Can travelling alter the brain?

Many of us will have encountered those who have been lucky enough to have had a gap year who or have ‘found themselves’ in Thailand. Nowadays, travelling the world seems to be at the top of every student to do list. The drive behind this need to travel is obvious; the social benefits of meeting new people and experiencing new cultures. However, new research suggests travelling may even be beneficial to your health and alter your brain for the better.

Research by Dr. Julia Zimmerman and Dr. Franz Neyer found the benefits of travelling went far beyond the obvious and impacted on personality and social interactions.  The study compared students who had travelled and lived abroad to students in the control group who had not. Those who had travelled were found to be greater extroverts, presenting higher social engagement and preference to social company, ultimately changing the way they interact with others. Individuals who had travelled showed a decrease in neuroticism in comparison to the control group. Neuroticism is a personality trait characterized by anxiety and loneliness, and is shown in individuals who have a relatively mild mental illness defined as neurosis.  There are further psychological studies that have emphasised this social change that exploring brings. Research by Jiyin Cao found a relationship between the amount of foreign travel experience a person had and an increase in generalised trust. Moving abroad to new places and cultures affected an individual’s interpersonal interactions for the better.

Not only can travel affect an individual’s psychological and social welfare, clinical neuropsychologist Dr. Paul Nussbaum suggested it could help minimize the risk of neurodegenerative diseases such as Alzheimer’s. The constant cognitive stimulation that backpacking brings is thought to keep the brain ‘switched on’ when it is exposed to the vibrancy and exhilaration of new places. The new language barriers that need to be overcome and getting lost around ancients ruins means the brain is faced with new and challenging situations which would not otherwise be encountered in the comfort of the home. These challenges are acknowledged by the brain, which responds by creating new, and re-enforcing old connections between neurons, via a process called synaptic plasticity. Synaptic plasticity is the change in the way neurons in the brain interact and signal to one another – the strength and efficacy of the messages may intensify. Travelling can alter the structure and function of the brain, consequently leading to an increase in plasticity and an enhanced ability to think and make decisions.

Holidays and city breaks are popular de-stress strategies, be it to take a break from a job or simply to take a step back from reality. The fast paced and multitasking lifestyles that are led today mean the ‘stress hormone’ cortisol is elevated massively. The Mayo Clinic states travelling can decrease cortisol levels, which can have positive effects on your mood and health – prolonged stress can lead to a weakened immune system and increase the risk of developing depression.

So be it a weekend retreat in Barcelona or backpacking around Bali, travelling at any age is beneficial. Travel whilst you are young to build social relations and carry this on into old age to halt dementia. If you were ever in need of an excuse to take a holiday, this is one. As Dr. Nussabaum says, travelling really is ‘a good medicine’.

Author – Rachel Coneys

Editor – Aisha Islam

References

Zimmermann J, Neyer F.J, 2013. Do we become a different person when hitting the road? Personality development of sojourners. Journal of Personality and Social Psychology [Online]. Volume 105 (3), p515-30.

Cao J, Galinsky A.D, Maddux W.W, 2014. Dose travel broaden the mind? Breadth of foreign experiences increases generalized trust. Journal of Personality and Social Psychology [Online]. Volume 5 (5), p517-25.

Global collation. Destination healthy aging [Online]. [Accessed 5.2.16]. Available from: http://www.globalcoalitiononaging.com/v2/data/uploads/documents/destination-healthy-aging-white-paper_final-web.pdf

Mayo Foundation for Medical Education and Research, 2011. Healthy aging [Online]. [Accessed 7.2.16]. Available from: http://www.mayoclinic.com/health/healthy-aging/MY00374

 

 

 

 

 

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Alzheimer’s Disease – What Do We Know?

