Oxytocin and Social Bonding

While most of us would be able to describe what being affectively close to someone feels like, we might find it harder to explain why and how such a connection forms.

Why do we love and what makes us love certain people? Why is love so different depending on the subject of our affection? Is it possible to measure love? What does the complete absence of love in an individual reveal about their health state? With so many questions having been formulated throughout centuries, no wonder love has become a universal conundrum. Traversing various disciplines, it not only represents the realm of the literary, but it has increasingly become one of the central focuses in philosophy, biology, social sciences and neuroscience.

As far as the neuroscientific approaches to love go, this concept is represented by affiliative bonds. Therefore, from now on we shall refer to love as such. For the sake of the reader’s personal interest, we shall further discuss affiliative interactions as they appear and manifest in humans. Affiliation describes the ability of an individual to form close interpersonal bonds with other individuals of the same species. Three prototypes of affiliation have been identified: parental (between children and their parents), pair (between romantic partners) and filial (between friends).

This article is intended to introduce the reader to the evolutionary significance and neurochemical mechanisms underlying social bonding/affiliation. As such, the above-mentioned types of affiliative behaviours will be only in part separately discussed. Instead, we shall focus on what these categories share in common, particularly, the hormone-neurotransmitter oxytocin and the concept of synchrony.

Synchrony refers to the process by which the members of a social group collaborate with each other, in order to achieve a social goal. This kind of collaboration involves concordance in time between members, at the level of behaviour and physiological processes (e.g. hormonal release, neural firing). Through these synchronous processes underlying social reciprocity, each member is introduced to the social milieu, becomes adapted to his/her environment and learns how to survive.

Intimate reciprocal relationships between two individuals in a social group help shape the individual’s moral, empathic and pro-social orientation, as well as social adaptation and self-regulation. The interaction between mother and infant is critical to the social maturation and well-being of the young. Human mothers, just like other mammals, exhibit specific postpartum behaviours, such as affectionate touch, high-pitched vocalisations, expressing positive affect, which lead to the notoriously strong mother-infant bond.

This type of specific attachment relationship coordinates the physiology of the infant with the behaviours of the mother. Moreover, this mother-infant synchrony enables the temporal alignment of the infant’s inner state with the responses of the social environment (via the mother). The absence of a proper interaction between mother and child, especially within the critical period (between 3 and 9 months after birth), has been shown to contribute to the development of autism spectrum disorders (for more information on autism, check out this previous article – Decoding autism).

Romantic attachment is another type of social bonding in humans, with significant implications to the normal psychological functioning of the individual. According to recent studies, both parental and romantic relationships share similar behavioural characteristics (gaze, touch, affects, vocalisations and coordination of these behaviours between the members of the pair) and rely on similar neuroendocrine mechanisms. These mechanisms mainly involve a nine amino-acid neuropeptide known as oxytocin.

Oxytocin acts as both a hormone and a neurotransmitter. It is associated with a variety of functions including the initiation of uterine contractions during parturition, homeostatic, appetitive and reward processes, and last but certainly not least, the formation of affiliative bonds. For the latter, oxytocin plays a very important role in social recognition, maternal behaviour and development of partner preferences.

Oxytocin is produced in the hypothalamus, by the magnocellular neurones clustered in two types of nuclei: the supraoptic and paraventricular. These neurones send projections to the posterior pituitary gland, thus engaging the oxytocin system with the hypothalamic-pituitary-adrenal axis, mediating the stress response, as well as parturition, lactation and milk ejection. Other projections from the paraventricular nucleus go to various forebrain limbic structures (e.g. amygdala, hippocampus), brainstem (e.g. ventral tegmental area) and spinal cord. There are also other areas, apart from the brain and spinal cord, which receive oxytocin signalling, such as the heart, gastrointestinal tract, uterus, placenta, testes etc. With such extensive projections, it comes as no surprise that oxytocin is involved in a wide variety of processes.

In romantic and parental attachment, oxytocin induces the motivation to initiate sexual behaviour, the formation of sexual preferences and the increased stimulant value of the infant for its mother, via its connectivity with the mesolimbic dopaminergic neurones. The neurotransmitter dopamine plays a major role in the reward-motivated behaviour. Therefore, the oxytocin-dopamine interaction is key to the motivation to bond between members of romantic or child-parent relationships.

