Two new network of neurons in the brainstem identified in appetite regulation.

Hunger, driven by negative energy balance, elicits the craving and consumption of food. Whilst this 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 The Rockefeller University identifies two new networks of cells in the brain which regulate appetite.  The team state that 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 that drive the need and consumption of food.  The opensource study is published in the journal Cell.

Past studies from the team showed that 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.  The researchers concluded that obesity is generally associated 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 that this part of the brain becomes activated in hungry mice.  Results show that mice which were fed more than their normal amount of food, until they were full, exhibit a different pattern of DRN activity. Data findings show that neurons in that part of the brain played a role in feeding behaviour.

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

The lab state that similarly, flipping on the GABA-releasing neurons in the same part of the brain had the opposite effect and increased food intake, and turning on the ‘hunger neurons’ automatically turned off the ‘satiety neurons,’ thus maximizing the effect.  They go on to add that switching off hunger neurons in obese mice prolonged inhibition of these neurons which dramatically reduces body weight

The team surmise that 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 that 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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