Risk factors for Alzheimer’s; what we can do to prevent the disease.
In today’s population, Alzheimer’s disease (AD) is becoming more and more prevalent. This is because it is a disease associated with ageing; as we live longer, the incidence of Alzheimer’s becomes greater. It is therefore becoming increasingly important for us to learn more about the disease so that one day we can find a cure. What is Alzheimer’s and how can we reduce the risk?

What is Alzheimer’s?
Alzheimer’s is a neurodegenerative disease resulting from neuronal cell death in the brain. Alzheimer’s is characterised by a large number of amyloid plaques in the brain that surround neurones, and this can result in vascular damage. The main component of these damaging plaques is amyloid-β protein, and it is the deposition of this protein that leads to neurofibrillary tangles and cells loss. Many people know someone with this disease, however there is currently no cure and the disease kills more people than breast cancer and prostate cancer combined. There’s a variety of symptoms that you can spot in a person with Alzheimer’s. Note that it is advisable that anyone with the below symptoms should visit a doctor. A typical symptom is a gradually worsening ability to remember new information, which occurs as a result of the death of neurones which are involved in memory. Other symptoms include challenges in solving problems, problems with words, misplacing things, confusion and mood changes.

brain

Figure 1: Image showing the loss of brain mass that occurs as a result of Alzheimer’s. Note that the ventricles (spaces within the brain) are larger in the pathological condition case. Image sourced from http://aforalzheimer.blogspot.co.uk/.

What are the risk factors for Alzheimer’s?
Unfortunately there are many risk factors for this neurodegenerative disease that we cannot change. The greatest risk factor for Alzheimer’s is age; as an individual gets older, their chance of developing Alzheimer’s increases. This was found in a study on the age-specific incidence of Alzheimer’s in a community (Liesi et al., 1995). They found that the incidence of Alzheimer’s disease was 14 times high among persons older than 85 years compared with those between 65 and 69 years of age. Another risk factor is family history; the more family members a person has with Alzheimer’s, the greater their risk of developing the disease. This is because there are genes known to be involved in Alzheimer’s. A study into the genetic background of Alzheimer’s (A.Rocchi et al., 2003) identified three genes responsible for the rare early-onset (where symptoms are typically seen before the age of 60) form of the disease. These are the amyloid precursor protein (APP) gene, the presenilin 1 (PSEN1) gene and the presenilin 2 (PSEN2) gene. These are called deterministic genes, meaning that anyone who inherits them will develop the disorder. However this rare, familial form of AD accounts for only 5% of all cases. The remaining 95% are mostly late-onset cases, of which the cause is a complex one involving environmental factors as well as genetic ones. A gene called apolipoprotein E (APOE-e4) has been found to be associated with sporadic late-onset AD cases, as well as being the only gene with a confirmed role in AD. Scientists estimate that APOE-e4 may be a factor in up to 25% of Alzheimer’s cases. If a person inherits this form of APOE, they have an increased wisk of developing the disease. Genetic testing for the above genes is available, however not routinely recommended by doctors.

There are various risk factors for Alzheimer’s based on a person’s medical history. Conditions that affect the cardiovascular system, such as diabetes, high blood cholesterol and strokes are implicated in developing Alzheimer’s disease: if an older person has had a stroke, it doubles their risk of dementia. Although the link isn’t clear yet to scientists, people who have had depression later in life are significantly more likely to develop dementia. In addition, a link between Alzheimer’s and Down’s syndrome has also been observed.

