Tag Archives: Neuroscience

The Neuroscience of Causality and Animacy

n 1998, Heberlein and colleges showed patients the Heider and Simmel movie. They found discovered that patients with amygdala damage did not describe the shapes using any social or anthropomorphic terms. These findings make sense since the amygdala is responsible for experiencing emotions. Even though the amygdala was damaged, the participants were able to judge causality and animacy suggesting other parts of the brain are necessary for judging these perceptions.

brain sliceA PET study conducted by Happe and Firth (1999) found that that intentional movement activated more activity in the random-movement displays in the tempoparietal junction, fusiform gyrus, occipital gyrus and medial frontal cortex compared to goal-directed movement. Processing in these parts appear to be domain specific or organised into modules. Evidence is based on Fodor’s (1975) descriptions of modality. Perception of causality and animacy is domain specific, processing is restricted to specific causal and intentional interpretations, the process is entirely a visual phenomenon and the causality and animacy are fast, automatic and innate.

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.

Basal Ganglia: Substance P

As mentioned in my last post on basal ganglia, the majority of the striatum consists of medium spiny neurons. These medium spiny neurons are GABAergic and organised based on the peptide they contain as well the dopamine receptors they contain. One these peptides is called substance P (SP). As a neuropeptide, SP functions as a neurotransmitter as well as a neuromodulator. Other than GABA, SP functions as a neurotransmitter in MSNs. Specifically, SP-releasing neurons mediate “synaptic communication between MSNs” (Blomeley, et al. , 2009).


Previously it was thought that striatal projection neurons like MSNs only inhibit each other; however, a study by Blomeley, et al. , 2009 has proven that they can also interact in an excitatory manner. Studies have shown the synaptic NK1 receptors, whose major receptor molecule is SP are present in a glutamteric terminals in the stiratum (Jakab et al., 1996). In the study by Blomeley, the importance of these NK1 receptors was investigated. The results suggest that SP plays a crucial role in facilitating the release of glutamate between medium spiny neurons. In other words, communication between the neurons is increased by SP attaching NK1 receptors found on the terminals of glutamate releasing MSNs.


Blomeley, C. P., Kehoe, L. A., & Bracci, E. (2009). Substance P mediates excitatory interactions between striatal projection neurons. The Journal of Neuroscience29(15), 4953-4963.

Heroin and the Brain


According to the medical journal the Lancet (2007), heroin is the most deadly and addictive of the twenty most common recreational drugs. Even though heroin does not carry the allure of cocaine, heroin usage is still an international problem. An opiate drug extracted from the opium poppy, heroin is an extremely potent analgesic (NHS). Remarkably, the effects of heroin can remain for up to five hours, and a single use is enough to fuel a life-long addiction.


Heroin and the other opiates (morphine, codeine, etc.)  when taken orally or inhaled must undergo first-pass metabolism, which decreases the potency of the drug (Sawynok, 1986). However, when heroin is injected it is able to by pass the blood-brain barrier as well as the fast-pass system. Once inside the brain, heroin breaks down into three different components, the quintessential and final form being morphine (Dubuc, 2002).  Morphine, an μ-opioid agonist, binds to μ-opioid receptors present in the brain, spinal cord and gut. The binding of the morphine to these receptors creates the sedative, euphoric and pain-relieving effects. The pleasurable feelings produced the heroin are positively reinforcing because they activate the limbic system or pleasure centre of the brain.

The High

Prior to heroin entering the system, inhibitory neurotransmitters (GABA) are active in the synapse (Dubuc, 2002). These inhibitory neurotransmitters inhibit dopamine  from being released. Natural opiates (endorphins, enkephalins, etc.) block the release of neurotransmitters that inhibit dopamine release. As such, when the natural opiates attach to the opioid receptor dopamine floods into the synapses. Heroin mimics the natural opiates released by our system when morphine attaches to the opiate receptor. The release of dopamine causes an immediate sense of welling being or euphoria, sedation and pain-relief.

Physiological Symptoms

Just like with cocaine abuse the effects are not just limited to the brain. Addiction not only destroys relationships and financial security; overdose does not need to be the only cause of death.


heroin 3Heroin was first synthesised by C.R. Adler Wright in 1874 when he added two acetyl groups to the morphine molecule (Sawynok, 1986).  Morphine itself comes from latex harvested from green capsules of the opium poppy. The use of opium predates written history with evidence of the poppy found in Mesopotamia. Wright’s discovery of heroin, however, was largely ignored until it was accidentally re-synthesised by Felix Hoffman of what is now Bayer pharmaceutical company. Hoffman ironically was trying to synthesise codeine (a less addictive and less potent form of morphine), however, instead also produce an acetylated form of morphine otherwise known as heroin (Chemical Heritage Foundation, 2010).

heroin 4The medical name for heroin is diacetylmorphine or morphine diacetate otherwise known as diamorphine. Today heroin is known by a variety of street names including H, horse, black tar, brown and smack.

