Although chemical and biological warfare has been internationally condemned since the 1600s, scientific research has continued to uncover chemicals which can have a devastating effect on the nervous system. Indeed, at the end of last year there were reports of an alleged government attack on civilians using an unidentified nerve gas in the city of Homs in Syria.  It is thought that Assad’s regime have been developing and stockpiling chemical weapons. If this is true, the situation shows disturbing similarity to Saddam Hussein’s use of the nerve gases against Iranian civilians during the Gulf War in the 1980s.

Interestingly, the discovery of nerve gases was made more or less by accident. The organophosphate (OP) family of nerve gases, including sarin and tabun, were being studied by German scientist Dr. Gerhard Schrader during the 1930s as possible insecticides. Whilst studying these chemicals Dr. Schrader accidentally spilled a drop of tabun onto the bench and, within minutes, was overwhelmed with dizziness and had difficulty breathing. It took him and his colleague three weeks to fully recover from this exposure.

By Mr.Henk [GFDL ( or CC-BY-SA-3.0-2.5-2.0-1.0 (], via Wikimedia Commons

OP nerve gases work by stopping the enzyme acetylcholinesterase (AChE) from breaking down the neurotransmitter acetylcholine (ACh). Normally, when ACh is released by nerve cells it is rapidly broken down by AChE, meaning that it can’t build up around target cells. However, when AChE stops working ACh collects around cells, overstimulating them. The effects are often seen as over-stimulation of muscle cells and glands which produce bodily fluids. After very high exposure to OP a victim will suffer a huge number of horrible symptoms, including, a runny nose, tight chest, blurred vision, shortness of breath, nausea, muscle spasms, drooling, crying, incontinence, vomiting and abdominal pain. In this case, death usually follows quickly, either due to choking or from suffocation caused by overstimulation of the diaphragm. Sarin was infamously used by the Japanese terrorist group Aum in an attack in a Tokyo subway station in 1995, which killed 13 and left thousands with temporary vision problems.

Another family of chemicals that affect the nervous system are anti-cholinergics.  Anticholinergics stop ACh from activating receptors on target cell (muscles and glands).  As a result, these chemicals have almost entirely the opposite effect to OP nerve gases. The symptoms include a dry mouth, muscle weakness, blurred vision, as well as hallucinations and some pretty strange delirious behaviour. Anticholinergics could have a potential (though still illegal) use as a ‘non-lethal’ weapon to incapacitate people – since people can’t really fight back if they’re delirious. Saddam Hussein was accused of stockpiling the anticholinergic Agent 15 to use in the Persian Gulf War against Kurds and Iranians. Another similar chemical known as BZ was weaponised by the U.S. military during the Cold War. Thankfully, stocks were uncovered and destroyed before it was deployed. BZ was also discovered by accident by a scientist innocently working on digestive disorders.

By: Staff Sgt. Steve Faulisi, U.S. Air Force [Public domain], via Wikimedia Commons

Despite some of these examples, where dangerous biological weaponry has emerged from otherwise benign research; there would be no sense in avoiding all scientific research in the fear that someone might accidentally stumble across the next weapon of mass destruction. Scientists certainly have a duty to be aware of the potential uses for their work, especially since research is (or should be) freely accessible online. However, ceasing research into potentially hazardous chemicals altogether would inhibit some pretty important discoveries; especially since many chemicals which are beneficial in small doses, could have a lethal ‘dual-use’. Indeed, drugs which inhibit AChE are not just potential biological weapons, they are also currently the most widely used treatment for Alzheimer’s disease.

Perhaps, since the discovery of the occasional nasty seems unavoidable if important biological research is to continue, the best course of action would be to fund counter research into possible treatments.

At the University of Sheffield, Prof. Mike Blackburn and his collaborators have recently developed a ‘bioscavenger’ to mop up OP chemicals, preventing them from attaching to AChE. This kind of treatment will hopefully help save lives in the event of nerve agent attacks. Last year, Dr. Moshe Goldsmith at the Weizmann Institute in Israel mutated a human liver enzyme so that it could break down OP nerve gas molecules. While this research holds obvious benefits to humanity, the implications of this work also raises an ethical dilemma. If the gene code for this newly-evolved enzyme could be put into soliders, we could be faced with a scenario where armies can be genetically manipulated to become immune to chemical or biological weapons. Unfortunately, this hypothetically amazing feat of science could result in an biological arms race…a situation it’s hard to envisage anyone winning.