What are lifestyle factors that we can change in order to reduce the risk?
Recent research is beginning to tell us more about risk factors that we could influence through lifestyle choices, and effective control of other health conditions. One known risk which we can prevent is head trauma. It has been suggested that deposits that form in the brain as a result of a head injury lead to dementia. A study which investigated this risk factor was conducted by A. Borenstein Graves et al, (1989). They explored a case study of 130 matched pairs, matched by age and sex. They found that a history of head injury resulting in loss of consciousness or that caused the subject to seek medical care was recorded in 24% of the cases and 8.5% of the controls, leading to an odds ratio of 3.5. Ischemic heart disease is implicated in vascular dementia. Your brain requires oxygen, and as each heartbeat pumps approximately 25% of your blood to your head, if this is not saturated with oxygen then the brain is also deprived. You can manage this risk by monitoring your blood pressure and cholesterol levels, and speaking to your doctor about how to reduce the risk of cardiovascular disease. Weight management is another factor important in preventing Alzheimer’s. Managing your diet can reduce the risk of high blood pressure and heart disease which, as mentioned above, increases the risk of dementia. Reducing the consumption of saturated fat is one way we can reduce the narrowing of the arteries, thus reducing the risk of developing vascular dementia.

Another dietary element that we can manage is the consumption of vitamin D; low levels are associated with an increased risk of dementia. Vitamin D can be obtained from eggs and oily fish. You should avoid cigarettes as it has an extremely harmful effect all over the body, including blood vessels in the brain. Research suggests that light to moderate amounts of alcohol may protect the brain against Alzheimer’s. However drinking above the recommended amounts of alcohol can significantly increase the risk of Alzheimer’s. In addition, ongoing research into the effect of social activity has suggested that people who are more socially active have a reduced risk of developing the disease. Puzzles that challenge the brain are considered as increasing the brain’s ability to compensate for damage that Alzheimer’s may incur, and so are encouraged to prevent disease onset. A study into the 7 main risk factors for Alzheimer’s, namely diabetes, midlife hypertension, midlife obesity, smoking, depression, cognitive inactivity or low educational attainment, and physical inactivity, found that up to half of AD cases worldwide (17·2 million) and in the USA (2·9 million) could be attributable to these factors (Barnes, D. et al., 2011). The study suggested that a 10–25% reduction in all seven risk factors could prevent as many as 1–3 million AD cases worldwide.

 

How can we help Alzheimer’s suffers?
We can help fund the amazing research that is supported by Alzheimer’s Research UK by donating to the cause via the following link: http://www.alzheimersresearchuk.org/support-us/donate/ . If you’d like to learn more about Alzheimer’s, you can click on the following link https://www.alzheimers.org.uk/ . Look out for volunteer groups in your area to help the ageing community. You can also help by educating friends and family about Alzheimer’s so that they know how to recognise the symptoms and are more aware of the causes.

References

https://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=102

http://www.alzheimersresearchuk.org/research-projects/research-early-onset-dementia/

American Psychiatric association. 1994. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV).  4th Revised edition. American Psychiatric Press Inc.

Hebert, L., Scherr, P., Beckett, L., Albert, M., Pilgrim, D., Chown, M.,Funkenstein, H., and Evans, D. 1995. Age-Specific Incidence of Alzheimer’s Disease in a Community Population. JAMA. 273(17), pp. 1354-1359.

Rocchi, A., Pellegrini, S., Siciliano, G., Murri, L. 2003. Causative and susceptibility genes for Alzheimer’s disease: a review. Brain Research Bulletin. 61(1), pp. 1-24.

Borenstein Graves, A., White, E., Koepsell, T., Reifler, B., Van Belle, G., Larson, E., and Raskind, M. 1990. The Association Between Head Trauma and Alzheimer’s Disease. American Journal of Epidemiology. 131(3), pp. 491-501).

Barnes, D., and Yaffe, K. 2011. The Projected Risk Factor Reduction On Alzheimer’s Disease Prevalence. The Lancet Neurology. 10(9), pp. 819-828.

Author: Jess Stonehouse 

Editor: Molly Campbell 

Zika Fever

The recent observed link between the Zika virus and neurodevelopmental disorders in Latin America has forced the world health organisation to place the outbreak as a public health emergency. So what is Zika and what are its effects on the nervous system?

