugars and other small molecules. Gap junctions are found in embryonic and heart tissue. 


Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. Peroxisomes. Available from:

Reece, Jane B., and Neil A. Campbell. Biology. San Francisco: Pearson Benjamin Cummings, 2008. Print.


The Four Humours

Claudius Galenus was a Greek philosopher and physician who practiced medicine among the Romans circa AD 160. Galen brought the approach known as Humourism to the mainstream. Humourism is a philosophical theory originating from he Greek philosopher Empedocles who implied that all things are combinations of the four basic elements: earth, water, fire and air. 

Earth: cold and dry

Air: warm and wet

Fire: warm and dry

Water: cold and wet

However, Galen like the father of modern medicine, Hippocrates, believed that these basic elements were mirrored in corpus. Hippocrates stated that the qualities of the four elements are reflected in our bodily fluids namely blood, phlegm, yellow bile and black bile. They both set about classifying illnesses in terms of excess of these fluids (Mukherjee, 2010). 

Excess blood: prompted inflammation: red, warm, painful.

Excess phlegm: prompted “tubercles, pustules, catarrh and nodules of the lymph” (ibid): cold, white, soggy, heavy. 

Excess yellow bile: prompted jaundice: yellow. 

Excess black: prompted depression (or melancholy, literally black (melass) bile (khole) and cancer: oily, viscous, dark. 


Cancer was believed to be the static form of black accumulating into a solid mass (ibid), whereas depression was viewed as the excess of fluid black bile circulating through the system. 

Galen explored this the approach of Humourism further, expanding into a theory of personality. Galen saw a direct relationship between the levels of the humours in the body and the emotional and behavioral inclinations known as temperaments. He described these temperaments as sanguine (blood), phlegmatic (phlegm), choleric (yellow bile) and melancholic (black bile). Imbalances in the humours determined personality as well as susceptibility to certain illnesses. Unfortunately, this interesting yet erroneous belief about illness continued beyond Galen’s death in AD 199. Medicine focused all curative and therapeutic efforts in Galen method. Surgery was thought pointless as the humour would only flow back. 

Galen’s falsely held beliefs about anatomy stood uncorrected until Andreas Vesalius’s attempts to confirm his heroes hypothesis disconfirmed it. Due to Vesalius discontent with the state of anatomical training at the University of Paris, he began to his own exploratory autopsies (ibid). These exploratory autopsies on the bodies left at the city gallows and in poorly covered graces, revealed to Vesalius that the possibility of Galen’s theories were non-existent. Blood, yellow bile and phlegm were found aplenty but black bile (the corner stone to Galen’s theory) was no where to be found (ibid). Vesalius’s discoveries and intricate anatomical drawings soon shattered the idea of humourism, opening up the doors to effective treatment. 


The theory of Humourism, did not however completely disappear. In fact, in psychology a major theory of personality still owes its root to the Greek physicians.

If one of the humours developed uncontrollably, becoming obviously dominant to the other three humours, the corresponding personality type would also become dominant. As a paradigm, a sanguine person has too much blood and as a result shows characteristics such as cheerfulness and optimism but can be selfish and overconfident. A phlegmatic person suffers from too much phlegm and would be rational and consistent but often slow and quiet. A choleric person suffers from too much bile and would be passionate and energetic but could also be tempered. Finally, a melancholic person suffers from excess bile and would be characterised as the artists, poetic and artistic but often depressed and fearful.

During Galen’s time, the Medieval Ages and up until the Renaissance it was considered accurate that certain people were born predisposed to one of the four temperaments and imbalances could be cured by changes in diet, exercise or the extremes of purging and blood-letting. By the 1500s, hundreds of errors were found in Galen’s work but he would later come to influence Hans Eysenck that concluded that temperaments are in fact biologically based but not through humours. Eysenck identified two personality traits he called neuroticism and extraversion, a nod to Galen.


Collin, Catherine. The Psychology Book. New York: DK Pub., 2012. Print.

Mukherjee, Siddhartha. The Emperor of All Maladies: A Biography of Cancer. New York: Scribner., 2010. Print. 

