Category Archives: Neuroscience/Neurology

The Striatum

The striatum is the largest collection of neurons in the basal ganglia. Composed of the caudate nucleus and putamen, the basal ganglia, as the name suggests, sits at the base of the cerebrum. It receives input from regions of the cerebral cortex, the limbic system, and the sensorimotor and motivational systems via the thalamus. In addition to the cerebrum, the striatum receives input from the brainstem including the substantia nigra and the raphe nuclei of the reticular formation. The dopamine and serotonin of these two structures serve a modulatory function. Anatomists organise the striatum on the “basis of differential connectivity and distribution of neurochemical markers” (Redgrave, 2007). Processing strong excitatory input, the striatal neural circuits generate a strong inhibitory output, which controls the output of basal ganglia further along in the motor loop.


The major cytology of the striatum is GABAergic medium spiny neurons (MSN), making up about 95% of the total cellular structure. MSNs are organised into two groups based on the peptide they contain, substance P and enkephalin and the proportion of dopamine receptors (D1 or D2) they contain. MSNs create dense networks of axon collaterals. As projection neurons, the MSNs create this dense network by forming axon collaterals with one another. Tunstall et al, 2002 found that almost 30% form an axon collateral with a neighbouring MSN. Research has shown that the function of these collaterals is in cellular recognition and “classification of cortical patterns” (Blomeley, et al. , 2009).

The striatum is a vital part of the basal ganglia, and all pathways run through it. From the striatum onwards, the pathway either becomes direct or indirect. As shown in the figure below.









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.

Redgrave, P. (2007). Basal ganglia. Scholarpedia, 2(6): 1825.

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.

Neuroscience: The Nervous System

he nervous system is the body’s speedy, electrochemical communication system. It consists of all the nerve cells of the peripheral and central nervous systems.

The central nervous system consists of the brain and spinal cord. The peripheral nervous system is the sensory and motor neurons that connect the central nervous system to the rest of the body. Nerves are the neural cables of the nervous system containing many axons. They are part of the peripheral nervous system. They are connected to the central nervous system by muscles, glands, and sense organs.

Sensory neurons carry incoming information from the sense receptors to the central nervous system. Interneurons are part of the central nervous system. They internally communicate and intervene between the sensory inputs and motor inputs. They are the most common type of neuron. Motor neurons carry outgoing information from the central nervous system to the muscles and glands.


– The Peripheral Nervous System –

The peripheral nervous system is made up of the somatic nervous system and the autonomic nervous system. The somatic nervous system controls the body’s skeletal muscles. The autonomic nervous controls the glands and muscles of the internal organs. It is broken down into the sympathetic and the parasympathetic nervous system. The sympathetic nervous system arouse the body, mobilising its energy in stressful situations (fight or flight response). The parasympathetic nervous system calms the body, conserving its energy.


– The Central Nervous System –

The spinal cord is the information highway connecting the peripheral nervous system to the brain. Ascending neural tracts send up sensory information. Descending neural tracts send down motor control information. Reflexes are the body’s autonomic response to stimuli controlled by the spinal cord. They are composed of 1 sensory neuron and 1 motor neuron that communicate through one interneuron. Because they only run through your spinal cord, they react automatically without your brain being involved in the process. The spine sends information back to the brain. Bodily pain or pleasure is controlled by the brain.

The brain receives information, interprets it and then decides on a response. It functions like a computer, receiving slightly differing images of an object from the eyes, it computes the differences and infers how far the object must be to project such a difference.

Neural networks are interconnected neural cells which, with experience, can learn, as feedback strengthens or inhibits connections that produce certain results. Stephen Kosslyn and Oliver Koening proposed to think of neural networks as networks of people. Neuron network with nearby neurons with which the can have short, fast connections. Each layer of a neural connects with various cells in the next layer. Learning occurs as feedback strengthens connections that produce certain results. New computer models simulate this process plus the excitatory and inhibitory conniptions to mimic the brain’s capacity for learning.


The Brain: Introduction, Brain Scans and Imagery

Scanning of a human brain by X-rays

Scanning of a human brain by X-rays

The brain enables the mind: seeing, hearing, remembering, thinking, feeling, speaking and dreaming.

Science now enables us to know about the living brain through lesions. Lesions are destroyed tissue. A brain lesion is naturally or experimentally caused destruction of brain tissue, which selectively removes tiny clusters of normal or defective brain cells without harming the surroundings. We can also probe the brain with tiny electrical pulses. Scientists can look upon on the messages of individual neurons and on mass action of billions of neurons. We can see colour representations of the brain’s energy – their consuming activity. These tools facilitated the neuroscience revolution.

The oldest method of studying the brain-mind connection is to observe the effects of brain disease and injuries. This has been going on for more than five thousand years. In the past two centuries, physicians have been recording the results of damage to specific brain areas. Some noticed that damage to one side of the brain often caused numbness or paralysis on the opposite side of body. This suggested that that somehow the right side of the body is wires to the left side and vice versa.

Other scientists noticed that damage of the back of brain disrupted vision and that damage to the left front part of the brain caused speech difficulties. These discoveries have helped scientists map the brain. Today scientists are able to electrically, chemically or magnetically stimulate various parts of the brain to record the effects. Modern electrodes are so small that they can detect the electro pulse in a single neuron.

scan2An electroencephalogram or EEG is an amplified recording of the waves of electrical activity that travels across the brain’s surface. These waves are measured by electrodes placed on the scalp when presented with a stimulus.

A positron emission tomography or PET scan is a visual display of brain activity. It detects where a radioactive form of glucose travels to whists the brain performs a given task.

A magnetic resonance imaging system or an MRI is a technique that uses magnetic fields and radio waves to produce computer generated images that distinguish among different types of soft tissue. It also allows us to see structures within in the brain. MRIs align the spinning atoms in our brain through the use of a magnetic field as well as causing a pulse of radio waves that disorients them momentarily. When the atoms return to normal spin the release detectable signals. MRIs can also detect oxygen-laden blood flow.


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

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. Psychology. Web. 03 Sept. 2012. <;.

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