Zika

The first reported infection from the Zika virus occurred in Uganda in 1947. Although the virus does show a wide geographical distribution, the outbreaks remained small and narrowly distributed until 2007 when there was a large epidemic, effecting 75% of the population on Yap Island. Zika, a mosquito-borne virus, belongs to the Flaviviridae family, which also includes the virus yellow fever. The species of Mosquito thought to be the main vector of the virus in South and South East Asia is the Aedes aegypti (Yssel et al., 2015). Studies have shown that there is a widespread distribution in North Africa as well as countries in Southeast Asia, including India and the Phillipines. These large outbreaks are characterised by mild flu like symptoms such as fever, rash, arthralgia, muscle and joint pain, malaise, headache and conjunctivitis (Yssel et al., 2015). Recent reports have suggested that the virus can also be spread through sexual transmission, however only two reported cases suggest this, and so the main focus of research remains on transmission via mosquito bite. The Zika virus is particularly a concern for pregnant mothers who are infected with the virus, as it can give rise to microcephaly.

Microcephaly

Approximately 3 million babies are born in Brazil every year. In a normal scenario an estimated 150 babies would be diagnosed with microcephaly, whereas now Brazil are said to be investigating around 4000 cases. Many post mortems of infants who died with microcephaly have been shown to present the Zika virus within their brains, and it has also been detected in the placenta and amniotic fluid.

Microcephaly is a disorder that affects neurological development. New-borns with the disorder tend to have smaller than average intracranial brain volume. There are two main types of microcephaly; primary microcephaly: when the brain is smaller at birth, and secondary microcephaly: when the brain is of normal size at birth but there is failure of the brain to develop normally post-natal (Woods 2004). The face develops at a normal rate which leads to an infant with a receding hair line and in many cases a wrinkled scalp. The cerebral cortex is particularly reduced which leads to a simplified gyral pattern and MRI studies have shown the frontal lobes to be particularly affected. Primary microcephaly is thought to be caused by a decrease in neurones produced by neurogenesis, whereas secondary microcephaly is characterised by a reduced amount of dendritic endings and synaptic connections (Woods,2004). Primary usually occurs before 32 weeks of gestation. The majority of neurones are formed by week 21 of foetal development, whereas dendritic connections and myelination mainly occur after birth; this explains the differences in the two variations of the disorder. Abnormalities are not just seen in regards to the brain and skull, later in life the body is usually seen to be underweight and dwarfed. Seizures severely impair intellectual development and disturbances in motor functions may also develop later due to the demyelination and reduced connectivity.

It is important to note that genetic factors, alcohol consumption of the mother during the pregnancy, maternal syphilis infections and poor pre-natal care can all be the cause of microcephaly. Thus further investigations are required to determine whether this causal link between Zika infection and microcephaly is directly related.

The infection is also thought to affect adults, resulting in temporary paralysis known as Guillain- Barré syndrome.

17256

(Kaneshiro and Black, 2013)

 

Guillain- Barré syndrome

During the recent outbreak in French Polynesia (2013 and 2015) the reports of individuals with Guillain- Barré syndrome (GBS) increased 20-fold (Yssel et al., 2015). GBS is a disorder in which the immune system begins to attack part of the peripheral nervous system. These immune cells begin to destroy the myelin sheath and in some cases the axons also. When demyelination occurs the speed of electrical transmission is greatly reduced. This causes problems with both motor and sensory transmission, as the limbs receive and transmit information over longer distances, and thus are more susceptible to the adverse effects of demyelination. Initial symptoms of the disorder include myasthenia (weakness) and tingling sensations known as paraesthesia in the lower limbs. These go on to spread to the upper limbs. Because there is reduced sensory afferent feedback the individual becomes unable to detect and respond to mechanical, thermal and nociceptive stimuli efficiently. These effects increase in intensity until the point of paralysis, where specific muscles can no longer be used. If this syndrome progresses then there is a high risk of mortality as the paralysis can affect respiratory muscles and the cardiovascular system. Research suggests that when a virus like Zika causes this syndrome it may be due to the virus changing the cells of the nervous system In such a way that the immune system begins to recognise them as foreign, or removes the ability of the immune system to distinguish between its own cells and those that are foreign. This leads to immune cells such as macrophages phagocytosing and destroying cells of the peripheral nervous system, particularly the Schwann cells, which lay the myelin sheath.

