The "Love Hormone" of 2012

Hello and welcome to the Love Hormone Pageant Results Show!  You have cast your votes, the results are in, and the “Love Hormone” of 2012 is… (dramatic pause)… Dopamine!

Dopamine is arguably the most exciting of love hormones. A neurotransmitter produced in the brain, dopamine plays a key role in many motivated behaviors (and love, especially falling in love, involves a lot of motivated behavior). It does this mostly through the mesolimbic reward system, which largely consists of dopamine-producing neuron cells in a brain region called the ventral tegmental area and their projections to other brain regions, including the nucleus accumbens. The mesolimbic reward system exists and has been studied in mammals, birds, reptiles and fish, but the story of how dopamine may be involved in “love” has been explored most with one particular mammal species, the prairie vole.

Photo of a prairie vole pair from Young, Gobrogge, Liu
and Wang paper in Frontiers in Neuroendocrinology (2011)

The prairie vole is a small rodent from the grasslands of the central United States. Unlike approximately 97% of mammal species, prairie voles are socially monogamous and form long-term pair bonds. Male and female pairs travel together, nest together and share parenting duties. Pairs tend to stay together for life and when one partner dies, the surviving partner may never re-pair with a new mate. The role that dopamine plays in how these pair bonds are formed between prairie vole couples has been studied extensively over the last 13 years by Zuoxin Wang at Florida State University and over 30 of his colleagues. Kimberly Young, Kyle Gobrogge, Yan Liu and Zuoxin Wang summarize much of this work in a recent review.

Graph showing that prairie voles prefer to
spend time with their partner after 24 hours
of living together and mating:fromYoung,
Gobrogge, Liu and Wang paper in
Frontiers in Neuroendocrinology (2011)

If you put a virgin male and a virgin female prairie vole in an enclosure and let them live together and mate for 24 hours, they will reliably prefer to spend time with each other rather than with a stranger if given that choice – this is called partner preference. If you enhance dopamine action in the brain, this partner preference will happen even sooner and if you block dopamine receptors throughout the brain, it won’t happen at all. This pattern is even true if you change dopamine action only in the nucleus accumbens, showing that dopamine binding in the nucleus accumbens is critical for the formation of partner preference and pair bonds.

The effect of a hormone or neurotransmitter is completely dependent on its receptors: where they are, how many there are, and how well things bind to them. Dopamine receptors can be classified into two main families, called D1-like and D2-like receptors, and they often have opposite effects. For example, in the prairie vole nucleus accumbens, activating D2 receptors or blocking D1 receptors will cause partner preference to form faster, whereas blocking D2 receptors or activating D1 receptors will prevent it from forming at all. Furthermore, male prairie voles develop more D1 receptors in the nucleus accumbens during pair bonding, which likely work to prevent the animal from forming a pair bond with a second female and keeping him faithful to his mate. Interestingly, promiscuous meadow voles generally have more D1-like receptors in the nucleus accumbens than closely related but monogamous prairie voles. So in the prairie vole nucleus accumbens, activation of D2 receptors promotes the formation of pair bonds and activation of D1 receptors prevents the formation of pair bonds.

However, dopamine is not all roses and chocolate hearts. The action of dopamine in the mesolimbic reward system, and especially in the nucleus accumbens, regulates much more than pair bonding; It regulates a whole suite of motivated social behaviors, like sexual, parental, play, and aggressive behaviors, as well as other motivated behaviors, like seeking food and drugs of addiction. Furthermore, mesolimbic dopamine seems to be at the heart of the interactions between drugs of abuse and social behavior. In another recent review by the same research group, Wang and his colleagues point out that brief exposure to any known drug of abuse activates dopamine activity in the nucleus accumbens and repeated drug exposure causes long-lasting or permanent changes to mesolimbic reward brain areas like the nucleus accumbens. For example, repeated exposure to psychostimulants increases the number and sensitivity of D1 receptors in the nucleus accumbens…Wait, what do active D1 receptors in the nucleus accumbens do? Oh yeah, they prevent pair bonding and partner preference formation. And not surprisingly, giving amphetamine (a psychostimulant) to prairie voles prevents them from forming partner preferences and pair bonds. So if you don’t want to hurt your chances of falling in love some day, just say “No” to drugs, mmmkay?

Dopamine is a busy neurohormone: It is not only involved in love and motivated behaviors, but is also involved in everything from voluntary movement, mood, punishment and reward, cognition, memory, learning, aggression, pain perception and sleep. It is also important to keep in mind that dopamine does not work alone. To regulate pair bonding and partner preference, dopamine interacts with oxytocin, vasopressin, glutamate, GABA, and corticotrophin-releasing factor. But then again, love is about as complex a brain function as you can get – we couldn’t expect a single hormone to go it alone!

So put your hands together one last time to celebrate the “Love Hormone” of 2012: Dopamine!

Want to know more? Check these out:

Young, K., Gobrogge, K., Liu, Y., & Wang, Z. (2011). The neurobiology of pair bonding: Insights from a socially monogamous rodent Frontiers in Neuroendocrinology, 32 (1), 53-69 DOI: 10.1016/j.yfrne.2010.07.006

Young, K., Gobrogge, K., & Wang, Z. (2011). The role of mesocorticolimbic dopamine in regulating interactions between drugs of abuse and social behavior Neuroscience & Biobehavioral Reviews, 35 (3), 498-515 DOI: 10.1016/j.neubiorev.2010.06.004