A study published in today's Science shows that the appetite-regulating hormone leptin causes neurons to be rewired in areas of the brain that regulates feeding behavior.

The research team, led by HHMI investigator Jeffrey M. Friedman, provides an important clue about how leptin exerts its effects on the brain to cause decreased food intake and increased energy expenditure.

"Leptin decreases feeding and fat deposition by acting on two classes of neurons. Leptin suppresses the activity of neuropeptide Y (NPY) neurons and it enhances the activity of proopiomelanocortin (POMC) neurons. Conversely, the absence of leptin increases feeding and fat deposition by exciting NPY neurons and suppressing the activity of POMC neurons."

So here is the problem for the neuroceutical industry:

“If you just look at a region of the brain, you can't tell one neuron from the next,” Friedman said. “And in this case, you had in one brain region neurons theorized to stimulate appetite right next to those believed to inhibit appetite.”

As I mentioned in Addicted, Overweight? specificity at the neuron level will be necessary to develop effective neuroceuticals. Not an easy task.