Prognosis for the disease is fairly good: most individuals recover fully with only a few (around 30%) suffering from prolonged weakness. This may pose the question as to why there is such a panic over the Zika outbreak. However, regions where there is the highest number of cases do not have efficient access to healthcare, and therefore there is an increased risk of mortality, which must be considered.

Conclusion

Brazilian authorities are currently investigation other potential causes of microcephaly, but it seems that there is an increasing amount of evidence linking the virus with these disorders. The greatest problem is that 80% of Zika cases are asymptomatic; therefore pregnant women may not be aware that they’ve even contracted the infection. If there is a confirmed link between the virus and microcephaly, then research developments are required that enable efficient and prompt diagnosis, in addition to preventing the disease infecting pregnant women and those of childbearing age in the first place.

References

Kaneshiro, N.K. and Black, B. (2013) Microcephaly: MedlinePlus medical encyclopedia image. Available at: https://www.nlm.nih.gov/medlineplus/ency/imagepages/17256.htm (Accessed: 8 February 2016).

Woods, C.G. (2004) ‘Human microcephaly’, Current Opinion in Neurobiology, 14(1), pp. 112–117. doi: 10.1016/j.conb.2004.01.003

Yssel, H., Dejarnac, O., Wichit, S., Ekchariyawat, P., Neyret, A., Natthanej, L., Perera-Lecoin, M., Hamel, R., Talignani, L., Thomas, F., Cao-Lormeau, V.-M., Choumet, V., Briant, L., Desprès, P., Amara, A., Surasombatpattana, P., Missé, D., (2015) ‘biology of zika virus infection in human skin cells’, Journal of Virology, pp. 15–354.

 

Article by: Kate Pearman

Edited by Molly Campbell

Cure for Schizophrenia?

A Cure for Schizophrenia?

I decided to write an article on schizophrenia, seeing as it has been prevalent in the news recently. If you’re unsure why, a scientific breakthrough regarding schizophrenia development has been discovered by Steve McCarroll (Associate Professor and Director of Genetics for Harvard) and his research team. After almost two decades of research and billions of pounds spent, these scientists from Harvard Medical School have may have discovered the biological origin of the illness – the role of the gene complement component 4 (C4).

Before we get into the science, I’ll cover a bit about the illness. So what is schizophrenia? If we split the word up, we have ‘schizo’ or the Greek term ‘skhizein’, meaning ‘to split’, and the ending ‘phren’ meaning ‘mind’. But contrary to popular belief, this mental disorder doesn’t really have anything to do with having a split personality, or drastically changing from a calm and collected mood to a raging, manic episode. It’s an illness affecting over 200,000 individuals in the UK alone and over 200 million people across the globe with onset starting from late adolescence to early adulthood. It involves symptoms that have been split into categories of positive and negative. Positive symptoms represent delusions, auditory and visual hallucinations, and negative symptoms refer to feelings of disconnection from yourself, people around you and a lack of interest in general life. This tends to have a pretty big impact on your day to day activities and maintaining responsibilities including going to work, looking after your family etc.

Schizophrenia is probably one of the most misunderstood mental disorders that is heavily stigmatised and feared by many people in the public. It’s usually due to lack of understanding of the illness or the ability to empathise with people affected by schizophrenia. Portrayal of schizophrenia and mental illnesses in general in the media and on screen is usually associated with violence and sinister behaviour, which is probably the stem of the fear behind this illness. It’s easy enough for you to believe that you suddenly know everything you could possibly know about schizophrenia after watching a 90 minute psychological thriller about it on Netflix one night, but there’s more to the disorder that is usually forgotten about – the direct impact on the patient having to deal with the illness itself, in addition to knowing that your peers are perceiving you as strange or out of the ordinary. One of the main ways we can change the public perception on many psychiatric illnesses is to be able to educate people about areas they are unfamiliar about. This really emphasises how important it is for scientists to continue research and why we’re so excited by the recent breakthrough discovered that could possibly lead to the development of new therapies and treatment.