The Arts and Humanities Research Council has a Neuroscience Ethics Network that bring together researchers from all over the UK. Some of this article has been based on prospective lectures initiated by the Network, intended for undergraduate Neuroscience students. If you’d like to read more about the Network, please click here:

Post by Natasha Bray

Toys for Girls and Boys

I don’t know why it comes as a surprise every year; but as soon as the pumpkins are sold out and the fireworks over, supermarkets start playing Noddy Holder and for the next month and a half we are reminded constantly of the upcoming festive season. The desperate panic felt as I realise how many presents I need to buy is dampened only by copious amounts of mulled wine. There is, however, one person for whom I actually look forward to buying a Christmas present; my godson Sam. Sam is four years old and extremely passionate about trains, fire engines, tractors…in fact, give him any sort of miniaturised mode of transport and he’ll be happy for hours. This love of miniature machines is typical for a boy of his age whilst many of his female contemporaries will be putting altogether different toys on their Christmas list: dolls, tea sets, play kitchens to name but a few. Indeed, once again this year the majority of young boys and girls will have their stockings filled with gender-appropriate toys, but what causes these preferences?

Last year, Dr. Laura Nelson (a neuroscientist) persuaded London’s largest toy shop ‘Hamleys’ to stop marketing their toys as being either ‘for girls’ or ‘for boys’. She felt that such marketing influenced the types of toys children chose, therefore reinforcing gender stereotypes: girls playing with tea sets encourages domestic, passive playtime, whereas boys might engage in more active and aggressive play if given a pirate ship. While we already assume that environmental factors (toys, parents, friends) can influence a child’s gender-identity, are there any biological reasons why girls like ‘sugar and spice and everything nice’, while boys are happier playing with a lorry that turns into a robot?

Since it would be very hard, not to mention unethical, to hide a child away from all gender-biasing environmental influences, the majority of current research is based on animal studies; specifically monkeys! Since most monkeys have no interest to advertising campaigns and few have played with a teddy or toy car before, they make pretty good ‘naive’ experimental subjects. Prof. Melissa Hines and her fellow scientists from Cambridge allowed male and female vervet monkeys to ‘take their pick’ of masculine and feminine children’s toys, then recorded how long they spent playing with each one. As it turns out, female vervet monkeys spent more time with the typical girls’ toys, while male monkeys spent more time with typical boys’ toys. This sex-determined preference for different types of toy suggests that there could actually be fundamental differences between male and female brains; perhaps not just in monkeys, but in humans too.

So does gender change the wiring of a child’s brain, biasing their choice towards more gender-appropriate toys? Professor Gerianne Alexander studied three month-old babies – or rather, how these babies looked at toys. The longer a baby looks at something, the more he or she is believed to like that object. The length of babies’ glances at either dolls (feminine), trucks (masculine) or balls (neutral) were measured and then compared to the level of testosterone they were exposed to in the womb. Testosterone is made by both boys and girls but boys produce much more since they have… well, testes. Interestingly, Gerianne found that the level of testosterone in the womb correlated with how much the babies liked typically masculine toys. So the lads swimming around in more testosterone looked longer at the trucks, while girls who weren’t exposed to high levels of testosterone looked longer at the dolls.

Incredibly enough, in a similar experiment with newborn babies (conducted just 24 hours after birth) Prof. Simon Baron-Cohen and his colleagues found that, even at this early time-point, (at least the earliest possible considering hospital guidelines), there seems to be biological differences between the sexes. These studies suggest that the level of circulating testosterone in the womb may be enough to impact brain development and possibly behaviour, even before Christmas TV adverts can brainwash them.

Further proof of the gender-biasing effect of prenatal testosterone comes from cases of congenital adrenal hyperplasia (CAH). CAH is a genetic disorder which leads to the overproduction of testosterone. CAH is usually diagnosed at birth and can be successfully treated with steroids. Children suffering from this disorder usually go on to lead a totally normal life, despite their brain’s prenatal exposure to high levels of testosterone. Interestingly, though, Prof. Hines has found that girls with CAH tend to be tomboys through their childhood. They are seen to play more like boys, favouring ‘rough and tumble’ games and typical boys’ toys over more feminine play times. So, levels of prenatal testosterone seem to predict toy choice more accurately than the actual sex of the child.

