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V1aR: The Fidelity Gene?


The Buzz

In June of 2004, the BBC News announced that scientists had found a gene capable of turning the "Don Juan of voles into an attentive home-loving husband" (Kettlewell). The article reports the findings of Dr. Larry Young of Emory University and his colleagues. By manipulating expression of a vasopressin receptor in meadow voles (Microtus pennsylvanicus), Dr. Young caused the males of this normally promiscuous species to "reform their ways" and behave more like their cousins, the monogamous prairie voles (Microtus ochrogaster). Previous research indicated the importance of the hormone vasopressin in social interactions such as pair-bonding; Dr. Young mused that vasopressin might be involved in normal human social behavior and may play a role in diseases like autism where people lack social skills.

Image from BBC News


The Science

Dr. Young has been conducting research on vasopressin for several years. He and his colleagues found that arginine vasopressin (V1a) affects male social and reproductive behavior in several species and that the distribution of V1a receptors within the brain varies between species with different forms of social organization (Figure 1). Vasopressin administered to the ventral palladium strenthened "affiliative behaviors" in the monogamous prairie vole but not the relatively asocial, promiscuous montane vole; the montane vole lacks the high densities of the V1a receptor and thus is unaffected by increases in vasopressin concentration. To further test the effects of the V1a receptor, Dr. Young created a strain of mice transgenic for the prairie vole receptor and found that pair-bonding formation increased with administration of vasopressin to the ventral palladium, indicating that the pattern of expression of the receptor in the brain regulates reproductive behaviors like partner selection (Young 1999).

Figure 1: V1a receptor distribution in montane and prairie voles.
Prairie voles have relatively high densities of receptors in the ventral palladium (VP) compared to the more promiscuous montane voles. *permission pending from Nature*

In the study that caught the attention of the popular press, Dr. Young and his colleagues compared the distribution of dopamine and vasopressin receptors in male prairie and meadow voles. The two hormones dopamine and vasopressin both act in the ventral forebrain and regulate pair-bond formation. Dopamine receptor distribution is similar in the two species, however, while vasopressin receptor distribution varies, as Dr. Young previously demonstrated. When the prairie vole V1aR gene was transferred via a viral vector to the ventral palladium of male meadow voles, pair-bond formation was substantially increased in this normally promiscuous species, demonstrating that this one gene profoundly affects social behavior and organization . The researchers stated that they did not know the mechanism by which vasopressin affects reproductive behaviors, but they speculated that vasopressin is released during mating and activates a "reward center" in prairie vole forebrains, causing the male voles to become attached to the female vole with which they mated. The male meadow voles, who lack the vasopressin receptors in the forebrain, would not experience this "mating reward" (Lim 2004).

In addition to studies concerning its effects on fidelity, the vasopressin receptor has been the subject of research on aggressive behavior, anxiety, and other problems in social interactions. An investigation into a possible link between V1aR and autism began with the recognition that vasopressin greatly influences social behavior, thus making vasopressin receptors reasonable candidates for susceptibility to autism. Autistic individuals were screened for nonconservative coding sequence changes; none were found, although evidence of linkage disequilibrium led the researchers to conclude that there may yet be a modest link between autism and V1aR (Wassink 2004). In a study of high-anxiety rats, vasopressin mRNA was found at higher levels in certain areas of the brain in the high-anxiety rats as compared to normal or hypo-anxiety rats. Binding patterns to the vasopressin receptor were unchanged, although anxiety- and depression-related bahavior decreased when the rats were treated with a V1aR antagonist (Wigger 2003). Thus vasopressin seems to be involved in anxiety and depression as well as positive social attachments like pair-bonding.

The Popular Press: Did They Get It Right?

Whenever scientists identify a gene with potential medical ramifications, the popular press gets excited. V1aR has profound implications for human social behavior, and a greater understanding of the vasopressin pathway may open doors for treatment of anxiety disorders, depression, and autism. Media "hype" might be understandable. In this case, the BBC News article was a fairly accurate portrayal of Dr. Young's discovery. The article briefly summarized previous research and this study's findings; however, rather more colorful language was used to describe the gene than is found in the scientific publications. Kettlewell wrote that the V1aR gene caused male meadow voles to "fall in love" and made the "former playboys reform their ways...even when other females tried to tempt them" (2004). The researchers avoided such anthropomorphic concepts in their analysis of the effects of vasopressin, stating simply that vasopressin "increased affiliative behaviors" (Young 1999). The BBC News article also simplified the scientists' description of the way in which vasopressin causes the formation of pair-bonds, mentioning only in passing that the exact mechanism is still unknown and concluding that the reward system "makes [the voles] feel happy...makes the voles think, 'when I'm with this partner I feel good'" (Kettlewell 2004).

In terms of potential medical ramifications, Kettlewell dwelled on the possible link bewteen V1aR and autism susceptibility far longer than evidence for such a connection would suggest. Despite quotes from cautious scientists suggesting merely that vassopressin could play a role in normal human social interactions and therefore in disorders that affect social behavior, the article seems to side with scientists who believe there is a stronger connection between the two. The authors of the study investigating a link between V1aR and autism certainly believed there was a link, although they themselves found little supporting evidence. It seems that both scientists and laypeople are clinging to the idea of a connection to autism susceptibility because of the influential role vasopressin plays in social behavior; even the cautious scientists believe there may be a "modest" link (Kettlewell 2004). It would be a neat solution, to be sure, but so far there is no conclusive proof that V1aR an "autism susceptibility gene." Even labeling it the "fidelity gene" is going a bit far, since research has shown that V1aR is involved in social interactions other than partner selection and faithfulness. To label it as such greatly simplifies its function and its influence. Overall, the article retains accuracy while presenting the discovery in more interesting language than science usually uses. It's not a "bad" source of information for the general public.


Kettlewell, J. 16 June 2004. Fidelity gene found in voles. BBC News. <> Accessed 13 September 2004.

Lim, M.M., et al. June 2004. Enhanced partner preference in a promiscuous species by manipulating the expression of a single gene. Nature 429: 754-757.

Wassink, T.H., et al. April 2004. Examination of AVPR1a as an autism susceptibility gene. Molecular Psychiatry advance online publication. <> Accessed 14 September 2004.

Wigger, A., et al. August 2003. Alterations in central neuropeptide expression, release, and receptor binding in rats bred for high anxiety: critical role of vasopressin. Neuropsychopharmacology 29: 1-14.

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

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