Maps and Infinite Homuncular Regression

Although maps provide an excellent structural representation of what is going on the brain, in themselves they have no intrinsic value (Deacon, 2012). Maps do not really tell us about how the brain is interpreting or processing the information, only how it stores and forwards the information. To be fair, even that is only based on visual interpretation not on concrete behaviour. Unfortunately, that brings up the issue of whether or not topological maps are of any value. The retinotopic map may just be a consequence of development and evolution, an attempt to minimise wiring of the brain. Deacon (2012) stresses that there is massive flaw with the current use of mapping; he summarizes it as the ‘infinite homuncular regression.’ Basically, we have come to a point where other maps are just reading maps. The actual perceptual neurology has not been determined. Deacon warns scientists of the dangerous of neuroimaging and maps when trying to prove the existence of neural activity and behaviour. All this boils down to really is the classic argument in psychology; correlation does not prove causation.

Fortunately, Graziano and his colleges (2009) suggest that perhaps a homunculus does exist that can bridge perception and behaviour: the motor cortex. To put it plainly, a motor homunculus represents the sensitivity and innervation dedicated to particular muscles in our body. This homunculus can be mapped onto our motor cortex, and stimulation of these regions leads to an immediate motor response. Hence, we can bridge the gap between map and action. In other words, the motor cortex may in fact put an end to the infinite homoncular regression. A recent study carried out by Bouchard et al. (2013) found that when participants vocalised constants and vowels, scans showed smooth trajectories in the motor cortex.

Extra-Striate Visual Areas

Due to the heavy burden of the packing problem, the brain alleviates some responsibility of off-loading information to the extra-striate visual areas. These areas are specialised for particular visual data. Colour information is relayed to V4, motor information is relayed to V5, and lastly, object

Secondary visual cortex: V2

The secondary visual cortex envelops V1 and is organised into parallel stripes running perpendicular to the V1/V2 border. Stripes that respond to the same region of the retina run adjacent to each other, preserving the retinotopic map. These stripes come in three types: thick, think and pale. Pale stripes are known as interstripes as they run between thick and thin stripes. Input is fed to the pale stripes from the hypercomplex cells of V1, and it is then forwarded to the LGN via the parvocellular layer. The main job of the pale stripes is to respond to oriented lines. Secondly, thick stripes receive input from layer 4B of V1 and respond to specific orientations as well as cells of binocular disparity. Output from the thick stripes is passed onto V5 via the magnocellular pathway. Lastly, thin stripes receive inputs from colour blobs of V1, hence they are sensitive to colour or brightness. Output from the thin strips project to V4 via the parvocellular stream.


V4 is the colour area, and cells here respond to colour, simple shapes and objects. As colour does not have its own parameter, it does not have an accurate retinotoic map. As such, V4 serves as the first indication of decline in retinal location and the rise of feature based primary indices.


As mentioned above, the thick stripes of V2 project to V5. V5 is known as the motor areas it responds to motion and stereo disparity. Non-spatial parameters are beginning to take precedence over maintaining the retinotopic map as it is no longer maintained here. Zeki (1990) confirmed the hypothesis found when he found that paths across the retina become more chaotic the further they are from the striate cortex.

The Inferotemporal Cortex

Each point of the inferotemporal cortex represents a different view of a face. Despite the highly abstract parameter, nearby cells represent similar views of the face. Over the past years, there has been discussion over whether inferotemporal cortex cells are grandmother cells. The inferotemporal cortex was monitored while a patient was shown various faces; one cell seemed to respond only to pictures of Jennifer Aniston of Friends (Connor, 2005). Nearby cells did not seem to respond to different views of Jennifer Anniston, but they did respond to characters from the same shows. These findings suggest that nearby cells represent many parameters that occur nearby in time. The temporal proximity of views experienced in everyday life may be reflected in the physical proximity of cells in the cortex.

Seeing Objects

Binocular disparity is the subtle difference between the left and right images. The left eye sees more of the scene than the right eye to the left of the centre and vice versa. Neighbouring layers responding to the left and right eye can inhibit one another when necessary. Optic nerves from the eye join at the optic chiasm and some of the fibres decussate. Optic nerves contain axons that emanate from retinal ganglion cells in the eye.  Regardless if the fibres decussate, all the fibres pass through the lateral geniculate nucleus. From the lateral geniculate nucleus, fibres feed into the striate cortex. Importantly, the striate cortex preserves the neighbourhood relations between the retinal ganglion cells. In other words, the striate cortex has a retinotopic map. The map is stretch and magnified around the fovea, which is consistent with the quality of foveal vision. Also the quality reflects the number of cells dedicated to this part of the retinal patch.