I should emphasise that while prenatal testosterone levels might correlate well with the tricky choice of Action Man vs. Barbie, it doesn’t necessarily mean that testosterone causes kids to pick one or the other. Impatient parents can’t just inject their kids with testosterone to make Christmas shopping easier. It’s also likely that the timing of exposures to certain hormones may influence the brain in different ways. What’s interesting, though is that something as ubiquitous as toys can be used as a way of investigating the science behind gender-stereotyped behaviours. Also, something tells me my godson would have plenty of excuses to be ungrateful if I get him a My Little Pony this year. Best start looking for a space rocket…

Post by: Natasha Bray

Is your brain wired for facebook?

I ‘like’ Facebook as much as the next person, or rather any of the other 950+ million users. The fact that people can stay in touch so easily in a metaphorically shrinking world without having to use a pen, paper, stamp or pigeon carrier is brilliant. However, what really amazes me about Facebook, Twitter, Tumblr, LinkedIn or any other social media is the phenomenon of ‘socialness’ itself.

In order to find the ‘social’ or ‘friend’ centre of the brain, scientists measured the size of different brain structures associated with making and maintaining friendships. In two different studies, they found that the size of an individual’s amygdala (the emotional centre of the brain) and their orbital prefrontal cortex (oPFC) were proportional to the number of real friends and social groups they had. In other words either having a larger amygdala or oPFC means you are more likely to be friendlier, or the more friends you ‘add’ to your social network, the larger those parts of the brain become. In fact, it’s probably a mix of both situations.

Robert Dunbar, a British anthropologist interested in the evolution of society, also attempted to define how the structure of the brain linked to the size of an individual’s social group: the equivalent to the average Facebook friend count. His early work focused on the brains of various species of monkey. From this work he found that he could predict the size of the animal’s social group from the size of their neocortex compared to the rest of their brain. He discovered that primate species which have a larger neocortex relative to the rest of the brain hang out in larger social groups, whereas those with a smaller neocortex have fewer ‘friends’. These monkeys’ brains have either evolved or changed to maintain friendships with a certain average number of other monkeys. From this Dunbar was able to predict that, if humans are like monkeys (which we are), our neocortex:brain ratio predicts that we should be cliquing into social groups of around 147.8 (with an upper limit of 300). What’s interesting is that this is essentially the case in real life: 150 is the average size of a tribal village, the optimum size in the Roman army’s military unit and the average number of friends on Facebook is actually creepily close too.

One question raised by Dunbar’s research is how or why the neocortex developed in the first place? The “Social Brain Hypothesis” suggests that primates evolved a larger neocortex and bigger social networks when they started eating fruit instead of leaves. Fruits contain way more calories than leaves, but are also harder to obtain and have a much shorter ‘shelf life’, meaning they pose more problems for a hungry monkey. Therefore if a monkey is to maintain a fruit-rich diet it is important for it to learn where to find fruit and how to tell whether or not it is ripe or safe to eat. It is thought that being part of a bigger social group allows all individuals to benefit from the group’s collective knowledge and thus from the extra energy found in fruit. Since the brain uses up so much energy to develop, it may be that this extra food source is partially responsible for the increase in neocortex size in these primate species.

Whether or not we realise it, most of us are hard-wired to seek out friendship. Our brains are social and we have evolved to cooperate and share – that’s why Facebook is such a massive phenomenon. But what does the size of our ‘friends’ section say about us? In a very modern experiment, psychologists asked people to rate another person’s attractiveness based on a fictional Facebook profile. These profiles were identical other than one factor: for each profile the experimenters altered the number of friends these fictional people had, either 103, 303, 503 or 703. These experiments found that 303 seemed to be the magic number, with participants rating profiles with this number of friends as being most ‘attractive’. Perhaps this could be a reflection of the upper limit of Dunbar’s number. Interestingly, both profiles with lower and higher friend counts were rated as being less attractive. Perhaps fewer friends is taken as an indication that a person is less sociable, whilst having too many friends may be seen as ‘trying too hard’. So when honing your online persona it’s more than just the pictures of that dodgy night out you have to worry about.

