(MCT) -- In their hunt for a switch in the brain that turns on and off the drive to eat, obesity researchers have come up with a bright idea: They have tried a relatively new technique to activate or suppress certain neurons' electrical activity - introducing tiny molecular lights called optogenetics into cells' midst. In mice, at least, the technique has helped identify both the exact brain cells and complex cascade of processes that prompt the dispatch of a "stop eating" signal from the brain to the gut.
The team's findings, published recently in the journal Nature Neuroscience, underscore that satiety signaling is a far from simple process. When a sensation of fullness - or of distaste or sickness - prompts us to stop eating, that appears to be the orchestrated result of the activation of one class of neurons and the inhibition of a distinct but related class of neurons, all located in the same tiny region.
To make matters even more complex, the region of the brain from which satiety signals are sent forth - the amygdala central nucleus - is a center of emotional processing, specifically of fear and anxiety. So researchers needed to test whether flipping the satiety switch to "on" would also turn on emotional angst or malaise. That's a key concern for those who will someday use these findings to devise new weight-loss medications.
On that question, at least, the news was good. When scientists "turned the lights on" and activated a unique cluster of cells in the amygdala central nucleus associated with satiety, the effect was not increased anxiety, but calm: In lab tests, mice whose satiety neurons were activated by molecular light were no more likely to show signs of fear than were control mice: They just ate less. A lot less.
The researchers were able to glean which neurons process satiety signals by genetically engineering light-sensitivity into certain cells. Then they were able to learn about those cells' roles in a given process - in this case, satiety - by shining lights on those cells, activating them. In this case, they learned that satiety signals resulted when one group of cells sensitive to the neurotransmitter GABA are activated, and that they were suppressed when a second group of GABA-sensitive cells were turned on.
Gauging the presence and strength of a satiety signal was easy enough: they could see how much - or little - mice would eat when different clusters of GABA-sensitive cells in the amygdala were activated.
The population of amygdala central nucleus neurons identified by the researchers as implicated in satiety "suggests that these cells could provide a target for therapeutic interventions to treat obesity, anorexia or other eating disorders," the researchers wrote.
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