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have produced dozens of different strains of mice, each with their own behavioural ticks, temperaments, and characters.
Interestingly, this quest for new and better experimental fodder has itself become grounds for an experiment. What makes these mice different from one another? The obvious answer would be their genes. A series of small mutations occurring over the span of multiple generations have manifested themselves in the mice’s tiny brains, changing how each breed looks and behaves. Mice, spanning as many as six generations in a single year, can evolve a lot quicker than humans, who hobble miles behind them with a 20-year generational lag. When assisted by the informed hands of professional breeders, a mouse’s evolutionary timeframe can be easily put on fast forward.
But Dr. Michael Meaney and his team questioned this assumption in their 2004 study. To them, a purely genetic explanation for interspecies variation seemed too simplistic. Differences between breeds could be pretty radical, and natural selection is a notoriously slow process, often taking thousands or tens of thousands of years to produce very slight adjustments to the genome. Even when factoring in human intervention, Meaney felt that things were going too fast for genes alone to manage. Something else must be working behind the scenes as well. To prove it, he first selected two very different breeds of mice. The first, called Type A, were skittish, docile, and easily frightened by new places or objects. The second, called Type B, were confident, curious, and almost wholly indifferent to threat.
| Mouse Type | Mouse Behaviour |
| Type A | skittish, docile, and react strongly to stress |
| Type B | confident, curious, and more or less unfazed by new places or experiences |
Meaney took both breeds and performed a cross-fostering study. Six hours after they were born, Type A and Type B mice were taken from their mothers and randomly fostered to mothers of the opposite type. Type A mothers raised Type B infants, and Type B mothers raised Type A infants, hence “cross-fostering.” As a control, some infants were taken and fostered to mothers of the same type — Type A infants with Type A mothers and Type B infants with Type B mothers. The mothers raised their adoptive offspring as their own, and Meaney let the infants reach maturity without any further intervention on his part.
When the mice were roughly 70 days old, they participated in a step-down test. Each mouse was placed on a small raised platform in the centre of an open plain. Meaney observed the mouse’s behaviour for the next five minutes, noting in particular its willingness to explore its new surroundings — though “explore” is perhaps overselling it. The study broke exploration down into three stages: extending the head over the edge of the platform, stepping two feet off of the platform, and stepping completely off of the platform. Hardly a venture worthy of Magellan or Columbus, but for a laboratory-raised rodent weighing little more than an ounce, step-down testing can be a truly harrowing experience. It evokes a deep-seated fear in a creature whose survival strategies have, for thousands of years, relied principally on its ability to scurry and hide. Aloft on a platform, surrounded by flat, open terrain devoid of grass or rocks or any sort of protective crevice or camouflage, they sense the atavistic dread of their wild ancestors, ears and eyes and nose trained to detect the first sign of an incoming hawk, fox, or bobcat. When confronted with the step-down test, docile mice tend to freeze, overcome by terror, while their more adventurous peers waste little time in exploring the boundaries of their new habitat.
It should come as no surprise, then, that Type A mice tend to take far longer than Type B mice to progress through the stages of exploration. Occasionally, Type A mice don’t leave the platform at all, but remain exactly where they’re placed, rigid with terror, until the experimenters remove them. Type B mice, on the other hand, barely hesitate before leaping nimbly from the platform and sniffing inquisitively around the perimeter of the cage.
Here was the crux of Meaney’s experiment. If Type A mice’s skittishness and Type B mice’s fearlessness comes hardwired into their genes, then they should exhibit it regardless of who raised them. However, if their dispositions were instead the product of their environment, then adopted mice should behave much like their step brothers and stepsisters, even though they are born from different breeds.
So which was it? Here’s the strange thing: it was sort of both.
When raised by Type A mothers, Type A mice acted as skittish as ever. They performed poorly on the step-down test, leaving their platforms with great reluctance or freezing with catatonic fright. But when raised by Type B mothers, Type A mice passed the test with flying colours, exploring their cage with the same gusto as their natural-born Type B brothers and sisters. Though mother mice don’t teach their offspring how to react to step-down testing in the conventional sense — few if any of the mothers will have ever even experienced such a thing — something in Type B mice’s maternal behaviour imparts in their foster children a bravado they would have otherwise lacked.
It seems that nurture has won the day. Except that Type B mice would beg to differ. Unlike their Type A peers, Type B mice displayed the same inquisitive, devil-may-care attitudes regardless of who raised them. When raised by Type A mothers, they nevertheless acted like their other biological siblings, sniffing eagerly around the testing site.
| Raised by Type A mothers | Raised by Type B mothers | |
| Type A mice | Skittish, fearful, performed poorly on test | Fearless, curious, performed well on test |
| Type B mice | Fearless, curious, performed well on test | Fearless, curious, performed well on test |
You can see why questions like “nature or nurture?” don’t have easy answers. They seem to lead us only to more questions. Why do environmental influences only work one way? How can Type B mothers subvert the ingrained timidity of Type A mice while Type A mothers are powerless to uproot the brash gusto of their adopted Type B offspring? What separates these two breeds? Meaney’s study can’t answer these questions, but it does at least pose them. And in science, new questions can be just as important as answers.
Of Mice and Men
Dr. Meaney’s study left us wondering what made Type A mice bend like putty beneath the sculpting hands of their environment, while Type B mice were, behaviourally speaking, rigid as stones. Enquiring scientific minds, spellbound as ever by those vast molecular blueprints, turned once again to genes. Of course, as an answer to Meaney’s questions, “genes” is distressingly vague. For the theory to hold any weight, its aim would have to be narrowed considerably. It would have to focus on one gene in particular.
Dr. Joan Kaufman suspected the culprit might be the serotonin transporter gene, known by the tongue-twisting moniker 5-HTTLPR.[18] As we discussed last chapter, the 5-HTT gene comes in two different varieties, long (l) and short (s), so named because one of them is built from a larger nucleotide sequence, making it physically longer than the other. In genetic parlance, these varieties are called alleles. Everybody has the same genes, but not everyone has the same alleles, which is why we are not all genetically identical. For instance, imagine two individuals named Tim and Patricia. Tim has brown eyes and Patricia has blue eyes. The gene determining their eye colour is largely similar — it sits on the same chromosome, is more or less the same length, contains an almost identical series of nucleotides, and does the same job in either of them. It is, essentially, the same gene, except that very slight changes have caused it to produce a different outcome in Tim than it does in Patricia. Tim has the brown eye allele of the eye colour gene, while Patricia has the blue eye allele.
Almost every gene in the human body comes in different alleles, which accounts for the tremendous variety of traits between individuals. In the 5-HTT gene’s case, the short allele is less efficient than the long allele, meaning it can generate fewer serotonin transporters in a given time. As serotonin is responsible for regulating mood, digestion, and a number of other important biological functions, a less efficient 5-HTT can, under the wrong circumstances, cause a lot of trouble.
5-HTT sits on the 17th chromosome of every human being and non-human primate, and is present in a similar form in most mammals. Since humans have two copies of chromosome 17, they also have two copies of 5-HTT, and they make good use of both of them. This means that a person can have two long alleles (l/l), two short alleles (s/s), or one copy of each (l/s).
Dr. Kaufman knew about 5-HTT ’s