ps418

In the thread on early human mating habits, Pyrrho wrote:

As it happens, by chance I've been studying some research on precisely this topic, and this gives a perfect opportunity to bring it up (though I'm still tracking down sources). The following should not in any way suggesting that monogamy is "all in the genes," because it isn't, and all behavior is the result of multiple influences. What I take the data to show is that genetic differences definitely play a role in between-species differences in social behavior patterns like monogamy/polygamy, and may also play a difference in within-species differences in social behavior patterns as well. Obviously though we should be cautious in extrapolating these results to humans or other primates, but they are interesting nonetheless.


About 5% of mammals are monogamous and form pair-bonds (Kleiman, 1977), while most other species are not monogamous and show weak or no pair-bonding. Even closely-related mammal species may differ dramatically in their affiliation and pair-bonding behavior, such as the monogamous Prairie voles and the no social-bond-forming Montane voles (Microtus montanus).

Prairie voles (Microtus ochrogaster) for instance form adult-adult pair bonds after mating, while Montane voles do not. And while Prairie voles spend most of their time in close physical contact with each other, particularly their mating partner (a partner preference), Montane voles are basically antisocial, and spend only a few percent of their time around other voles, and do not form a partner preference (Young et al, 1998). They tend to be more explorers than homebodies. Also, whereas the monogamous voles show mate-guarding agression in an "intruder" test, the nonmonogamous voles do not.

What if any bioogical differences underly these behavioral differences? It has been established that neuroendocrinological processes play a major role in pair-bonding and other aspects of social behavior. In particular, oxytocin and vasopressin are known to play a major role in adult-adult pair bond formation in mammals. In the Prairie voles, injections of these hormones will induce pair bond formation even without mating, and adminstation of vasopressin receptor antagonists before mating prevents the formation of post-mating pair bonds. Injection of vasopressin antagonists also blocks the mate-guarding aggression (Bester-Meredith et al, 1999).

In the nonmonogamous Montane voles, on the other hand, injecting vasopressin has no effect on pair-bonding or affiliative behavior. The reason is that even though both species utilize vasopressin, the distribution of vasopressin receptors in their brains are quite different. In particular, the Prairie voles have high density of receptors in the nucleus accumbens and ventral palladium, areas that are associated with reinforcement and conditioning, while the nonmonoamous Montane vole has few or no such receptors in this region. Interestingly, injection of some drugs (cocaine, amphetamines) into the ventral palladium results in the formation of a place preference -- mice will prefer the place they were at when they recieved the injection (Gong et al, 1996). It may be, therefore, that the activation of the VP by vasopressin following mating in Prairie voles results in a conditioned preference for the mating partner, i.e. monogomy is something like a conditioned preference for a particular conspecific.

In the case of vasopressin 1a receptors, it has been shown that the reason for the different expression of receptors in these brain regions is due to a ~460bp microsattelite insertion into the 5’ flanking region of the V1aR gene (the coding regions are the same). Young et al (1999) demonstrated this by creating transgenic mice which possessed the prairie vole V1aR gene along with 2.2 kb of the 5' flanking region and 2.4 kb of the 3' flanking region. This not only resulted in a Prairie vole like pattern of V1aR expression in the transgenic mice, but behavioral tests showed that the trangenic mice respond to vasopressin with increased affiliative behavior (defined here as as olfactory investigation or grooming of a stimulus female), as do prairie voles. Young et al comment that:

Thus, a fairly trivial genetic difference in a noncoding region can result in a marked difference in the expression of a gene in the brain, which in turn has a major impact of the social behavior of these voles. And it is likely that the association of certain social behaviors with the pattern of vasopressin receptor expression is not peculiar to Montane and Prairie voles, but exists in many other mammals as well. Pitkow et al (2001) states:

And finally, it is also likely that within-species individual differences in expression of V1a receptors are partly responsible for within-species individual differences in attachment and social behavior (Pitkow et al, p. 7395), although this is more speculative.

Refs

Bester-Meredith et al, 1999. Species differences in paternal behavior and aggression in Peromyscus and their associations with vasopressin immunoreactivity and receptors. Hormones and Behavior 36, 25–38.

Gong et al, 1996. Conditioned place preference and locomotor activation produced by injection of psychostimulants in ventral pallidum. Brain Research 707, 64–74.

Kleiman, D.G., 1977. Monogamy in mammals. Quarterly Review Biology 52,39–69.

Pitkow et al, 2001. Facilitation of Affiliation and Pair-Bond Formation by Vasopressin

Receptor Gene Transfer into the Ventral Forebrain of a Monogamous Vole. Journal of Neuroscience 21, 7392–7396.

Young et al,1998. Neuroendocrine bases of monogamy. Trends in Neuroscience 21, 71-75.

Young, L.J., 1999. Oxytocin and vasopressin receptors and species-typical social behaviors. Hormones and Behavior 36, 212–221.

Young et al, 1999. Increased affiliative response to vasopressin in mice expressing the V1a receptor from a monogamous vole. Nature 400, 766-768.