If you were wondering why the parental attachment has so far been presented only from the perspective of the mother-child relationship, that is because in males a different hormone mediates parental behaviour. Vasopressin can be seen as the male equivalent of oxytocin, as it modulates affiliation, aggression, juvenile recognition, partner preference and parental behaviour in males. Having said that, there are studies which show that oxytocin also supports paternal behaviour and is linked to the father-typical affiliative behaviour.

Oxytocin is also very important in establishing close connection with our best friends (what is known as filial attachment). According to research in this area, children start showing selective attachment to a ‘best friend’ around the age of 3. This kind of interpersonal interaction represents the first attachment to non-kin members of society, therefore, a crucial step in the normal development of any human being.

Depending on the level of synchronous parenting children experienced during infancy, their interactions with best friends can vary in the degree of reciprocity, emotional involvement and concern for the friend’s needs. These behaviours are modulated by oxytocin. During the first 3 years of life, oxytocin secretion in humans depends on the parent’s postpartum behaviour (which is predicted by the parents’ own levels of oxytocin) and, in turn, determines the degree of empathy between close friends. Therefore, a reasonable assumption, which has been recently proven, is that children benefiting from high parental reciprocity during infancy develop better social adaptation, are more friendly and cooperative, and show greater empathy.

All in all, the social bonds we form with members of our social group, be they our family, romantic partners or friends, are dependent on certain hormones and behaviours occurring at critical stages of development. Close attachment bonds with our parents, during early infancy, are later translated into affiliations to non-kin members of the social groups, who we come across during childhood, evolving into intimate friendships during adolescence, which eventually shape the ability of the adult human to form and maintain romantic connections and provide nurture for the next generation.

What we have just discussed is of importance for different aspects. Focusing on oxytocin and synchrony provides better understanding of neurodevelopmental disorders such as autism. At the same time, this focus offers some answers to questions regarding the reasons and mechanisms underlying the many types of love us humans experience throughout our lives.


Feldman, R. (2012). Oxytocin and social affiliation in humans. Hormones and Behavior, 61(3),  380-391. 

Hammock, E. A. ., & Young, L. J. (2006) Oxytocin, vasopressin and pair bonding: implications for autism. Philosophical Transactions of the Royal Society B: Biological Sciences, 361(1476), 2187–2198. 

Decoding autism

About a year ago, I posted an article entitled Autism, which was meant to be more of an introduction into autistic spectrum disorders. Since then, I’ve been meaning to come back to this topic and provide more details about the mechanisms leading to autism, but I knew I need to do some proper research, which my student schedule didn’t really allow at that point.

The reason why I didn’t post any articles in the past three months is mainly my uni dissertation, which took up a lot of time. My chosen topic was Cellular mechanisms of autistic spectrum disorders. This assignment offered me the chance to read a lot of scientific papers and have a far better understanding of autism than I had before. As you probably guessed, this article draws quite a lot on my dissertation.

Some clarifications

When we refer to autism, we must be well aware that this is just an extreme end of the spectrum and that different neurodevelopmental disorders, sharing particular symptoms, are grouped under the term autistic spectrum disorders (ASD). The symptoms that characterise ASD are: impairments in social interaction, communication deficits and repetitive behaviours. Several factors have been linked to ASD, including gene dysregulations, alterations of the immune system and even environmental risk factors.

Discussing all the possible causes of ASD, could probably fit in a book, rather than a blog article, so I will only focus on gene dysregulations. However, if you have any kind of questions, feel free to post them in the comment section and I will try my best to answer them.

About glutamate and one its receptors

In biochemistry there are 20 different amino acids (the building blocks of proteins) and one of them is glutamate. This particular amino acid is very important because, apart from its role in the formation of proteins, it is also the main excitatory neurotransmitter in the brain. This means that glutamate is used to help the neurons communicate with each other and give rise to all sorts of brain activities we know about, including learning and memory.