So why is Facebook in particular so popular so, dare I say it…addictive? There have been countless studies which show that going onto your Facebook account makes the pleasure centres of the brain, the same ones which activate when eating chocolate or having sex, ‘light up’. It seems that thinking and talking about ourselves is something we all enjoy. Psychologists found that participants in a study were happy to receive very little payment to talk about themselves whereas if they were required to chat about someone else they generally expected at least double the amount. The participants, on average, found talking about themselves so much more enjoyable that they would actually give up money in order to avoid talking about another person instead. Maybe that will help explain why people insist on posting mundane statuses online. (It doesn’t, however, give any excuses for those who use hashtags on Facebook…#wrongsocialmedia.)

But there are many more important benefits from having a strong, optimally-sized social group. Researchers in Kenya watched wild baboons to see how long higher socially ranking males and lower socially ranking males took to heal or recover from naturally occurring injuries and illnesses. Despite the highest and lowest ranked baboons experiencing a similar amount of biological stress, the lower-ranked baboons took an average of six days longer to heal or recover than alpha males. The researchers think this could be due to the positive impact that close friendships have on the immune and repair systems.

I’m definitely not saying that everyone should use Facebook in order to avoid getting ill, or that we should all frantically cull or add friends until our account reaches the magic ‘Dunbar’ number. But next time you log on to your account and scroll aimlessly through the trivial happenings recorded in your newsfeed or indulge in a little chat with an old friend, don’t blame yourself. Our brains are wired up to be social.

Post by: Natasha Bray

Politics vs. Science – from Galileo to Professor David Nutt

In 2009 Professor David Nutt caused controversy for the UK government’s Advisory Council on the Misuse of Drugs after stating the cannabis should be declassified to a Class C (rather than Class B) illegal drug.  During his time on the Council, Prof. Nutt had also claimed that recreational use of ecstasy is less dangerous than horse-riding. He was sacked from his government-advice post by Alan Johnson, the then Labour UK Home Secretary, who wrote to Nutt, “I cannot have public confusion between scientific advice and policy and have therefore lost confidence in your ability to advise me as chair of the ACMD.” By that logic, Johnson must have breathed a huge sigh of relief when three more scientist experts on the Council soon resigned.

Science and politics share a very complicated relationship, and have done since time began. Galilieo was condemned for stating that the Earth revolved around the sun. He was kept under life-long house arrest for his theory. Darwin’s theory of evolution has been exploited as an argument for any number of political agendas, all the way from communists to Nazis. Global warming was (and still is) a political minefield for climate scientists. The disciplines of science and politics are so intertwined such that good science is intrinsically political and policies should always be informed by science. Unfortunately, in today’s society there is a massive disconnection between scientists and politicians.

This rift is exemplified by the shocking fact that there is only one British Member of Parliament out of 650 that has a scientific, research-based PhD (Lib Dem MP for Cambridge Julian Huppert, Biological Chemistry, in case you’re wondering). Similarly in the United States, 3 in 435 people in the House of Representatives have a non-medical, scientific background. And considering Prof. Nutt’s dismissal, it seems that scientists are seen by politicians as commodity experts whose advice can be cherry-picked for a bit of ‘policy-based evidence-making’. Winston Churchill once said that science should be ‘on tap but not on top’. But what’s stopping us scientists from getting properly involved in politics?

I’m tempted to argue that, to a certain degree, it’s our own fault. As scientists, we are notoriously rubbish at PR. I imagine many of us wouldn’t want to be seen dead testiculating* with the rest of the mob in Parliament. Sadly, a lot of scientists’ work is viewed as slow, expensive, secretive and not immediately socially beneficial. The current stereotype of a scientist is sadly pretty much the same. Politicians, on the other hand, work to very tough deadlines in order to combine ethical, social, moral and economic factors into their party’s policies. These policies actually make a huge difference to people’s daily lives. As if that wasn’t enough, politicians have to try and kiss babies, refrain from calling women bigots and avoid cameras when beating up youths during the Election. Makes the lab seem pretty cushy.

The main thing scientists have got going for them if they fancy residing in Downing Street is the doctrine of science itself. As Carl Sagan (the American Brian Cox of his time) said, “science is a way of thinking much more than it is a body of knowledge”. The knowledge bit isn’t bad either and it lasts far beyond the sell-by date of parties’ policies.  The logic that underlies the analysis of data gathered from random, blinded, controlled trials is the perfect way of objectively testing different policies. And we’ve got buckets of that logic to share with our MPs.

