|22 Oct 2001 @ 13:17, by sindy|
In Shakespeare's enchanted midsummer forest, a quick sprinkle of magic dust allowed for some very unlikely pairs to fall suddenly, hopelessly, in love. How did Puck so masterfully manage these affairs of the heart? Emory scientists have an answer. They say it's really the brain that orchestrates the forming of such heartfelt, lasting emotional bonds.
These bonds make up the pulse of life--life with lovers, family, friends, business associates. Virtually every form of psychopathology is characterized by abnormal social attachments. Yet, very little is known about social bond formation: its anatomy, chemistry, and physiology.
It may sound a bit clinical to the romantics among us, who envision the complex processes of falling in love or being a loyal friend as more soulful than biologic. However, according to Thomas R. Insel, Emory neuroscientist and director of the Yerkes Regional Primate Research Center, the various forms of attachment, including parent-infant, male-female, and filial, are not unique to humans.
Insel suggests that "at least the neural basis of attachment can be investigated in animal models." These neural pathways, he proposes, also may prove to be important in treating clinical disorders such as autism and schizophrenia, both of which result in social isolation and detachment.
Neuroscientist Tom Insel, who has studied social attachment for the past 15 years, is known for developing the best laboratory model, a rodent from the Midwest call a vole.
aving studied social attachment for 15 years, Insel is known for developing the best laboratory model, using a mouse-sized rodent found in the Midwest called a vole. Voles come in various species, including prairie and montane voles. These two species are 99% genetically identical, "but that last 1% results in some very different social behaviors," Insel explains wryly.
Different, indeed. Field biologists in the wild discovered that highly social prairie voles are the model of family values. They naturally form lasting, monogamous pair bonds (male-female) after mating and prefer the company of their mate to others. The male reacts aggressively toward other males once he's bonded with a female. Vole breeding pairs nest together, and both parents provide extensive and prolonged parental care, with offspring remaining in the nest for several weeks beyond weaning.
By contrast, the montane vole is a loner, nesting in isolation. Love doesn't last beyond a brief interlude. Montanes, who do not form a pair bond after mating, breed promiscuously. The males make terrible dads. Even the females abandon offspring soon after birth.
In the laboratory, Insel and his research team have been able to duplicate the natural behavioral differences of voles in the field. Lining the walls of Insel's laboratory are stacks of variously shaped cages and mazes which help him quantify affiliate behaviors. For instance, he knows that when placed in large cages, prairie voles will spend more than 50% of their time huddled together with their mates. Montane voles will spend less than 5% of the time close to another individual. He has seen that when a pair-bonded prairie vole dies, the surviving partner prefers living alone to taking a new mate. As in the wild, prairie vole dads in the lab are extremely involved with their pups, the very model of Mr. Mom. When separated from their parents, prairie vole pups get very upset, as demonstrated in ultrasonic distress calls. Laboratory montanes, true to form, take no interest in their pups whatsoever, and pups take it all in stride.
As it turns out, one of the major contributing factors to these enormous differences are the peptide hormones oxytocin (OT), active in females, and vasopressin (AVP), active in males. In mammals, cells in the hypothalamus produce these hormones. In rodents, scientists have associated OT and AVP with various social behaviors such as parenting behavior (including parturition and nursing), social memory, territorial behavior, and aggression. Other mammals, like sheep, also exhibit maternal behaviors when the oxytocin switch is turned on. "It's remarkable, really, that the two different peptide systems have been adapted for different roles in male and female mammals," says Insel. "Apparently, at least in voles, they are activated by pair bonding."
As for humans, the role of central oxytocin or vasopressin in forming enduring, selective bonds has remained largely unexplored. "Across human cultures, sexual behavior is consistently associated with pair bonding," Insel says, "although sex is neither necessary nor sufficient for human pair bond formation." In men, AVP peaks during arousal, and oxytocin peaks with ejaculation. While no data from humans regarding OT or AVP in pair bonding exist, studies in monkeys show that increased transmission of the peptides does increase social interaction.