When two neurons interact at the synapse (the space between the terminals of two interacting neurons), the neurotransmitter is released from the first neuron’s terminal and comes in contact with the second neuron’s terminal. But here’s the trick: in order for the neurotransmitter to have an effect on the second neuron, it has to activate certain structures on its terminal, called receptors. In the case of glutamate, there are three types of receptors, involved in different functions and with different mechanisms. The one we will be focusing on is the type I metabotropic glutamate receptor (mGluR). When this receptor interacts with glutamate, it leads to the translation of specific proteins involved in a process known as long-term depression (LTD), which influences learning and memory. Increased LTD is thought to play a key role in the development of ASD.

The FMRP protein

A few genes have been found to regulate the activity of mGluR and, through it, several cognitive processes. The Fragile X Mental Retardation 1 (FMR1) gene, which codes for the FMRP protein, is one of these genes. It interacts with mGluR-dependent proteins and is thought to regulate synaptic plasticity. During embryonic development, FMRP plays an important role in neural differentiation. Therefore, a mutation in the FMR1 gene leading to the absence of FMRP (a loss-of-function mutation) results in restricted brain development, impaired cognitive functions and autistic symptoms (previously mentioned). This mutation has been found in patients suffering from autism and especially from another brain disease, Fragile X Sydrome, which is the most common monogenic (determined by a mutation in a single gene) cause of autism. The activity of FMRP suppresses mGluR-dependent LTD, by inhibiting the synthesis of proteins involved in this process. Therefore, the absence of FMRP results in LTD, which primarily leads to mental disability.

Neuroligins and Neurexins

These represent transgenic protein families, which mediate synapse maturation in neurons using glutamate. Mutations affecting members of neuroligin and neurexin families have been found to be associated with autistic-like behaviours. The effects of these mutations on the brain are very specific, affecting cells in brain regions involved in learning and memory (CA1 pyramidal cells of the hippocampus, the Purkinje cells of the cerebellum), language (brainstem) and social interaction (somatosensory cortex). In normal situations, neuroligins and neurexins trigger mGluR-induced LTD, but their translation is inhibited by FMRP. The absence of FMRP leads to the loss of this inhibition, which results in mGluR-induced LTD.

Possible therapeutic strategies

Research on the links between mGluR transmission and genes involved in neural development resulted in a variety of therapeutic strategies for ASD. Genetic mGluR reduction and mGluR antagonists (drugs that act on this receptor by preventing glutamate to activate it) are the most common examples of treatments. Potential therapeutic candidates are Fenobam and Lithium, which act as antagonists at mGluR. Administered on animal models and on humans suffering from Fragile X Syndrome, these drugs have resulted in cognitive and behavioural improvements. Although there is hope in treating ASD, there is still a lot of research that needs to be done, especially since even diagnosing different autistic spectrum disorders is still a challenging task.

I hope this article gave you a little more insight into the mechanisms underlying autism and that you enjoyed reading it. As I mentioned above, any questions about this topic are welcomed.


Baudouin, S. J. (2014). Heterogeneity and convergence: the synaptic pathophysiology of autism. European Journal of Neuroscience, 39(7), 1107-1113.

Berry-Kravis, E., Hessl, D., Coffey, S., Hervey, C., Schneider, A., Yuhas, J., Hutchison, J., Snape, M., Tranfaglia, M., Nguyen, D. V. & Hagerman, R. (2009). A pilot open label, single dose trial of fenobam in adults with fragile X syndrome. Journal of Medical Genetics, 46(4), 266-271.

Espinosa, F., Xuan, Z., Liu, S. & Powell, C. M. (2015). Neuroligin 1 modulates striatal glutamatergic neurotransmission in a pathway and NMDAR subunit-specific manner. Frontiers in synaptic neuroscience, 7, 11-11.

Etherton, M., Foeldy, C., Sharma, M., Tabuchi, K., Liu, X., Shamloo, M., Malenka, R. C. & Suedhof, T. C. (2011). Autism-linked neuroligin-3 R451C mutation differentially alters hippocampal and cortical synaptic function. Proceedings of the National Academy of Sciences of the United States of America, 108(33), 13764-13769.