U.S. President Barack Obama praises his ‘dream team’ of scientific advisors for their advice, “even when it’s inconvenient, indeed, especially when it is inconvenient”. As scientists we may not have rhetoric on our side to sugar-coat the facts; but shouldn’t that
be an advantage? We should not just be ready to inform and educate policy-makers; we should be ready to objectively challenge their decisions. In return, politicians shouldn’t dispose of us when they don’t like what we have to say. Professor Nutt hasn’t given up; he has now formed the Independent Scientific Committee on Drugs (win). Personally I think he sets an outstanding example to both scientists and politicians alike.

*to testiculate (verb): to gesture animatedly whilst spouting absolute b*llocks.

Post by Natasha Bray

Blame it on the brain: can you be held legally responsible for your brain?

Earlier this year, Edwin Hart Turner (38) was executed by lethal injection after being convicted of murdering Eddie Brooks and Everett Curry in a robbing spree near Mississippi. Shortly before the murders, Turner had been admitted at a mental hospital for depression after an attempted suicide. The defence attorneys’ main argument against Turner’s execution was his unstable state of mental health. Guilty or not guilty, Turner’s lawyers argued that a mentally ill person should be exempt from state execution.

Charles Whitman was a sporty, popular man who became increasingly aggressive and violent, while complaining of ‘tremendous headaches’. In 1966 he shot 13 people dead and wounded 32 others at the University of Texas in Austin before committing suicide. His autopsy discovered a cancerous tumour the size of a walnut invading his amygdala – a part of the brain important in regulating fear and rage.

Currently, the trial of Norwegian Anders Behring Breivik is dividing both social and professional opinion. Breivik, led by his far right-wing views, killed 8 people with a car bomb in Oslo and 69 more on the island of Utoya, a camp for the youth wing of the Norwegian Labour Party. Breivik maintains that he is not legally insane and that he should be held fully culpable for his acts. Legally this would mean the difference between him being sectioned in a mental hospital, possibly indefinitely, or being incarcerated for a very long time. Professional opinions of Breivik’s mental health vary from him being ‘lucid but lonely’, to having personality disorders, including extreme narcissism; paranoid schizophrenia or psychosis; being both suicidal and homicidal; to having ‘a rare form of Asperger’s and Tourette’s syndrome’.

Admittedly, cases such as these aren’t exactly common. However, with further advances in our understanding of mental illness these stories are increasingly relevant, necessitating a level of crossover between neuroscience and legal ethics. This crossover poses a major dilemma for society, the question of how much personal control we have over our own brains and whether or not we can be held entirely responsible for our actions? Must all mass-murderers be, to some extent, mentally ill since they fall so far outside a ‘normal’ moral spectrum? Are we less accountable for our actions and decisions since our brains’ functions are a product of our biology and social influences?

These more general philosophical questions lead us to specific practical questions about how society should act. Should all criminals be psychologically and neurologically tested when being trialled? Should brain scans be used as evidence in a court of law? How should we treat people who have committed terrible crimes but are psychologically or neurologically unwell and should there be a distinction between the two?

At the end of 2011 The Royal Society published a report stating that in the USA, neurological or behavioural genetics were used as evidence for 722 legal defences between 2005 and 2009. In Italy, a woman had her sentence for murdering her sister reduced after the defence lawyers presented genetic and imaging evidence that her brain’s anatomy was different to that of 10 normal women. On the other hand, in 2008 an Indian woman was convicted of poisoning her husband when a scan of brain activity allegedly revealed that she had knowledge of events surrounding her spouses death which could only have been gained through experience. Neuroscientists are now often called upon as expert witnesses and so should have a understanding of the legal and ethical implications of their testimonies.

Following this, there has been a lot of research investigating how people perceive neurological or psychological evidence. In this research, mock-jurors were asked to decide whether a virtual defendant was guilty or ‘not guilty by reason of insanity’ (NGRI). The virtual defendants had different levels of neurological or psychological evidence to support their claim of insanity. For example, in some cases medical evidence was provided proving the defendant had suffered brain damage, whilst in other cases the results of psychological analysis was given showing various types of personality disorder. This research found that around 50% of mock-jurors will find the defendant NGRI on the basis of evidence suggesting the defendant has suffered physical brain injury or neurological disease, especially if this is backed up by a brain scan. However, only about 10-12% of mock-jurors find virtual defendants with a personality disorder or psychopathy to be NGRI.