Insel and his colleagues, Zuoxin Wang and Larry Young, are further investigating OT and AVP and their wide-ranging effects in a series of behavioral, cellular, and molecular studies.
In Insel's laboratory, colleague Zuoxin Wang records a female prairie vole's preference in choosing a mate. Typically, prairie voles form lasting, monogamous pair bonds and prefer the company of their mates to others. They are the model of family values, with both parents providing prolonged care. By contrast, montane voles fail to form pair bonds after mating and breed promiscuously. The males make terrible dads, and the females abandon offspring soon after birth.
Study Sheds Light on Why Sex Evolved
Most organisms pass on only half their genes when they reproduce, mingling their genome with that of another. Sexual reproduction not only halves an individual's contribution to the next generation, it leads to all sorts of trouble and expense. Scientists have thus long wondered why sex evolved in the first place. Indeed, as William R. Rice, a biologist at the University of California, Santa Barbara, puts it: "My son only has half of my genes; the other half are from his mother.... However, if I were an asexual female, my offspring would carry all of my genome. I would put twice as many genes into the next generation." Now a study described in the current issue of the journal Science offers new insight.
Popular explanations for the evolution of sexual reproduction hold that sexual recombination of genes allows beneficial mutations to accumulate faster and that it helps to limit the spread of harmful mutations. Rice and UCSB colleague Adam K. Chippindale tested the idea that sexual reproduction also separates beneficial and harmful mutations from each other, allowing good mutations to break free of bad company. Creating artificial populations of asexual fruit flies, the team studied 17 of these asexual populations and 17 populations of normal, sexually reproducing fruit flies for 10 generations. They salted each of the 34 populations with some individuals that had a gene for red eyes instead of white, and arranged for this trait to exert a positive influence on reproductive success. The red-eyed flies thrived in both populations for a few generations, as expected. But the proportion of flies with red eyes eventually ceased to grow in the asexual population. The advantage of having red eyes was balanced by whatever relatively unfit qualities were present in the original carriers of mutation. In the sexual population, however, the red-eye gene continued to penetrate the population.
The researchers predict that given enough generations the red-eye gene would eventually have been present in every individual in the sexual fruit fly population. Moreover, they predict that it would have disappeared in the asexual population. The flies they used varied greatly in reproductive fitness, so each lineage of asexual red-eyed flies was randomly dropped into a background of genetic material that could help or hinder it. In such circumstances, Rice and Chippindale found, even an extremely beneficial mutation cannot itself guarantee reproductive success. Different parts of the genetic background will, over time, determine the survival of a beneficial mutation in an asexual population. Thus, the great benefit of sex is to free good mutations from the limitations of the larger genome in which they occur. By recombining them with other genomes, beneficial mutations are judged by natural selection on their own merits and can emerge into an entire population. —David Labrador
Why Have Sex?
Bacteria don't do it, fungi don't do it, certain sea cucumbers don't do it--have sex, that is. These organisms reproduce asexually, and their method makes our own reproductive strategy seem a bit clunky. Why go to all the trouble of sex when asexual reproduction is so much more efficient? One popular explanation holds that sexual reproduction reduces the number of harmful mutations that can accumulate in a genome. By that reasoning, the higher the rate of dangerous mutations, the more advantageous sexual reproduction should be. Peter D. Keightley of the University of Edinburgh and Adam Eyre-Walker of the University of Sussex set out to test that hypothesis by calculating mutation rates in a number of species. And the results of their study, published today in the journal Science, call the mutation-reduction idea into question.
Examinations of sexually reproducing species ranging from fruit flies to humans revealed that each of the organisms appears to have a lower mutation rate than that necessary to benefit from sexual reproduction, "suggesting that sex is not maintained by its capacity to purge the genome of deleterious mutations," Keightly and Eyre-Walker report. Another widely held explanation--namely that sexual reproduction enables organisms to adapt more quickly to changing environments--may fare better. "While this [study] leaves many other hypotheses to test," they write, "they all share a common feature: it is adaptive evolution that principally drives the evolution of sex, perhaps in combination with other mechanism." --Kate Wong