Researchers have discovered that by activating a neuron in the pre-frontal cortex of a mouse, they can cause the same mouse to eat more than he would have if it had not been stimulated.
For a long time, the notions and discoveries about the brain's role in obesity have been hotly debated. The arguments were all about how the appetite regulation was generated either by higher or lower processes in the brain.
A previous discovery highlighted how the consumption of fructose led to increased activity in the hypothalamus, insula and striatum areas of the brain, where the reward/motivation impulse is originated. Fructose then, prevented the full stimulus from being sent, so that the person eating ate more than would have if fructose had not been consumed since he/she did not receive the 'full' signal from the brain.
The pre-frontal cortex, then, has become the focus of the studies in neuroscience that are trying to pinpoint the exact mechanisms that can cause obesity or overeating.
Dopamine, a neurotransmitter that regulates the pleasure and reward areas of the brain, also regulates appetite. Mice with low dopamine levels lose their appetite and slowly die of starvation.
This led to the present discovery of D1 dopamine-receptor neurons in the pre-frontal cortex. The activation of D1 receptors causes mice to eat more, while switching off D1 receptor caused the mouse to stop eating.
Scientists in the study believe that the discovery reveals how eating behavior is a synergy of decision making and primitive emotional responses.
More importantly, this discovery could lead to therapy that more effectively tackles obesity problems.
Source: MNT/ 1.27.14