Heroin Addiction

As with all other drugs that work on the reward-system, overtime pleasure experienced by the excess release of dopamine diminishes. As a result, an addict must increase their dosage to experience the same high. It is often by addicts that no high ever measures up to the first one. Remarkably, this shows how quickly the drug effects our normal ability to feel pleasure and relief.

Physiological and psychological effects of addiction (Timberline Knolls Residential Treatment Center, 2013):

– Dry mouth

– Cycles of hyper alertness followed by extreme drowsiness

– Disorientation

– Sudden behavioural changes

– Constricted pupils

– Shortness of breath

– A droopy appearance

Heroin Overdose and Treatment

heroin 5Like all class A drugs, the risk of heroin overdose is common. As such it is important that these symptoms are recognised by medical professionals as well as anyone else witnessing any of the following (U.S. National Library of Medicine, 2013):

– Spasms  of the stomach and/or intestinal tract

– Low blood pressure

– Weak pulse

– Dry mouth

– Extreme pupil constriction

– Tongue discolouration

– Slow, shallow or no breathing

– Bluish nails and lips

– Delirium

– Disorientation

– Constipation

– Extreme drowsiness

– Muscle spasticity

– Coma

Even if you are not medical professional, if you notice any of these symptoms you should call poison control.


Dubuc, Bruno. “THE BRAIN FROM TOP TO BOTTOM.” THE BRAIN FROM TOP TO BOTTOM. Douglas Hospital Research Centre, Sept. 2002. Web. 17 Nov. 2013.

“Felix Hoffmann.” Homepage of the Chemical Heritage Foundation. N.p., 2010. Web. 17 Nov. 2013.

“Heroin Addiction Symptoms and Effects.” Heroin Addiction. Timberline Knolls Residential Treatment Center, 2013. Web. 17 Nov. 2013.

“Heroin Overdose: MedlinePlus Medical Encyclopedia.” U.S National Library of Medicine. U.S. National Library of Medicine, 31 Oct. 2013. Web. 17 Nov. 2013.

Nutt, David, et al. “Development of a rational scale to assess the harm of drugs of potential misuse.” The Lancet 369.9566 (2007): 1047-1053.

Sawynok, Jana. “The therapeutic use of heroin: a review of the pharmacological literature.” Canadian journal of physiology and pharmacology64.1 (1986): 1-6.


The Genetics Behind Huntington’s

Huntington Disease is a rare genetic condition that most people have never even heard of unless a) they study it b) they personally know someone with the disease or c) they are a fan of House. Luckily for me only a) and c) apply in this situation. However, I believe Huntington’s like a variety of other diseases is something the public needs to be educated about because awareness really is the greatest way to inspire research into any field.

As autosomal dominant disorder this makes Huntington’s especially dangerous because as a dominant trait a person only needs one affected allele to develop the disorder. Were the trait recessive such as the trait for hemophaelia, for example, then the likelihood of having Huntington’s is significantly lowered. When a trait is autosomal this means that it is no carried by any of the sex chromosomes (X or Y), rather is carried by any of the other 22 chromosomes the human body has. In Huntington’s the gene affected is located on chromosome 4, specially on the p (upper, shorter) arm.













The symptoms of Huntington’s has already been discussed on a previous post on basal ganglia disorders; however, in summation it results in damage to the striatum and cerebral cortex causing changes in personality including mood swings, involuntary movements known as hypokinesia and eventually dementia. As is common with most genetic disorders, the symptoms do not appear until adulthood. In Huntington’s the symptoms usually arise around mid-age, but unfortunately it can arise earlier than our 30s or 40s if unlucky. Once symptoms start appearing the person usually has about another 5 to 15 years until death. The age at which symptoms appear directly correlates with the genetics behind the abnormal gene.

Huntington’s is part of numerous diseases including varies ataxias and fragile X syndrome that result due to trinucleotide repeat. Specifically, Huntington’s is due to a repeat of the CAG trinucleotide. Normal alleles carry about 10 to 35 copies, but those suffering from Huntington’s and various other neurodegenerative diseases have more than 40 repeats. People with around 60 repeats with develop Huntington’s around the age of 20. These repeats in CAG result in the production of a “mutant protein” that eventually fill the striatum and cerebral cortex causing degeneration and ultimately death of these brain cells. In healthy individuals the gene involved in Huntington’s encodes for a large protein known as huntingtin (Htt), which when normal enhances the production of a protein (BDNF) necessary for the survival of the cells in the striatum and cerebral cortex.

Stay tuned for a post later this week on current experimental treatment on Huntington’s! Thank you for reading :)


Cummings, Michael. “Genetics of Behavior.” Human Heredity: Principles and Issues. 9th ed. Belmont: Brooks/Cole, 2011. 405-06. Print.