So now I should probably tell you what the breakthrough actually is. After McCarroll et. al analysed 100,000 human DNA samples from 30 different countries, they were able to locate genetic variants in particular regions of the genomes that are related to the increased risk of schizophrenia. The gene that stood out to them the most was C4, which is involved in the complement cascade and is part of the immune system. The variability in structure of most human genes is not usually much, unlike the gene C4. By genetically analysing more than 65,000 people, it was found that individuals with a particular form or structure of the gene showed higher expression of C4, consequently having a higher risk of developing schizophrenia.

 

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Figure 1 – Image credit: Psychiatric Genomics Consortiu. Studies by McCarroll et al., 2016.

You can see in Figure 1 how the C4 gene on chromosome 6 is pretty much dominating and is much higher than the other genes, all of which have been linked to schizophrenia. This is indicating that C4 may possibly pose the strongest risk for the disorder. But how is the C4 gene related to this disorder? C4 is a critical component of the classic complement cascade and has a key role in pruning synapses whilst the brain matures. Previous studies and this study in particular have found that animals with a high level of C4 activity had more of their synapses eliminated during a key stage of brain development. Elimination of connections between cells has long been associated with schizophrenic patients.

 

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Figure 2 – C4 protein localisation in human brain tissue (McCarroll et al.)

The group of confocal images in Figure 2 show the localisation of the C4 gene in hippocampal tissue. This increased C4 activity is thought to lead to impairment in cognition, which is a symptom seen in schizophrenia. These findings suggest that therapies in the future may involve reducing C4 activity to prevent synaptic pruning in patients showing early symptoms and help prevent further progression of the disorder.

This study has been described as a crucial turning point in the fight against mental illness by the director of the US National Institute of Mental Health. For over a hundred years, the pathology of complex brain diseases that comprise cognition have been studied using carefully constructed behavioural tasks and it is thought that the regulation of biogenic amine neurotransmitters is abnormal in psychiatric disorders such as schizophrenia. Findings by McCarroll et al. have provided additional knowledge that may be important in dealing with many symptoms associated with the disorder, which are fundamental in scientists’ quest to try and find a cure. Although this breakthrough is unlikely to lead towards immediate treatments, researchers are one step closer towards understanding the key molecular and cellular events of the illness.

If you’d like to read about McCarroll’s study in depth, here’s a link to the journal that was published in Nature: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature16549.html

References:

http://www.nhs.uk/Conditions/Schizophrenia/Pages/Introduction.aspx

http://www.mind.org.uk/information-support/types-of-mental-health-problems/schizophrenia/#.VrEYqrKLTIU

http://www.independent.co.uk/life-style/health-and-families/features/schizophrenia-the-most-misunderstood-mental-illness-9546654.html

Whiteman, Honor. “Schizophrenia breakthrough: scientists shed light on biological cause.” Medical News Today. Available from: http://www.medicalnewstoday.com/articles/306063.php

https://www.theguardian.com/science/2016/jan/27/schizophrenia-breakthrough-as-genetic-study-reveals-link-to-brain-changes

Purves D. & Augustine G.J. et al. 2001. Neuroscience. 2nd ed. Sunderland MA: Sinauer Associates.