Types of Retinal Ganglion Cells

First, the midget retinal ganglion cells are the most common, making up about 80%. These cells respond to static form and project to the parvocellular layer of the lateral geniculate nucleus, specifically bilayers 3 through 6. Second, the parasol retinal ganglion cells consist of 8-10% of all retinal ganglion cells.  These cells contain on/off receptive fields and receive their light input from rods. As expected, they respond to increases and decreases in light conditions. In addition, they also respond to motion. Output from the parasol retinal ganglion cells project to the magnoceullar layer of the lateral geniculate nucleus, specifically to bilayers 1 and 2. Thirdly, the bistratified retinal ganglion cells make up less than 10% of all retinal ganglion cells. They respond to short (blue) wavelengths by increasing their frequency rate and to middle wavelengths (yellow) by decreasing their frequency rates. Output then projects to the konio sublayers 3 and 4. Lastly, the biplexiform retinal ganglion cells are equally rare making up less than 10%. The exact function of these cells in unknown, but it is known that they connect directly to rods and contain on-centre receptive field. It is believed that they provide information about ambient light.

Features of the Lateral Geniculate Nucleus

The nucleus consists of six major layers; each layer has a major layer plus a konio cell sub-layer. Each layer is responsible for carrying information from one eye. All of the layers of one lateral geniculate nucleus receive input from half the visual space. Even though layers 2, 3 and 5 correspond with the left eye, they only receive half of the information of the retina in that eye; the other half corresponds to the right visual field. As with the striate cortex, cells in each layer are organised retinotopically. In addition, each layer encodes a different aspect of the retinal image. Each lateral geniculate nucleus contains twelve copies of half the visual field (2/bilayer). However, it is important to note that only 10% of inputs come from the retina. 30% of input comes from outputs including the striate cortex and the midbrain. Thorpe (1996) proposed that the brain uses feed forward connections of retina to lateral geniculate nucleus to striate cortex to perform “quick and dirty” analysis. Feedback then makes connections to the retinal image. Thorpe’s hypothesis is supported by his demonstration that people can make quick visual interpretations from briefly flashed images. 

The Striate Cortex (V1)

The striate cortex is responsible for early feature detection representations including colour. Stimulation of the striate cortex produces hallucinations of swirling colour (Frisby and Stone, 2010). In additional, all cells in the striate cortex have orientation-tuned columns except for layer 4B. The LGN and retinal ganglion cell are not orientation-tuned like the striate. Like the lateral geniculate nucleus, however, it is organised in layers: horizontal, vertical and retinotopy. The top layer of V1 contains pyramidal cells and their dendrites. On the other hand, the bottom layer of V1 contains pyramidal cells as they exit the cortical layer. Neurons in these layers are arranged into vertical columns with each column dedicated to one retinal patch and a specific characteristic. Retinal progress decreases the further you move from the edge of V1.

In 1978 a study was carried out by Hubel et al. to illustrate the existence of orientation-tuned cells in the striate cortex. Anesthetized macaque monkeys had their eyes exposed to a pattern of vertical stripes, continuously for 45 minutes. The stripes were of irregular width, filled the entire visual field, and moved about to activate the entire striate cortex. A chemical was then injected to be taken in by any active cells. Immediately afterwards, an autopsy was performed, which showed increased chemical uptake in the vertical columns.

Now these orientation-tuned columns are called hypercolumns. Each hypercolumn contains a mass of different types of cells that together process the same retinal patch. The patch of the retinal image that each hypercolumn deals with is called the hyperfield. Hyperfields must overlap to some degree, which allows for edge features to be detected (Frisby and Stone, 2010). As well as overlap, inter-hypercolumn communications links edge features together to create on unified image. This communication is possible due to the horizontal fibres that run along the vertical columns.  The area dedicated to a particular area remains quite constant; however, processing decreases the further you move from the centre, which is why feature detection becomes cruder the further you move into the periphery. In addition to orientation, these cells can also be tuned to colour, scales and ocularity (Frisby and Stone, 2010). The ice-cube model (Hubel and Weisel, 1962) argues that each hypercolumn functions as an image-processing mechanism.