Basal Ganglia Disorders: Parkinson’s and Huntington’s Disease

My last post was exclusively about basal ganglia and the reason for this was to help clarify the parts of the brain directly involved in two very infamous disorders: Parkinson’s and Huntington’s Disease.


Parkinson’s Disease

Parkinson’s disease is far more recognized that Huntington’s disease; however, thanks to the character Thirteen on the tv show House that might be changing. Parkinson’s disease effects about 1% of all people over the age of 50; however, as you can see from the video posted below, this is not always the case. Another example is actor Michael J. Fox, who was diagnosed with Parkinson’s at the age of 30. He has since become an activist for the cure of Parkinson’s, which led him to found the Michael J. Fox Foundation. It is not that uncommon to know someone with the disease. Many people can in fact recognize it based on the very characteristic tremors.


Parkinson’s is classified by hypokinesia. The symptoms of Parkinson’s include slowness of movement or bradykinesiadifficulty in initiating ‘willed’ movements or akinesia, increases muscle tone or rigidity, and of course, tremors in the hands and jaws even at rest. Many  of those who suffer from the disease will eventually show signs of cognitive decline. More specifically, the substantia nigra’s input to the striatum. This input features the neurotransmitter dopamine, which facilitates the activity of the motor loop by activating cells in the putamen. As noted in the previous post, the putamen forms an inhibitory connection with neurons in the globus pallidus, which then forms an inhibitory connection with the thalamus (VLo). Due to the depletion of dopamine, the ‘funnel’ between VLo and the supplementary motor area (SMA) closes. As a result, the victim of Parkinson’s will have impaired motor function with symptoms such as ones listed above.

Treatment Options for Parkinson’s Disease

Even through Parkinson’s cannot be cured, therapies do exist to try to ease or deter the symptoms. Most therapies aim at enhancing the levels of dopamine delivered to the caudate nucleus and the putamen. The most common type of medication is known as L-dopa, which is a precursor for dopamine. This means that it participates the chemical reaction that produces dopamine. This treatment does alleviate some of the symptoms; however, it cannot do anything to stop the progressive course of the disease, nor slow the rate of cell degeneration in the substantia nigra. Currently, experiments are being conducted to test whether graftng non-neural cells, manipulated to produce dopamine, into the basal ganglia can help. Also, stem cell research shows promise to one day provide an effective treatment as well.

Huntington’s Disease

Whereas Parkinson’s is characterized by hypokinesia, Huntington’s is characterized by hyperkinesia or excessive movement. As tragic as Parkinson’s disease is, Huntington’s does seem far more frightening. A hereditary, progressive and always fatal disorder, Huntington’s  symptoms include dyskinesia or abnormal movements, dementia and disorder of the personality. The scariest part of the disorder is that the symptoms do not appear until adulthood, so unless the person knows that they have a history of the disorder, they can easily pass on the genes of Huntington’s to their children without even knowing that they have it. Genetic tests can be performed to find out for sure, but for many people it is too late at that point. The name Huntington’s comes from the abnormal gene carried by the patient. The first and most notable sign of the disease is known chorea: spontaneous, uncontrollable movements with rapid, irregular flow resulting a flicking movement in various parts of the body. In fact, Huntington’s disease can also be called Huntington’s Chorea. The devastating effects of the disease is due to the profound neuron loss in caudate nucleus, putamen and globus pallidus as well as cell loss in any other part of the cerebral cortex. The fact that Huntington’s can strike any part of the brain means that many patients suffer a variety of different symptoms, sometimes making it difficult to diagnose without a genetic test. Damage to the basal ganglia results in a loss of inhibitory output to the thalamus (VLo) resulting in the abnormal movements.

brainslice3Unfortunately, due to the progressive nature of the disorder and the genetic component, treatment for Huntington’s is virtually non-existent. Most patients with the disorder have their symptoms treated with various medications ranging from anti-depressants to sedatives and anti-psychotics.


The Brain: The Cerebral Cortex


The cerebral cortex is the intricate fabric of interconnected neural cells that covers the cerebral hemisphere. It serves as the ultimate control and information processing centre. Humans have larger cortexes which enables us to be more adaptable, which gives us the ability to learn and think beyond basic survival instincts.