So what does this mean in real life? Today, it is estimated that 90% of UK prisoners have a diagnosable mental illness or substance abuse problem (Office for national statistics). About 1 in 7 of all prisoners in the UK are thought to have four concurrent mental health problems, often not simply associated with the time spent in prison. Also more than half the reported prisoners who commit suicide in prison exhibit symptoms of mental health problems on entering prison. Whether or not these mental health issues preceded or even contributed to their crime is unknown (and I can’t say how one would ever prove that beyond reasonable doubt), but I think that this has huge implications for the prison system. Seeing as people outside prison with mental illnesses are treated as patients rather than criminals, I think the government should focus on treating and rehabilitating, rather than punishing, prisoners who have been incarcerated on their brain’s behalf.

Post by: Natasha Bray

Optogenetics: The ultimate ‘light bulb’ moment

If the system underlying the ‘mind’ is a network of neurons constantly firing and wiring, then surely ‘mind control’ could be achieved by controlling the activity of neurons? Imagine being able to switch groups of neurons on and off instantaneously as simply as flipping a light switch. In fact, why not use light itself to control neurons; to control minds? How would you turn neurons deep in the dark depths of your brain into light-responders?……….Welcome to optogenetics (‘opto’ comes from ‘optos’, Greek for ‘visible’).

Science has yet again used a once thought ‘lower’ organism to make massive steps in understanding the way our biology works. The simple algae Chlamydomonas reinhardtii looks pretty unremarkable – it swims about generally doing what algae do: photosynthesise, swim, repeat, etc. What makes it interesting, however, is that it can detect which way to swim using its ‘eyespot’. This eyespot, found on the surface of the alga, contains a pore called channel rhod-opsin that opens in response to light (in particular, blue light). When this channel is open, it lets calcium into the cell. In this case, calcium acts like the alga’s engine ignition. The calcium ions activate propeller-like flagellae, which do a sort of tiny breast-stroke towards the source of light.

As well as being an unexpectedly neat way of guiding this humble green blob towards the sun’s rays, this system is also a massively useful experimental tool. Until recently when scientists wanted to activate neurons they tended to rely on either drugs or electrical stimulation. These methods are far from perfect since drugs can be slow and may cause unwanted side effects; whilst electrical stimulation is too imprecise to target very specific groups of cells. Algae have now inspired scientists into designing similar light-responsive systems that they can whack into groups of neurons. With a bit of tinkering these systems can be targeted to any number of different neuron types and can respond to a variety of different coloured light. Some systems are slight tweaks on the basic channel rhod-opsin unit whilst others combine opsins from other types of algae or microbes that react to different coloured lights or for different lengths of time. Whatever the mechanism, these are tools that let you change the activity of specific groups of neurones at will – with millisecond precision.

So what can you do with these light-responsive systems – or ‘phototriggers’? Let’s start with flies. First install the DNA for a phototrigger system into neurons at the base of a fly’s wing, now from this DNA those neurons can construct their very own light-responsive receptors. These neurons become active when a light is shone on them, just like the algae. Shine a light, the neurons become active and fire, telling the wings to beat. Result: we have take-off. And just in case you’re thinking the fly just sees the light and tries to flee, the same happens in decapitated flies. Gross but true! If you want to know more or need to see it to believe it: see here.

So what else can we do with this amazing technology? Well, it has been used experimentally to help us understand a number of brain functions. For example, in order to understand how choices are made, optogenetic techniques were used to switched on and off a flies’ preference for certain smells. This led to the amazing discovery of the fly’s inner critic, an assembly of 12 neurones that govern the decisions flies make. Scientists have also inserted light-responsive elements into more complex animals in an attempt to prove a causal relationship between certain groups of brain cells and a specific behaviour. In the video below, a mouse runs around every time a blue light is shone into its brain, meaning that the switching on of the light-activated brain cells causes the mouse to run. Another study made a mouse ‘prefer’ to freeze on the spot by illuminating – and therefore activating – its reward centres every time it chanced upon a particular place in its cage. These experiments are elegant and powerful because they identify the particular set of brain cells that cause, or lead to some pretty complex actions. More recently, in a bid to unravel the mysteries of how the brain deals with fear and rewards, scientists have used a similar light sensitive system to make rats remember a fearful situation. If mice or rats have minds (the complexities of which, we don’t know), then surely this counts as mind control?


