Monogamous cheaters

In my previous post I wrote about vasopressin and oxytocin, so-called “love molecules” that promote attachment and pair-bonding in voles and humans. These molecules act on receptors found in the dopamine-reward system to enhance the dopamine “pleasure” response thereby re-enforcing monogamous activities. However, socially monogamous voles, like humans, are prone to “mistakes” or “slip-ups” with males and females frequency engaging in uncommitted sexual behaviors. Indeed, using genetic testing of offspring, researchers have found that many of the species first thought to be “monogamous” like birds and gibbons actually participate in extra-pair copulations. It’s now more exciting to find a species that is actually sexually monogamous (such as the recent discovery of a monogamous frog). Evolutionarily speaking this is not surprising; we want to get it on with as many people as possible to pass on our genes and increase genetic diversity, while at the same time having enough resources to take care of our young. Therefore, it is possible that two competing systems co-evolved in humans: one that promotes monogamy (vasopressin, oxytocin and others) and another previously uncharacterized system that promotes sleeping around with as many people as possible. This predicts that our tendencies towards infidelity and sexual promiscuity could also be genetically encoded.

Is unfaithfulness really all in the genes? A new study published recently in PLoS ONE suggests that it might be, at least in part. The authors linked a certain variant of the dopamine D4 receptor gene to the propensity towards one-night stands (but not the actual number) and the number of sexual partners in those that were unfaithful (but not to unfaithfulness per se, although there was a trend towards significance). Interestingly, people with this variant have less dopamine D4 receptors in the reward centers of the brain and these receptors show less binding to dopamine, suggesting that these individuals might need more dopamine floating around to reach the same feel-good mood. It’s not a surprise then, that this variant has also been associated with a slew of other behaviors that increase dopamine release including addictions, risky behavior and novelty-seeking.

So, what does this mean? The authors are careful to point out that the dopamine D4 receptor gene should not be labeled the “cheating gene” or the “promiscuity gene” (although it already has) since having the variant does not necessarily mean that you will sleep around or be unfaithful. Many other genetic, environmental (alcohol) and cultural influences are likely to play into an individual’s decision to sleep around or cheat. In addition, the variant may be associated with a third confounding variable like being more honest about sexual behavior, more attractive, etc. Or it may simply be associated with risky behavior and novelty-seeking, increasing the likelihood of wanting uncommitted sex.

For now, I’d hold off on sending your significant other for genetic testing.

Part 3 of 3: Stress and the Aging Brain

                 Perhaps where we see the most extensive effects of stress on the brain is in adulthood and into older age.  In rats, it has been discovered that acute and chronic stress can have very different effects.  An acute stressor (ie. something that only lasts for a short period of time) actually enhances learning and memory, up to a certain point, beyond which too much stress causes performance to deteriorate again.  A state of chronic stress, however, has been shown to have very negative effects on the brain.  Specifically, in rats, chronic stress has been associated with a shrunken hippocampus, specifically because dendrites in the hippocampal neurons begin to die off.  These rats also perform more poorly on memory tasks, especially those involving spatial memory. 

                In fact, if you expose a middle-aged rat to high levels of glucocorticoids, it will perform cognitive tasks similar to the way that a rat in old age would perform them, while reducing glucocorticoid levels in an old rat will enhance its performance.  So, could chronically high glucocorticoid levels contribute to the cognitive decline (memory and word-finding difficulties) that we know happen as we age?  Could they have anything to do with Alzheimer's Disease (AD), a disease characterised by both poor memory and reduced hippocampal volume?  The answer so far is that we're still not sure, but more and more evidence is suggesting that there is at least a correlation between chronic stress, a smaller hippocampus and the prevalence of Alzheimer's.  In monkeys, higher glucocorticoid levels have also been shown to increase Beta-amyloid in the brain, a protein that's known to be a precursor to the cell death seen in Alzheimer's Disease. 

                But why is this?  If you remember back to my first post about stress and the brain, I said that the hippocampus is one of the main mechanisms by which the HPA axis gets shut down.  If you have more and more glucocorticoids, you see hippocampus shrinkage.  This means that there's less and less hippocampal tissue to shut down the HPA axis, leading to chronically high glucocorticoid levels and consequently, a chronically shrinking hippocampus.  It's a feed-forward mechanism.  There's also the neurotoxicity hypothesis, which says that a lifetime of dealing with chronically high glucocorticoid levels may cause the hippocampus to be less able to deal with other aspects of normal aging and therefore its cells are more easily damaged and die off. 

                Don't panic yet.  There's no need to stress out about how your brain is responding to your stressful life.  You're not doomed to an ever-dwindling hippocampus.  It turns out that if you remove a chronic stressor, dendrites that had previously disappeared are actually able to grow back.  Obviously removing every stressor from our lives isn't likely to happen, so there are a few other minor changes that we can make to help us along.  Interestingly, one of the few things that we can do in order to grow new neurons (called neurogenesis, a phenomenon that neuroscientists only came to believe in fairly recently) is exercise.  Exercise has been shown to especially increase neurons in…wait for it…the hippocampus.  How convenient is that?  As if we needed another incentive to stick to our 2011 resolution to hit the gym! 

Cristina McHenry

Concordia University

Adapted from "Effects of Stress Throughout the Lifespan on the Brain, Behaviour and Cognition" by Sonia Lupien et al. and inspired by Wayne Brake's Neuropharmacology course at Concordia University.