Convultion images are used to give us an idea about the activity profile of the striate cortex, representing the output of simple cells (Frisby and Stone, 2010). Each point on a convultion image represents the response of a single simple cell, which is centered over the corresponding retinal image. White represents a large, positive output. Grey represents no output, and black represents a large negative output. Based on this scale, outputs are coded in terms of pixel grey level. Inside a hypercolumn is a pattern of activity corresponding to one area (point) of the convultion image, an area representing the hyperfield (ibid).

Complex Cell

Unlike simple cells, complex cells cannot be mapped into positive and negative regions. An optimal stimulus does not need fall on any particular region of the retinal field. However, a line or slit of a particular orientation is still the preferred stimulus. A theory of complex cells and receptive fields has been proposed (Frisby and Stone, 2010). This theory proposes that the receptive fields of complex cells can be predicted supposing they receive their input from a series of suitably placed simple cells. However, this theory cannot be true because some complex cells do not even receive input from the striate cortex.

Hypercomplex or “end topped” cells cannot be mapped into positive or negative regions either, but unlike simple and complex cells, they prefer moving stimuli. In addition, hypercomplex cells are selective to stimulus length. Of all stimuli, the best is either a bar of defined length or a corner.

Seeing Maps

A quintessential aspect of brain maps is differential magnification of various regions of the sensory map. The striatal cortical map of the retinal image has five  important properties (Frisby and Stone, 2010). First, the striatal cortical map has a continuous mapping of retinal points to corresponding cortical points. Second, the cortical representation is upside down. Thirdly, the cortical representation of the visual scene is cut down the middle. Each hemisphere processes half the visual field except for the central strip, which is processed by both halves. Fourthly, the cut in cortical representations places similar regions of the scene the furthest apart in the brain. Lastly, map contours intersect and right angles. 

All maps, whether they are used in the brain or not, represent a mathematical function (v = f(u)) transforming one points in space (the domain, u) to another (the codomain, v). For a map to be accurate, it must be continuous, without any breaks. Also, every pair of nearby points must correspond to two nearby points in the codomain. For example, take the cities Sheffield and Leeds. They represent two geographical points. For a map to be accurate, Sheffield and Leeds on a map must correspond proportionally in terms of distance, direction, etc. with Sheffield and Leeds in real life. The map of South Yorkshire would be the codomain and the real cities would be the domain. In the visual system, these points could be two retinal points (domain) accurately reflected onto the striatal cortex (codomain).  In addition, a map of the brain must specify direction. Direction here is not used in the common sense, direction refers to continuity between domain and codomain. For example, mapping from retina to the striate is actually discontinuous; however, mapping from each half of the retina to the striate cortex is continuous, giving rise to the retinotopic map. If you map against the specified direction, it is called inverse mapping. An example would be mapping from the cortex to the retina, which is discontinuous. This is because most nearby points in the striate cortex correspond to nearby points in the retina; however, if two striate points are located on different ocularity stripes, inverse mapping is discontinuous (Blasdel, 1992).

Connolly and van Essen (1984)

Connolly and van Essen (1984)

Scientists argue that the reason the striate cortex maintains the retinotopic map is because it economises the length of nerve fibres. Nerve fibres are necessary for inter-hypercolumn communication, and if neighbouring points were spread out, wiring would become chaotic.  Of course, mapping does not occur only in the visual system. The brain has a myriad of maps including ones for auditory, touch and motor output and many copies of these maps exist. All of these maps, like the retinotopic map must be continuous, suggesting spatial organisation is key to a healthy, functioning brain. Unfortunately, because there are so many features of the visual system that need to be represented in the map, singularities arise.

Singularities are jumps in continuity (Frisby and Stone, 2010), and they are the result of the packing problem. To put it simply, the brain wants to pack all features of the visual system into the brain; to maximise efficiency, the brain wants all similar variations of a feature in one place. In other words, the brain wants continuity. However, as was discussed with the binding problem, there are far too many variations and features of our visual system to account for them all in every possible detail. Hence, some continuity must be compromised (Hubel, 1981). The brain’s map of the visual system is continuous with respect to retinal position, but the map is discontinuous with respect to orientation. However, the brain still attempts to keep similar preferred orientations close together to maximise efficiency to the limited extent it can (Frisby and Stone, 2010).