When I first heard about optogenetics, I was gobsmacked at how clever and insightful the technology sounded. A small part of me was originally hesitant, however. I’ve obviously watched too many films that make me almost suspicious of a tool that could potentially enable mind control, or, dare I say it, ‘brainwashing’. Anthony Burgess’ Clockwork Orange springs to mind: “When a man cannot choose, he ceases to be a man.” (Anthony Burgess). The implications of this technology are massive and, without wanting to sound like too much of a film nerd, ‘with great power comes great responsibility’ (Spiderman, if you’re wondering). Luckily, though, after reading up on optogenetics, I’ve come round to realise that its potential for good far outweighs the fearsome idea that the technology would be used to construct an army full of mindless, Jason Bourne-esque zombies. Like I said, I watch far too many films.

Instead, the ability to manipulate the brain as we’ve never been able to in the past is being put to good use. Awful diseases like Parkinson’s, Alzheimer’s, multiple sclerosis – to name but a few – are currently not curable. In an aging population more prone to age-related brain disorders, it’s an increasingly big problem. Optogenetics is a valuable tool with which to study these diseases in order to find treatments. It may even prove a valuable tool in itself – for some Parkinson’s patients, who currently rely on drugs to switch on faulty neurones, optogenetics might offer a powerful alternative with no dodgy side effects. Not only that, but how the brain works is still, to a large extent, a mystery. Optogenetics allows scientists to essentially break the brain apart into its different components to isolate different groups of cells to study how each of them work and affect each other: ultimately leading to our ability to sense, think and act .

Post by: Natasha Bray

From secret agents to drunk rats

There’s a spy film (I can’t remember which one) with a famous scene where the secret agent and his enemy sit down for drinks. The agent secretly slips a pill into his mouth to counter the effects of the alcoholic beverages they both proceed to consume. Throughout the rest of the night, the spy retains all his mental faculties, knowing that meanwhile his enemy will succumb to impaired judgement, delayed reflexes and slurred speech. This is all caused by the alcohol slowing down the enemy’s brain by binding onto ‘depressant’ receptors, called GABAA receptors, making them more active – in turn, slowing down the brain.

Not to mention the secondary bodily actions alcohol has on the drunken enemy. Alcohol limits the production and release of the antidiuretic hormone vasopressin, meaning that important salts and fluids are excreted by the kidneys in his urine. The alcohol irritates the stomach lining so much that his brain concludes that the stomach’s contents must be harmful thus causing a feeling of nausea. The enemy’s sleep is also affected. As a compensatory reaction to the alcohol, his body produces glutamine; a stimulant which prevents deep restful sleep and can even trigger tremors, anxiety, restlessness and high blood pressure the next day. All in all, the next morning the enemy will experience the dreaded post-intoxication syndrome – also known as a hangover.

So what is the agent’s ‘magic’ pill that protected him from this dreaded sequence of events? Today the internet is full of suggestions, many herbal or vitamin-based. Not surprisingly, there is a huge market for ‘miracle’ hangover cures. Yet hardly any claim to be able to curb the primary effects of alcohol – feeling ‘drunk’. Recently, however, scientists at the University of California have tested a natural substance called DHM (taken from an Asian tree) on rats. The rats were given a dose of alcohol equivalent to a binge of 15-20 pints of beer. The rats that weren’t given the DHM lost their ‘flipping’ reflex (their ability to stand up after being pushed over) for over an hour. In contrast, the rats given DHM before the alcohol only lost their ‘flipping’ reflex for around 15 minutes. In other words, DHM made the rats extremely tolerant to alcohol.

Still, perhaps the most important finding from this study was DHM’s longer-term effects on alcohol addiction. Rats, just like humans, can become addicted to alcohol. If the alcohol was mixed with DHM, however, the rats drank much less than their untreated counterparts, possibly because it binds to the same GABA receptors that alcohol does but without the same ‘depressant’ effects. The researchers plan to test DHM on humans, with a view to hopefully using it to treat alcoholism.

Post by: Natasha Bray

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