Author: Aisha Islam 

Editor: Molly Campbell

Addictive Drugs and Their Reinforcing Capabilities

Introduction:

Almost every person in his or her lifetime will have taken some sort of drug, whether this is caffeine, nicotine or perhaps a recreational drug, such as cocaine. The taking of drugs seems to be a natural phenomenon within humans because as well as targeting the reward pathway within the brain, they provide an effect that is appealing to people; whether this is just a caffeine kick or the euphoria produced that allows people to escape from their usual way of thinking. The reward pathways within the brain are an evolutionary advantage that ensures that when a positive action is carried out (such as drinking water, eating food or having sex) it is repeated. Drugs target this pathway producing reinforcing affects. They do this by releasing dopamine, a neurotransmitter that activates the reward pathway, making the brain believe the effects of taking the drug are good, ‘rewarding’. In this article I will be talking about the reinforcing effects of cocaine, alcohol (ethanol) and nicotine.

The Reward Pathway: 

First the terms ‘rewarding’ and ‘reinforcing’ require definition. A rewarding stimulus is one in which, through activation of dopamine, the brain understands to be not only positive but a stimulus that must be approached. Reinforcement means that the action produces the increasingly intense feeling that repetition is necessary. The pathways within the brain that induce reinforcement are a set of forebrain structures, connected through a series of neural pathways. These include the nucleus accumbens (which is part of the ventral striatum), the basal forebrain (which includes the amygdala) and regions within the medial prefrontal cortex (Eric J. Nestler et al, 2001). These areas of the brain receive dopaminergic innervation from the ventral tegmental area (which is part of the midbrain). Reinforcing drugs induce a sense of reward by increasing that release of dopamine within these forebrain structures, via activation of the mesocorticolimbic dopaminergic system. The euphoric state of the drug also plays a role in their reinforcing nature, but without this release of dopamine they would not necessarily be addictive. This is seen in LSD which does not provide this rapid onset of positive reinforcement, so although the drug does produce a state of euphoria, this alone is not enough to cause chronic use and abuse (Eric J. NEstler et al, 2001).
The mesocorticolimbic pathway originates in the ventral tegmental area of the midbrain and the dopaminergic neurone efferents that synapse in the ventral tegmental area are the most important in reinforcement.

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Figure 1: The dopaminergic pathways of the brain.
Source: Bear et al., Neuroscience, 3rd edition.

Cocaine:

Cocaine is a psychostimulant which produces a state of euphoria that induces a state of extreme pleasure and gratification, which is accompanied by a separation from reality. Cocaine is highly addictive due to its capability to produce strong reinforcement. Cocaine’s affects are fast acting but short lasting which also adds to its reinforcing nature, and is why users will continuously take the drug throughout a short period of time. Although cocaine is reinforcing, addicts of cocaine are more likely to go through sessions of binges on the drug rather than continual use. This may be due to the fact that withdrawal of cocaine does not necessarily produce major adverse effects on the body, (although there are emotional withdrawal symptoms) such as the shakes that would cause users to need the drug to function normally. The psychostimulant effects of cocaine results from the increased level of monoamine neurotransmitter release, including: dopamine, serotonin and noradrenaline. Cocaine targets the reuptake proteins of these neurotransmitters, binding to them and antagonising them, inhibiting their action. This decreases the amount of neurotransmitter being removed from the synaptic cleft, causing an increased level of neurotransmitter and enhancing the response. The prevention of the removal of dopamine is the most important for the reinforcing nature of cocaine. Dopamine release is increased in the nucleus accumbens.

Alcohol (ethanol):

