Two new networks of neurons identified in appetite regulation.

The age-old feeling of hunger, driven by negative energy balance, elicits the craving and consumption of food, and whilst this survival response is in part mediated by neurons in the hypothalamus, the role of specific cell types in other brain regions is less well-defined.  Now, a study from researchers at Rockefeller University identifies two new networks of cells in the brain regulating appetite.  The team states the two types of cells, located in a part of the brainstem called the dorsal raphe nucleus, are potential targets for new drugs to treat obesity by controlling the hunger signals driving the need and consumption of food.  The opensource study is published in the journal Cell.

Past studies from the team showed a hormone called leptin acts on neurons in the brain’s hypothalamus region to suppress hunger. Injections of the hormone were shown to promote dramatic weight loss in patients with a rare leptin deficiency, however, many obese people didn’t respond to this therapy.  These findings led the researchers to conclude obesity must be linked with leptin resistance.  The current study shows modulation of the activity of specific neurons with drugs could bypass leptin resistance and provide a new means for reducing body weight.

The current study investigates the dorsal raphe nucleus, or DRN, using whole-brain imaging to show this part of the brain becomes activated in hungry mice.  Results show mice fed more than their normal amount of food, until they were full, exhibit a different pattern of DRN activity. Data findings show neurons in this part of the brain played a role in feeding behavior.

Results show activated cells in the two groups of mice were triggered by a full belly releasing glutamate, a chemical nerve cells use to signal one another, while the neurons triggered by hunger released a different neurotransmitter, known as GABA.  Data findings show turning on the glutamate-releasing cells in obese mice suppresses the animals’ food intake and causes them to lose weight, confirming the DRN neurons turned on by hunger did indeed drive food intake.

The lab states this was confirmed by flipping on the GABA-releasing neurons in the DRN to increase food intake, automatically turning off the ‘satiety neurons’ to maximize the effect.  They go on to add switching off hunger neurons in obese mice prolonged inhibition of these neurons to dramatically reduce body weight

The team surmises their findings establishes an important role for the dorsal raphe nucleus in regulating feeding and provides a potential pharmacological approach for modulating food intake and body weight.  For the future, the researchers state their findings open up new avenues of research into exactly how the brain controls eating, and possible drugs to treat obesity.

Source: The Rockefeller University

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