Another way of thinking of singularities and the packing problem is in terms of parameters. Two points, as discussed above, define each retinal position otherwise known as position parameters (x, y). Correspondingly, each retinal point must correspond to a point on the cortex (x’, y’). Even though our cortex exists in three dimensions, there is still a finite amount of space to store information and parameters limit us to representing information in 2D. As orientation brings its own parameter (theta), the brain has to represent x, y and theta in 2D.  This cannot be done without introducing discontinuities in at least one of the parameters because we are limited to two parameters. As the cortex must maintain a smooth map of the retinal map, discontinuities must be introduced into the representation of orientation. Based on this information the packing problem can be redefined in terms of parameters. The packing problem arises from attempting to pack all three dimensions of a 3D parameter space into a 2D one. As a solution to the packing problem, the cortex treats two of the parameters with varying priority, in this case the domain and codomain. Low priority is given to orientation, hence singularities.


As singularities exist for orientation, the topological index was introduced to describe the number of singularities. Specifically, the index tells us how orientation varies as we move around the centre of a singularity (Frisby and Stone, 2010). This can be done by drawing a circle around a singularity and moving clockwise. If the underlying representation orientation changes clockwise, the singularity is positive; however, if the orientation changes anticlockwise, the singularity is negative. Singularities in the striate cortex rotate no more than 180 degrees, so the singularity variable is always between + – ½. Hypothetically, a pinwheel is a full rotation, with an index of +1. To date, now pinwheels have been found in our visual cortex. Tal and Schwartz (1997) found that for any neighbouring singularities, you could usually draw a smooth curve between them. The remaining cells form columns along the curve with the same orientation preference (iso-orientation). In addition, Tal and Schwartz confirmed that nearby singularities have the same topological indices with opposite signs.

In addition to orientation, ocularity is another parameter that has to be represented in the striate cortex. Ocularity refers to the extent in which cells respond to our eyes. The brain as ocularity stripes meaning columns in the striate alternate between monocular and binocular cells. The stripes suggest that the brain wants to ensure that pairs of L and R stripes process every part of the visual field. Unfortunately, adding another feature parameter only furthers the packing problem. Researchers have found that the brain maximised economy by ensuring that each iso-orientation domain in the orientation maps tends to cover a pair of L-R ocularity columns; in other words, each orientation is represented for each eye (Hubel and Wiesel, 1971). Furthermore, the brain needs to perceive lines of different widths. The brain has solved this problem by having cells tuned to the same orientation, sensitive to various widths of spatial frequencies. As with orientation, representation of spatial frequency is continuous except for some singularities.  Lastly, directionality is packed together with orientation. Except for sudden changes in direction (180 degrees), the direction map is continuous. It overlays the orientation map; however, it does not effect the continuity of orientation as orientations defines two possible directions (Frisby and Stone, 2010).

Fortunately, colour does not add to the packing problem! This is because colour is represented exclusively at the centre of orientation singularities. At the centre of singularities, cells have no preferred orientation, so colour does not add any parameter. To fully understand how orientation, ocularity and colour come together, the polymap was constructed to show an overlay of all the parameters. Based on observations from a polymap, in addition to the specific wiring of the brain, some scientists argue that the cortex is not really trying to solve the packing problem. All the maps try to do is to minimise the amount of wiring the brain needs to employ (Frisby and Stone, 2010). In fact, Swindale et al. 2000 found that the cortex does attempt to maximise coverage, and if any small changes were made to the current mapping system, wiring efficiency would be reduced.

Receptive Fields: Simple Cells and Tuning Curves

Receptive Fields

The jumping spider makes use of pattern recognition to distinguish prey from mate. Their eyes allow them to detect specific features or templates, specifically, the bar-shaped feature similar to the legs of other spiders (Land, 1969). Frisby and Stone (2010) discuss the jumping spider because they provide an excellent paradigm for how template matching works through a series of steps.