Ethanol is a depressant within the central nervous system. This does not mean that taking alcohol makes the users depressed; in fact most of us know this is quite the contrary as alcohol usage is associated with increased happiness and a loss of social awkwardness, perhaps why people find it so pleasurable. What ‘depressant’ means in the case of ethanol is that it facilitates the action of GABAA receptors and inhibits glutamatergic NMDA receptors (Eric J. Nestler et al, 2001). The release of GABA within the brain acts to hyperpolarize the cell, making it more negative on the inside and decreasing the amount of action potential (hence depression). Glutamate is the main excitatory neurotransmitter within the brain and its release causes an increase in action potential firing. By inhibiting this, ethanol is again reducing the amount of action potential firing within the brain. If high doses of ethanol are taken then most ligand and voltage gated ion channels are affected. This is why alcohol has such a wide spread affect within the brain. The reinforcing nature of ethanol is not understood completely but is thought to be due to its effects on the NMDA receptors and its ability to activate the mesocorticolimbic pathway, although it is not yet know whether this reinforcing effect takes place in the ventral tegmental area or the nucleus accumbens. How dopamine is realised due to ethanol is also not confirmed as it could either be due to the facilitation of GABAA receptors or due to the inhibition of NMDA receptors (Eric J. Nestler et al, 2001). What is clear though it that one or both of these mechanism plays a role in inhibiting the tonic inhibition of the release of dopamine. Ethanol also reduces serotonergic function, which is thought to add to the reinforcing nature of ethanol. The fact that ethanol does affect so many systems within the brain is probably the main reason why it is so hard to find out why the drug is reinforcing, but it must be remembered that in many cases of drug abuse (this is very different from drug use) people are wanting to remove themselves from reality due to some underlying cause, and for some people this may be what motivates them to abuse alcohol or any other drug to such an extent.

Nicotine:

Nicotine is the addictive substance within the Tabaco plant and within cigarettes, and now also E-cigarettes. Nicotine is an interesting drug, firstly because it is highly addictive although it does not cause any state of euphoria, showing how this drugs addictive nature is so much to do with how it’s affects on the central and peripheral nervous system. Secondly, as most of us know smoking is not pleasurable and in fact quite deterring the first couple of times people smoke, and it must be taken quite frequently to become pleasurable. This shows how drug taking can be so associated to one’s social environment as without this most people would not force themselves to continue smoking. It is also shown in animal studies that the animals will not choose to take nicotine if they have the choice (Eric J. Nestler et al, 2001). Therefore the reinforcing nature of nicotine is not immediate as it is in cocaine for example, but is instead only reinforcing once the user has become addicted. Nicotine is similar in structure to acetylcholine and is therefore capable to binding to nicotinic acetylcholine receptors (nACh), causing the opening of ion channels, allowing sodium to enter and a response in the postsynaptic neurone to be initiated. In the central nervous system nACh receptors are located on the ventral tegmental dopamine neurones and through binding of nicotine cause a release in dopamine by creating an action potential (Eric J. Nestler, 2001). Nicotine may also cause the release of endogenous opioids adding to its reinforcing nature. Nicotine also causes withdrawal symptoms, such as an agitated mood and shaking of the hands. This could lead to continued use just to remove the uncomfortable symptoms that are accompanied with withdrawal.

Conclusion:

There is so much more that could be said on how drugs cause addiction and how the brain of an addict is altered from the normal state. The reinforcing nature of drugs is what causes people to seek the drug and to feel the need to take the drug again, as by hijacking the reward pathway our brains are fooled into thinking that the drug is good for the body and mind. This fact also demonstrates the strength of the reward pathway in its ability to unconsciously control the acts of the conscious mind. Each drug has its own mechanism in causing the release of dopamine but it is through this release that all drugs are reinforcing.

The consuming of drugs is a subjective topic. Whilst considered dangerous, drugs have been demonstrated to open the mind and make people observe the world in a fascinating and euphoric way. Some of the greatest pieces of literature in history, Alice in Wonderland to name an example, have been argued as products of the brain when under the effects of recreational drugs. What has to be understood is that there is a difference between taking and trying drugs and abusing them. It is the process of taking a drug regularly that causes long term alterations to the brain and enhances the reinforcing nature of the drug.

References:
Eric J. Nestler, Steven E. Hyman and Robert C. Malenka, 2001, Molecular Neuropharmacology A foundation for Clinical Neuroscience, The McGraw-Hill companies, Inc. Medical Publishing Division.

Article by Lara Cornish.
Edited by Molly Campbell.