Receptors and Personality

Are neural receptors a plausible basis for inheriting personality?

Posted Dec 05, 2016

Most personality traits are highly heritable. Still, there is a great deal of doubt about whether complex human behavior can be genetically determined. Receptors for neurotransmitters are products of gene expression. Perhaps the number of specific receptors in the brain links genotype and personality.

The Vole's Story

Some of the most compelling evidence of a role for neural receptors in personality comes not from humans but from voles. Prairie voles live in pairs with males caring for the young. Amongst mountain voles, males and females meet briefly for mating and then go their separate ways.

The “family-values” behavior of male prairie voles is related to the greater supply of oxytocin receptors in the brain (1, this being the “cuddling hormone” that mediates close social contacts in all mammals including humans).

When the amount of oxytocin receptors was experimentally increased in mountain voles, they changed to resemble prairie voles, establishing pair bonds for the first time (2). (This manipulation involved attaching receptors to cold viruses that served as a vector to carry them into the brain).

The success of the experiment showed that behavioral propensities are strongly affected by the population of neuroreceptors in the brain. The same is likely true of humans and personality theorists have long noted connections between personality types and neurotransmitter systems,

Personality and Neurotransmitters

Various personality theorists have correlated personality traits with activity in different regions of the brain, For instance, fearfulness is linked to the amygdala and pursuit of pleasure is connected to a pathway through the nucleus accumbens.

Such pathways use specific neurotransmitters with the pleasure system using dopamine and fearfulness being based on serotonin pathways.

Activity in neurotransmitter systems can be used to account for major personality dimensions. For instance, extroversion is associated with increased dopamine activity that promotes exploratory behavior.

Serotonin activity is connected to conscientiousness, agreeableness, and anxiety levels. So it is possible to tie some of the major personality dimensions to the level of activity in various neurotransmitter systems in the brain. If that reasoning is correct, how does that help to explain how personality types are inherited?

Personality and Dopamine Receptor Genes

When one neuron stimulates another, the neurotransmitter is released at a synapse and crosses the synaptic cleft before hooking up with a receptor and altering the electrical activity of the recipient neuron.

As complex protein molecules, receptors are products of gene expression and therefore provide a plausible mechanisms through which personality types might be inherited. The reasoning is that if more dopamine receptors are present, for example, the individual would be higher on sensation seeking.

We know that this is unlikely to be a simple relationship. After all, the amount of neurotransmitter available is also important, as is the presence of any degrading enzyme or other chemicals that interact with the neurotransmitter molecules.

Perhaps on account of these complications, it was with some fanfare that the news of dopamine genes being identified as a correlate of sensation seeking was received. The sensation seeking trait is of some interest to clinicians because it predicts earlier use of addictive drugs and other risky behaviors (3).

Dopamine genes are rather weakly correlated with sensation seeking – accounting for less than 4 percent of variability in the trait in one of the best-conducted studies that looked at four dopamine genes (having 273 single nucleotide polymorphisms, or variants) in 635 unrelated people.

Why Receptor Effects on Personality are Weak

The heritability of sensation seeking is around 58 percent and this sets a ceiling on the maximum amount of individual differences that could be explained by dopamine genes. The researchers point out that their study accounts for 6.6 percent of the heritable differences (leaving 93.4 percent unexplained).

Although sensation seeking is highly heritable, like other personality traits, most of these effects are unrelated to genes that code for dopamine receptors.

Perhaps there are many other genes involved, including those that are most active early in development and affect the emergence of dopaminergic pathways. Of course there are possible genetic effects on other neurotransmitter systems that influence sensation seeking. Then, one could point to the amounts of degradative enzymes, and neuromodulators.

Moreover, we are beginning to understand that how genes are expressed in the brain is affected by psychological experiences (4). So the cycle of abusive parenting is now linked to reduced expression of glucocorticoid receptors and increased methylation of the BDNF (brain derived neurotrophic factor) gene in the frontal cortex (that is itself associated with psychopathology in addition to having a role in learning and memory, 5).

At the end of the day, the receptor-neurotransmitter interaction is just one step in a complex chain of events by which neurons process information and trigger sensation-seeking. We are a long way from understanding the genetic basis of personality.

References

1 Insel, R., and Hulihan, T. (1995). A gender-specific mechanism for pair bonding: Oxytocin and partner preference formation in monogamous voles. Behavioral Neuroscience, 109, 782-789.

2 Barber, N. (2004). Kindness in a cruel world: The evolution of altruism. Amherst, NY: Prometheus.

3 Derringer, J., Kreuger, M. R. F., Dick, D. M., et al., (2010). Predicting sensation seeking from dopamine genes. Psychological Science, 21, 1282-1290.

4 Moore, D. S., (2015). The developing genome: An introduction to behavioral epigenetics. New York: Oxford University Press.

5 Franklin, T. B., and Mansuy, I. M. (2010). Epigenetic inheritance in mammals: Evidence for the impact of adverse environmental events. Neurobiology of Disease, 39, 61-65.