Gao, R. & Penzes, P. (2015). Common Mechanisms of Excitatory and Inhibitory Imbalance in Schizophrenia and Autism Spectrum Disorders. Current Molecular Medicine, 15(2), 146-167.

Nosyreva, E. D. & Huber, K. M. (2006). Metabotropic receptor-dependent long-term depression persists in the absence of protein synthesis in the mouse model of fragile X syndrome. Journal of Neurophysiology, 95(5), 3291-3295.

Rojas, D. C. (2014). The role of glutamate and its receptors in autism and the use of glutamate receptor antagonists in treatment. Journal of Neural Transmission, 121(8), 891-905.

Zalfa, F. & Bagni, C. (2004). Molecular insights into mental retardation: Multiple functions for the Fragile X mental retardation protein? Current Issues in Molecular Biology, 6, 73-88.

Image by Isuru Priyaranga


As I was thinking about the way I should structure this article, a question kept running through my head: ”If we were to choose, do we want to be cool idiots or anti-social geniuses?” At first, common sense kicked in: “You cannot really put things like this; when it comes to human beings (and living creatures, in general) there are many shades of grey. Therefore, you can be smart and socially able at the same time. People are complex!” But what is intelligence? What really distinguishes intelligence from geniality? Are geniuses narrow-minded and do they excel in only one or two areas? Doesn’t being smart require broaden interests and different abilities, including social skills? Does intelligence involve creativity? So many questions, so many myths, so much confusion… I decided to write an article about intelligence at some point in the near future, but until then, let us focus on today’s topic – Autism!

Autism Spectrum Disorder is a rather peculiar brain disorder with contradictory manifestations. It is one of the reasons for the avalanche of questions above, and it has often left scientists baffled. I am sure most of you are all well aware of the characteristic symptoms an autistic person portrays. If you remember when we talked about empathy and mirror neurones in a previous article, we mentioned autism in the context of a dysregulation in the activity of mirror neurones. As a result, autistic people do not understand and tend to avoid other people, and they might not allow others to touch them. They also develop stereotypical behaviours. Repetition and strict schedules is what people with autism need in order to feel calm and safe. Anything that is out of the ordinary, according to their particular set of rules, can wreak havoc.

Some of you might add that autistic people have severe mental disabilities. I would like to point out a relevant distinction here: patients with Asperger’s syndrome show normal intelligence and often impressive language skills, and are not characterised by the same anti-social behaviours as autistic patients. The latter was first described by Leo Kanner in 1943, whereas Asperger’s syndrome bears the name of its discoverer who, nevertheless, used the same term (autism) in 1944 to describe the disease.

What is amazing about many autistic people is that, despite their so-called “mental retardation” and subaverage IQ (between 30 and 60), they exhibit incredible and unique talents, usually in one or two fields. These fields can rage from art and music to maths and impressive arithmetic skills. Either they are multi-instrumentalists, polyglots, compulsive drawers or writers, or are able to do almost impossible mental calculations, and it comes as no surprise that autistic people were also notorious geniuses (e.g., Michelangelo Buonarroti, Pablo Picasso, Amadeus Mozart, Charles Darwin, John Nash).

On top of this, autistic people can learn a new language or a classical music composition in a matter of days or even instantaneously (as it is the case of multi-instrumentalist Leslie Lemke). And if you are still not impressed, some have an amazing memory, being able to retain every information they read. Kim Peak, the man who inspired the famous film ” Rain Man”, has stored in his memory all the details in the around nine thousand books he has read throughout his life. Nevertheless, he is regarded as retarded and is almost completely dependent on his father.

But what actually happens inside those incredible people’s brains? What makes them work in a way normal people cannot, and yet still, why do they lack what we have? One possible explanation comes down to genes. It appears that a mutation in the fmrp gene causes the loss of the encoded protein, leading to structural brain modifications. The FMRP protein regulates synthesis of proteins in neurones and its absence leads to overly developed brain tissue.