-       First, the original image is projected on to the retina of the spider’s eye

-       Second, the spider’s eye focuses on a specific feature, in this case the leg

-       Then the leg’s image is cast onto the retina, and receptors project this information to the primary visual cortex (V1)

-       Neurons in V1 receive inhibitory and excitatory input from the receptors in the retina

-       The receptors not blocked by the leg have increased activity and send an excitatory light signal

-       The receptors blocked by the leg have decreased activity and send an inhibitory light signal

-       The neuron gathers the total input and if it exceeds its threshold, firing indicates that a bar is present

Template matching, whether in a spider or human, relies on encoding of a pattern whose shape directly matches the input pattern to be detected. Striate cortex cells in V1 are found in all mammals. These cells receive input from the retinal fibres, and each cell is responsible for a limited patch of the retina (receptive field). Accordingly, cell types in the striate cortex are classified according to their receptive fields (Hubel and Wiesel, 1981). Striate cells are broken down into two parts: simple cells and complex cells.

Jumping Spider

Jumping Spider

Templates can, however, be impractical because the amount needed would be exponential resulting in a binding problem (Frisby and Stone, 2010). For example, if we have 18 templates for orientation sensitive to 18 sizes, which are sensitive to 18 shades, you can image the ridiculous amount of templates you would need. This problem is known as a combinatorial explosion.

Simple Cells

Simple cells are named simple because they can be simply mapped into excitatory and inhibitory sub-regions. Simple cells are optimally excited by bar-shapes, which is why it makes sense that simple cells are also called slit- and line – detectors. Slit-detectors respond to a light bar on a dark surrounding, and line-detectors respond to the opposite (Hubel, 1988).  Light on dark or vice versa is important because simple cells respond best to patterns that generate luminance differences, in other words, edges. However, because simple cells are so sensitive to edges, the orientation of a bar is important. The optimal stimulus for a simple cell, to emphasize luminance differences, is one that provides maximum excitation and minimum inhibition (Frisby and Stone, 2010).  To provide maximum excitation and minimum inhibition, different orientations are dealt with by different cells (Hubel and Weisel, 1962). The angle to which each cell is tuned is determined by the pattern of its excitatory and inhibitory regions. ‘Slit’ and ‘edge’ simple cells exist for a full range of orientations, which is reflected by the brain’s wiring; the fibres going from the retina to cortex differ depending on which orientation they represent (Frisby and Stone, 2010).

Population Code

As discussed in the previous section, bars maximally excite simple cells; however, cells still respond even when they are not maximally excited. If part of a cells visual field is activated, a partial response will be initiated. As such, context is vital to making sense of our visual field. For example, a non-vertical stimulus stimulates the vertically oriented receptive field just as well as the vertical but faint edge. In order to distinguish between the two outputs, they must be considered in context of the activities of cells examining the same retinal patch.

Fortunately, having sensitive simple cells makes interpolation between neighboring orientation measurements possible. This “talk” or interpolation between cells is known as a “population code.” Even though there are only simple cells for 18-20 different preferred orientations, we manage discriminations of less than <0.26 degrees (Frisby and Stone, 2010). Communication between cells allows us to discriminate when orientations vary very slightly, in the grey area between defined orientations. Populations of cells that have same preferred value of particular stimulus, like orientation, are called a channel. Scientists are able to measure the preferred orientation of cells by recording the symmetric pattern of firing rates.

Unfortunately, a major consequence of having a limited number of cells tuned to a large number of orientations is that cells taking each measurement need to be “broadly tuned” for “coarse coading.” Cognitive psychologists wanted to know how many channels are necessary to resolve the ambiguity problem. The answer is technically two but then the cells would be so broadly tuned that you would not be establishing any type of context. In addition, the tuning curve would turn far to slow to interpret anything. Unless the input to the cell coincided with the flank of the curve, there would be very little difference between the cells outputs. Hence, the brain uses a large number of broadly tuned cells with tuning so that the most sensitive part of the tuning curve can always be representative of one orientation with the less sensitive parts being representative of slight deviations from the optimal orientation (Frisby and Stone, 2010). 

Tuning Curve

The overall relationship between orientation of input edge and the output of the cell is called the tuning curve (Frisby and Stone, 2010). Tuning curves are important because they allow you to pinpoint which cells are sensitive to what orientation. The flank mentioned in the section above is where the slope of the tuning curve is the greatest; it also represents the point of greatest change in firing rate. This peak in sensitivity is found half way from the top of the curve. The trough or top of the curve is the least sensitive part because the slop is equal to zero. Regan and Beverly (1985) proved that humans do have peaks and troughs in their orientation sensitivity.

Skärmavbild 2014-01-20 kl. 16.56.48