People, scientists included, are always looking for simple, comprehensible explanations for complex phenomena. It’s so satisfying to be able to easily explain something in a sound bite, and sound bites are so much more easily accepted by an audience than some elaborate, difficult collection of details. For example, we often hear homosexual behavior reduced to being a “choice,” the product of a “gay gene,” a “sin,” or something similarly absolute and irreducible…suggesting that it is part of a diverse spectrum of sexual behaviors with multiple causes and that different individuals are different in their behaviors is almost certainly the more accurate description, but that doesn’t satisfy our need for straight, simple, linear causal mechanisms. This is true of most animal behavior, I think—you just can’t crunch it down to one single agent that drives much of anything.
I thought there was one excellent counter-example, though, one that suggested at least some complex behaviors might be reducible to a discrete source: the mating behavior of Microtus voles. It was such a simple, clean story; new results suggest that it was too clean, and that there’s much more to the behavior than was thought.
First, the simple story. There is a gene called the arginine vasopressin 1a receptor (avpr1a). This gene produces a protein that binds to a hormone signal, vasopressin, which is produced by the pituitary gland under a variety of circumstances. A close examination of this gene in voles revealed a variant that had series of short repeated sequences inserted into the regulatory region—an array of short terminal repeat (STR) sequences that were thought to affect the activity of the gene. So far, then we’ve found some voles that have an avpr1a gene with an STR insert (I’ll call them STR+ avpr1a voles), and some voles that lack the insert (STR- avpr1a voles). Variations like this are not surprising.
Now, the interesting part: the vole species first studied showed a strong correlation. The STR+ avpr1a voles, Microtus ochrogaster and Microtus pinetorum, were monogamous species—they got together with a partner and stuck with them for life. The STR- avpr1a voles, Microtus pennsylvanicus and Microtus montanus, were promiscuous and didn’t form that pair bond. The monogamous voles expressed the avpr1a gene in a region of the brain, the ventral palladium, where it was not expressed in promiscuous voles. You should all be thinking that that is an interesting similarity, but correlation is not causation, so what?
The next step was to make transgenic animals, both mice and voles, that contained the STR+ avpr1a. Male mice and Microtus pennsylvanicus were given copies of the STR+ gene, and they then exhibited increased affiliative behaviors—that is, they were more attentive to their mates, with an increase in sniffing (one way rodents show interest is by getting up close and inhaling the aroma of prospective partners) and grooming (another demonstration of affection.) As you might guess, this was a popular subject for a while—a single gene that might make males more affectionate and more loyal to their partner? Oooh, baby, bottle that and put it on the market. (I should clarify, though, that the demonstrations of its effect were all done in transgenic animals, and the gene was present throughout development, so application is a bit impractical.)
Now for the recent complication in the story. A survey of 25 species of voles and other rodents, including the mouse, has found that they all have the STR+ variant of the gene, except for the two closely related species, M. pennsylvanicus and M. montanus, in which this phenomenon was originally described. Loss of the STR insert is the unusual event which occurred just once in this lineage. Monogamy (starred species in the diagram below) is also a minority behavior, so many species are non-monogamous despite having the STR+ avpr1a gene.
They also examined a few primates. We humans also have an STR insertion in our avpr1a gene, but it’s in a different location and contains a different repeat pattern. These repeats in regulatory regions of the gene aren’t unusual at all.
You might be wondering if this means that those original studies with their provocative results were all wrong…and no, it doesn’t imply that at all. It is almost certainly true that avpr1a is one component of some kind of social learning circuitry in the mammalian brain, and tinkering with it can modulate some sociobehavioral traits. That isn’t in question at all. However, what has been tested here is the sufficiency of the avpr1a system for regulating pair bonding behavior, and it clearly is not. There are other neuropeptides besides vasopressin that have effects on social learning, such as oxytocin and dopamine, and they’re all tangled up in rather sophisticated circuits, so there are other pathways and strategies that can generate a preference for monogamy, and other species have used them. There is no single magic circuit to explain a complex behavior.
And sorry, ladies, there isn’t going to be a handy anti-philandering pill, either.
Fink S, Excoffier L, Heckel G (2006) Mammalian monogamy is not controlled by a single gene. Proc. Nat. Acad. Sci. USA 103(29):10956-10960.
Young LJ, Nilsen R, Waymire KG, MacGregor GR, Insel TR (1999) Increased affiliative response to vasopressin in mice expressing the V1a receptor from a monogamous vole. Nature 400:766-768.