Another theory has to do with brain trauma (such as in the case of epilepsy) at an early age, which can trigger different parts of the brain to be cross-activated. This, in turn, leads to another very interesting phenomenon – synaesthesia. Therefore, autistic individuals associate numbers or different other objects with colours, odours or shapes. This can account for their unbelievable abilities to memorise so much information. Some scientists believe that it is the loss of particular functions in the brain that trigger the genius abilities, more specifically the brain regions that control “higher” cognitive processes are or become inactivated. Ironic as it sounds, the talents of autistic people, which we all aim for, are actually linked to subcortical areas and in a normal individual are usually suppressed by the functions of the cerebral cortex. We can now understand why normal people are “normal” and autistic people are different.

As always, there is much more to tell, but unfortunately limited space requires this article to come to an end. I will come back to this in a future article about the creativity and intelligence. Until then, how about you reflect on the questions at the beginning of this article for a while? Also, I added a link to a very interesting video about an autistic young man who is not only extremely talented but also (surprisingly!) socially able.

For further information:

Antonio Damasio,1995. Decartes’ Error. Vintage Books

Bear et al., 2006. Neuroscience – Exploring the Brain. s.l.:Lippincott Williams & Wilknins pp. 706

Dick Swaab, 2014. We are our brains – From the womb to Alzheimer’s. Penguin Books, pp. 185-194

Video Daniel Tammet (highly recommended) 

Image by Damaris Pop

Empathy and…mirror neurons!

As I am quite sure all of you have watched Titanic at some point in your lives or at least know the story, I’m gonna ask you one simple question? How did you feel when Jack Dawson died at the end of the movie? Did you burst out into tears, did you feel an overwhelming sadness? If the answer is Yes! (and should be, unless you are some socio-paths, heartless people – just kidding, I didn’t cry either!), this article is meant to briefly explain what actually happened in our brain at that time. 

Psychologists would call this empathy. And that’s true. For a few moments you were experiencing what Rose was feeling while she was seeing her lover freezing to death and then drowning. But why did you empathize with a movie character? What do humans empathize at all? It all comes down to neurons. In order to try to understand this complex process that lies behind our ability to put ourselves in someone else’s place, we need to figure out the neurological mechanisms that triggers all this. (This could be a good excuse when someone calls you a wet blanket, for example: ‘It’s not me, it’s my mirror-neurons and oxytocine signalling in the anterior cingulate gyrus’, as you’ll see below) 

Some special motor neurons have been discovered in the frontal lobes of monkeys, that apparently signal both when the animal is performing a particular task and when it’s seeing someone else doing the same thing.They were called mirror neurons.  It’s important to bear in mind: “the same thing”, because for another type of action, other mirror neurons would show activity. Thus, these neurons are highly specific. Evidence of mirror neurons have been recorded in humans as well, using neuroimaging, but there isn’t a 100% certainty they actually exist, as it is in macaques and apes. 

Researchers now believe that mirror neurons (if they indeed exist in humans) are also involved in the development of learning (in particular, in language formation); they also appear to account for the evolution of mankind throughout the history (from homo sapiens to homo sapiens sapiens – around 200,000 years ago – and the development of arts, modern tools, religious beliefs – later on, around 40,000 years ago). Moreover, many scientists see dysregulation in mirror neurons’ activity as a possible cause of autism – one of the primary symptoms of this disease being the incapacity of the patient to relate himself to the exterior world, hence the anti-social behaviour. 

There are many other long-known brain structures which trigger emotions and empathy, such as the anterior cingulate gyrus, the amygdala, the hippocampus, the neurotransmitter oxytocin…But mirror neurons are a quite novel discovery and may set neuroscientists on track to explain complex processes that happen in our brains. Cool, right? 🙂 

This article is not only about mirror neurons, but also about empathy. I put a link to a short video filmed in India, in which a macaque monkey is being resuscitated by another one, after having been electrocuted. Some say this is a clear sign of empathy in animals (at least in the superior ones; also elephants, dolphins have shown many signs of empathy before). Other say it is a normal altruistic behaviour, present in most animals (from insects to mammals). Ethologists and population geneticists refer to altruism as one of the instincts of putting others in your species first in order to assure species’ survival and evolution and is mostly encountered in animals that have lived in groups. 

What do you think? Do some animals empathise or what we might see as an empathic behaviour is nothing more than pure adaptive instinct?

Monkey video

Interesting article about mirror neurons

Article – Empathy brain differences