The closer I get to the end of my Phd contract here in Germany, the heavier the workload as a PhD student and, consequently, I did not have any time to think nor write in the past weeks. Apart from the usual work with experiments, these past weeks I had to be an assistant for a practical course: I had to teach Master’s degree student how to use a pipette, how to perform a transformation of bacteria, how to mini prep plasmids, agarose gel run and a couple more experiments to give them an idea of what working in a lab means. Moreover, I am currently preparing presentations of my project, a couple of poster abstracts for some conferences and a quarterly report. Fortunately, one of the other tasks I will soon approach (and possibly finish sooner) is to write a couple of paragraphs for a review.
Due to all these commitments (and, of course, the experiments I need to complete before my contract ends), I think I will be only able to write once every two weeks, even though I will try my best to keep my blog updated every week. However, I will not talk about the chapters of the review I am currently for now, but today I would like to present to you one of the neuromodulators I am reading about and that I completely forgot during the months in which I was talking about neuromodulators in the brain. Therefore, this week I will talk about vasopressin.
Vasopressin is a neuropeptide of nine amino acids, synthesised by the neurons in the supraoptic and paraventricular nuclei in the hypothalamus. This neuromodulator has been identified as well in neurons belonging to the stria terminalis that project to the lateral septum and medial amygdala, that then project back to the hypothalamus from here (have a look below for a schematic of the areas involved in the vasopressin release/location).
This neuropeptide has some very interesting physiological and endocrinological effects on the whole body, as you could have seen from the schematics above. One of the roles of the vasopressin is to decrease the water loss: for example, the release of this neuromodulator in the body produces a very concentrated urine, while also inducing the constriction of arteries and, consequently, an increase of the blood pressure (that is where its name is coming from). Indeed, during haemorrhage or shock conditions, where there is a drop in blood pressure, there is an increase in the release of vasopressin in order to produce a rise in the blood pressure and bring the conditions back to normal.
Apart from the role of vasopressin on the whole body, since it is already February and we are getting close to Valentine’s day, I want to mention a study on the behaviour of prairie and Montane voles (have a look below for a picture of these two rodents) and how monogamy might actually be influenced by vasopressin and oxytocin (have a look here if you missed my post about this neuromodulators).
It is known that prairie voles create a stable monogamous relationship with the partner after mating, a moment in which there is the release of oxytocin and vasopressin. It seems that these two neuropeptides are involved in the formation of a monogamous relationship. Indeed, the cerebral injection of oxytocin and vasopressin produces the onset of monogamous behaviours in prairie voles that did not mate, while on the other hand, the injection of antagonists (a substance which interferes with or inhibits the physiological action of another) inhibits the formation of a monogamous bond, without altering the mating phase. It is therefore possible to infer that these two neuropeptides are necessary and sufficient to produce a monogamous relationship.
On the other hand, vasopressin and oxytocin have no effect on the promiscuous behaviour of the Montane voles. Even if there are no differences on the general levels of the two neuropeptides, researchers found differences in the regional distributions in the receptors. In the monogamous voles, the receptors are in brain areas associated with reinforcement and conditioning, while the promiscuous voles have fewer receptors in the same areas. This hypothesis is supported by the analogous distribution of vasopressin receptors in monogamous mice and primates, while a different regional distribution of these same receptors is present in promiscuous rodents and primates.
To sum up, a simple model of interpretation believes that the release of oxytocin and vasopressin during mating would lead to the activation of reinforcement circuits in monogamous species, while this cannot happen compared to promiscuous ones, due to the lack of oxytocin and vasopressin receptors in these areas.
But what about humans? I will try to talk about the (semi) monogamous human behaviour in my next post. Stay tuned, Valentine’s day is coming.