The cerebral cortex is made up of a sheet of cells that is 1/8 of an inch think and contains approximately 30 billion nerve cells. Glial cells or glue cells as they are commonly called, hold the nervous system together. They are NOT neurons but their own category of cells. Glial cells serve to support, nourish and protect neurons by communicating with them. Scientists are currently attempting to find connection between glial cells and information transmission and memory.

brain lobes

Folds of the brain increase the brain’s surface area allowing for maximised function and activity. As most people know, the brain’s cerebral cortex consists of four lobes: the parietal lobe, the occipital lobe, the temporal lobe and the frontal lobe. The frontal lobe is the front portion of the cerebral cortex, lying right behind the forehead. The frontal lobe is involved in speaking, muscle movement, high level cognition (planning, judgment, reasoning). Damage to the frontal lobe can result in changes in social skills, libido, attention and risk-taking. The parietal lobe is the part of the cerebral cortex at the top of head, behind the frontal lobe towards the back. It includes the sensory cortex. This means the parietal lobe processes sensory information such as pain, touch and pressure. Damage to the parietal lobe results in sensory problems such as impaired verbal memory and language skills. The occipital lobe lies at the base of te head and includes the visual areas; it receives visual information from the opposite visual field. This means that what is seen by our right is processed by the left side of our occipital lobe and vice versa. The temporal lobe lies above the ears and includes the auditory areas. These two areas receive auditory information from the opposite ear much like how the eye and occipital lobe work. 

– Functions of the Cerebral Cortex –

German physicians Fritsch and Hitzig electrically stimulated the cerebral cortexes of dogs. Through their experiments, Fritsch and Hitzig found that they could make different parts of the dogs’ bodies move. However, their ability to make the dogs move through stimulation was selective. Movement was only observable when a specific arch-shaped area of the back of the frontal lobe was stimulated. This area is know known as the motor cortex. Furthermore, the physicians discovered that the parts of the body that were moved, corresponded to stimulation on the opposite side of the brain.

Neurosurgeons Foerster and Denfield also investigated the functions of the cerebral cortex through stimulation. They found that precise control requires the greatest amount of cortical space. Furthering this idea, Jose Delgado found that specific parts of the cerebral cortex correspond with certain actions. Today it is evident, through the use of MRI scans, that precise actions require overlapping cortical sites.

brain lobes 2

The cerebral cortex specialises in receiving information from the skin senses and the movement of body parts. The greater the area devoted to specific body region, the more sensitive this area becomes. As a paradigm, our lips are far smaller than our back; however, relative to size, the cerebral cortex dedicates far greater area to our lips making them far more sensitive and kisses so enjoyable. It also explains why our backs are far less sensitive to pain than say our stomachs.

– Association Functions – 

The association areas consist of 3/4 of the cerebral cortex. Association areas are uncommitted to sensory of muscular activity. They associate with various sensory inputs with stored memories. The functions of the association areas cannot be triggered by stimulation or any other forms of probing. The existence of these areas are vital in disproving the popular belief that 90% of our brain is dormant. Our brain relies heavily on these unassociated areas for interpretation, integration and acting on processed sensory information.


Cherry, Kendra. “The Anatomy of the Brain.” The Four Lobes (2012): n. pag. About.com Psychology. Web. 03 Sept. 2012. <http://psychology.about.com/od/biopsychology/ss/brainstructure_2.htm&gt;.

Myers, David G. Psychology . 6. Worth Publishers, 2001. Print.Myers, David G. Psychology . 6. Worth Publishers,2001. Print.

Mental Retardation and Dendritic Spines


Dendrite is Greek for “tree-like” and to explain what they do in the simplest terms possible, they receive electrochemical signals from other neurons and then pass these signal down to the soma or neural cell body. Dendrites play a critical role in determining the frequency of the action potential, which drives the electrical signal down axons of the body of the neuron towards the axon terminals. Dendrites are so essential that their architecture is a great indicator of the complexity of our neural connections. In fact, our brain function depends on strong synaptic connections, connections which are cultivated during infancy and early childhood.

Unfortunately, as with all things complex, sometimes something goes wrong in the developing process. Mental retardation occurs when there is a disruption in this early refinement of dendrites that results in cognitive impairment severe enough to disrupt adaptive behaviour. There is a wide array of genetic disorders and poor environmental conditions that can result in mental retardation. For example, Down Syndrome and PKU (both genetic disorders), accidents during pregnancy and childbirth, maternal infections with rubella, Fetal Alcohol Syndrome and environmental impoverishment. Poor environmental conditions in young children such as poor nutrition, isolation and neglect can even result in brain damage severe enough to cause damage to these sensitive dendrites.

spine 2

Healthy dendrites have spines that look like small balloons that hang of the dendrite. In cases of mental retardation dendritic spines are very thin and long, resembling the dendritic spines of a fetus. This is clearly seen in the top most image, a) and c) are healthy dendrites. This clear difference reflects the failure of normal circuits in the brain’s development. Studies by Marin-Padilla and Purpura have discovered a correlation between extent of dendritic spine damage and degree of mental retardation.


Bear, Mark F., Barry W. Connors, and Michael Paradiso. “Neurons and Glia.”Neuroscience: Exploring the Brain. Baltimore, MD: Lippincott Williams & Wilkins, 2006. 43. Print.

Images courtesy of google images.