As a general rule, the cells of your body ought only grow, survive and proliferate when so directed by upstream messages, hormonal or otherwise. In light of the supreme importance of proper and well-timed growth, it is these messaging systems that have recently become the stars of the show. One area of particular importance is the systems governing the development and survival of neurons. Brain-derived neurotrophic factor (BDNF) is, as its name suggests, is produced in the brain that influences the growth and survival of neurons.
It seems that most everything of interest to the neuroscientist and psychologist involves BDNF functioning, at least at some level. Conditions of persistent stress or depression do not, of course, lend themselves to the survival, growth and prosperity of neurons in certain regions of the brain, and it is becoming clear that disrupted BDNF function is somehow at the root of all this. Curiously, in addition to its putative role in emotional and cognitive disturbances, BDNF has also been linked to obesity and over-eating, though this relationship is not well characterized.
In this study, Cordeira and colleagues began by generating knock-out mice that are incapable of producing BDNF. This may seem a hazardous state of affairs, as BDNF is quite important for normal brain development and function. The developmental abnormalities brought on by wholesale removal of BDNF were avoided by using a specific type of mutant mouse whose ability to produce BDNF only began to decline after birth. These animals showed increased consumption of both regular lab chow, and high-fat lab chow as compared to their unaltered control mice.
So it can therefore be argued that BDNF may have a role in regulating food intake. The next logical step for the researchers to take was to investigate whether BDNF and its receptor TrkB are themselves regulated by various conditions of food access. It seems that they are, as even brief access to high-fat food causes an increase in TrkB. These measures were taken in the ventral tegmental area (VTA), a key site of dopamine production in the brain. Because dopamine is a neurotransmitter involved in the response reward and pleasurable stimuli, it is here suggested that BDNF signaling may be involved in the hedonic aspects of tasty high-fat food.
The theory that BDNF helps make tasty food rewarding is furthered by the discovery here using a drug to activate one of the brain’s dopamine receptors helps to reverse the changes in food intake in the knock-out mice. In the normal mice, giving them this drug decreased their tendency to eat the high-fat food, at least in the period immediately following administration. This was also the case in mutants, but what is interesting is that during the four hours following administration, it was only the BDNF knock-outs that showed a persistent decline; the normal mice quickly resumed their eating. Ultimately this brought the relative caloric intakes of the two strains into much better agreement, suggesting that dopamine functioning is key in BDNF’s regulation of feeding.
So the basic issue we are left grappling with is the following: what role does BDNF really play in feeding? As I mentioned earlier, BDNF is not classically recognized as a feeding signal. Yet, BDNF has been implicated in drug addiction – and one could argue that chronic overeating is something like drug addiction. This argument, by the way, is quite controversial and likely warrants a post covering the debate. For now we shall simply say for some, food can be extremely rewarding and hard to resist, and it is perhaps this trait that underlies some fraction of obesity in our population. And, if this analogy to drug addiction does hold, then perhaps we can throw BDNF into the mix of putative therapeutic and experimental targets.
Cordeira, J., Frank, L., Sena-Esteves, M., Pothos, E., & Rios, M. (2010). Brain-Derived Neurotrophic Factor Regulates Hedonic Feeding by Acting on the Mesolimbic Dopamine System Journal of Neuroscience, 30 (7), 2533-2541 DOI: 10.1523/JNEUROSCI.5768-09.2010