Eating disorder researchers have discovered a neurocircuit in mice that, when activated, increased their stress levels while decreasing their desire to eat. Findings appear in Nature Communications.
The scientists believe their research could aid efforts to develop treatments for a serious eating disorder called anorexia nervosa, which has the highest mortality rate of any mental disorder, according to the National Institute of Mental Health. People with anorexia nervosa avoid food, severely restrict food, or eat very small quantities of only certain foods. Even when they are dangerously underweight, they may see themselves as overweight.
"We have identified a part of the brain in a mouse model that controls the impact of emotions on eating," said the study's senior author.
Because mice and humans have similar nervous systems, researchers believe their findings could shed light on the part of the human brain that regulates hunger.
The investigators believe they are among the first to demonstrate the role of this neurocircuit in the regulation of both stress and hunger.
While previous research has established that stress can both reduce and increase a person's desire to eat, the neural mechanisms that act on the regulation of eating by stress-related responses largely remain a mystery.
The team focused on a neurocircuit connecting two parts of the mouse brain: the paraventricular hypothalamus, an eating-related zone in the brain, and the ventral lateral septum, an emotional zone in the brain. The authors identify a novel projection from the paraventricular hypothalamus (PVH) to the ventral lateral septum (LSv) that shows a scalable regulation on feeding and behavioral changes related to emotion.
The neurocircuit acts as an on/off switch. When researchers activated the neurocircuit, there was an increase in anxiety levels and a decrease in appetite. Conversely, when the investigators inhibited the neurocircuit, anxiety levels dropped and hunger increased.
The scientists used a research technique called optogenetics to turn the neurons in question on and off.
Weak photostimulation of glutamatergic PVH→LSv terminals elicits stress-related self-grooming and strong photostimulation causes fear-related escape jumping associated with respective weak and strong inhibition on feeding. In contrast, inhibition of glutamatergic inputs to LSv increases feeding with signs of reduced anxiety. LSv-projecting neurons are concentrated in rostral PVH. LSv and LSv-projecting PVH neurons are activated by stressors in vivo, whereas feeding bouts were associated with reduced activity of these neurons. Thus, PVH→LSv neurotransmission underlies dynamic feeding by orchestrating emotional states, providing a novel neural circuit substrate underlying comorbidity between eating abnormalities and psychiatric disorders.
How stress can curb the desire to eat in an animal model
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