[MUSIC] So, welcome back. Neuroscientists are getting pretty good at relating the big five personality traits to the brain, in particular, to the important role played by the gaps between neurons, called synapses. So neuroscientists and geneticists have looked at the genetic variation that exists between individual people that affects how our synapses are used or how effectively or ineffectively they might be used in certain systems in the brain. Neurons speak to each other across synapses using neurotransmitters. There are about 50 neurotransmitters, and they allow nerve cells to communicate with each other. I'm gonna focus on serotonin and dopamine, as they're both involved in mental traits that affect our personality in very direct ways. So let's take neuroticism as an example, one of those five dimensions I mentioned. Neuroticism is a good example for us because it's related to politics which I just talked about it. Now neuroscientists know which part of the brain are involved in the response to threats. There's a circuit involving a structure in the [INAUDIBLE] brain called the amygdala. Which is shown here in red. The amygdala is involved in your emotional responses to the things you experience. So if someone invades your personal space and you fall on your knees. That's the amygdala squeaking away inside your brain. The amygdala is connected via nerves to the cingulate cortex which is shown here. These nerves form a circuit so the information can pass from the amygdala to the cingulate cortex, then from the cingulate cortex back to the amygdala. Your brain is full of circuits like this. Anyway, the cingulate cortex is one of three areas of the brain that are critical for self awareness and one of it's jobs is to think about the amygdala is doing. So if you go to a funny movie, the amygdala feels threatened and it starts firing as if you were in danger. The cingulate cortex working with your frontal cortex is kind of applied back, take it easy, it's just a movie. If one suffer from post-traumatic stress disorder they've got a lot more amygdala activity than they should have and less singular cortex activity. Now, the synapses of the nerves transmitting messages between the amygdala and the cingulate cortex use serotonin to connect them. And the law of the variation in how our amygdala and cingulate cortexes function relates to how the genes involved with serotonin are regulated. So remember, that genes consist of more than just the protein. There are also promoter regions in front of the coding part, which other proteins would go bind, and account for how much of a protein is made and when and where in the brain it's expressed. So, because brain function is specified by circuits, even small differences in the location of brain cells, or the amount of a particular receptor of enzyme, can produce large differences in function. I'll give you an example of how this might work. There are two common forms of the serotonin transporter gene, which codes for the protein that removes the serotonin from the synapse and returns it to the original cell. And they differ in their promoter regions so that one form of the promoter is much better at getting transporters produced than is the other. So some people have more transporters and some people have fewer transporters. And the point here is that if you produce a lot of transporter launching across the synapse fast, quick and then over. Any single gene's impact on motor behavior is gonna be limited, of course, and this single gene or candidate gene studies must be viewed with that in mind. Yet, many studies on these genes suggest that many people, monkeys and rodents With a short or no activity in the form of the transporter gene. Are more sensitive to the environment and tend to suffer significantly more anxiety and depression when faced with stressful life situations. Brain imaging has shown that when stressed, the singular cortex and amygdala light up differently and the circuits that connect these two areas are weakened in those with the low-activity allele. Now, if these studies are correct, the ultimate effect of the low-activity allele is that the part of the brain that's supposed to be dampening down your fear responses doesn't do the job very well. You might ask yourself, why would the low-activity allele have survived in human populations? Well, perhaps being low-stressed and happy is overrated. If what you're trying to do is survive in this route, researchers with that particular world view so that having a high activity allele lets you see the world through rose colored spectacles because you've filtered out bad news. So depending on your attitude when it's not being determined in part by your genes, you can say that the null activity allele isn't about making you prone to anxiety. It's about giving you a more realistic view of the world and the high-activity allele, okay. Putting aside neurosis, you probably have noticed that your worldview is particularly slanted when you're in the intense throes of romantic love, and particularly during orgasm. Well, brain scans show that an orgasm lights up 30 parts of the brain with a massive amount of activity in the cingulate cortex, while it smothers other parts of the brain, like the amygdala. Intense romantic love and orgasms release serotonin and feel-good chemicals, like the so-called cuddle hormone, oxytocin, and its close relation, vasopressin. It's believed to be the oxytocin that smothers the amygdala, and that this increases generosity, trust, and empathy. But unfortunately, that's not an amyloid good. Because the amygdala is the threat detector, it starts vibing when you see danger, risk, uncertainty. So the up-shot of dampening the amygdala is that the brain in love is prone to bad decisions, it's got trouble detecting threats. Like a jealous spouse and connecting with long-term consequences, like the effect of unprotected sex, for example. Now, there's a maxim in biology that for every problem, there's gonna be some animal on which it can be most conveniently studied. A control model system. Now, a lot of what we know about the impact of hormones on our love life was first worked out on some rodents called prairie voles. Now, prairie voles like these live in couples and a father, mother care for the young for many weeks. Now, Montane voles on the other hand, which look pretty much identical to prairie voles, they're much more typical of mammals. The mammals are promiscuous and they take no care of the children. It turns out that the difference between these two closely related species lie in the promoters of their molecular receptors for vasopressin and oxytocin. The receptor's job is to fire up the neurons in response to the hormones. The pair bonding prairie vole has far more receptors in various parts of the brain than the Montane vole. In a clever series of experiments, researchers took the prairie vole's vasopressin receptor gene And using gene therapy, inserted it into the brain of philandering Montane voles, which turned those little Casanovas into faithful husbands and fathers. Now although Montane voles and unfaithful husbands have some key differences, the general mechanisms may be similar. We've got several vasopressin alleles that differ from each other in their promoters and at least one of these alleles is associated with poor hair bonding and promiscuous behavior. You can now get genetically tested to see which variant you have. There's talk of past developing drugs that can modify a man's vasotransive centers. So think about that. The world. Well, as we're on the subject of orgasms, trend studies by Tim Spector and Spector is a king of twin studies, has shown that the ability of women to have orgasms has a strong genetic component. There's an extreme condition called Restless Genital Syndrome, where the nerves supplying the genitals are over excited, and a woman can have up to 100 orgasms a day. Has a common mechanism with a much commoner restless leg syndrome, which is about 60% heritable. Now some of the genes responsible for both conditions, in fact, the axons and nerves, they use the neurotransmitter, dopamine. Dopamine is involved in all kinds of awards, thing that make us feel good, eating, drinking winning a football game, making money, buying a new car. It's the motivation chemical which fuels our cravings, part of our brain require dopamine or they're not satisfied. And other parts of our brain, when carrying out functions essential to our lives and reproduction, they release dopamine to reward us. Oxytocin is also about reward, but it's usually more social. It's the reward about being around friends of going when you see a baby. It's about bonding and trust. Now there are times when you have the combination of oxytocin and dopamine, like when you're making love. Now just as with serotonin, there's a lot of variation among people in the functioning of the dopamine system. There's variation in how much dopamine is produced and then the dopamine receptors on the synapse system pick up the signal and transmit it. There's five different dopamine receptors, and different parts of the brain use different dopamine receptors to receive the same dopamine molecule. So having so many receptors allows different systems in our brain that all use dopamine, to evolve independently from each other. There's genetic variants in these receptive proteins, that cause the receptors to find dopamine less efficiently. That means there is less signal coming across the synapse. When these happen, now people with these mutations are stimulated to crave more stimulation. And this course is novelty-seeking behavior, which can lead to risk taking. It's really dopamine craving that is leading us to seek novelty and risk. Now if we consider whole populations, there be a benefit in it of having Individuals who are risk-takers, and people who avoid risks. For the individual, the golden mean applies. If you avoid all risk, then you aren't likely to achieve anything. If you take risks all the time, you're probably gonna get yourself killed. [SOUND]
