Aug 3, 2026 03:26 PM
https://www.eurekalert.org/news-releases/1138157
EXCERPTS: What enables us to sustain effort toward goals, even when the task becomes increasingly difficult? A recent study by researchers at Nagoya University in Japan revealed the underlying brain mechanism, showing that orexin neurons play a crucial role in driving and regulating motivated behavior. The findings were published in Proceedings of the National Academy of Sciences of the United States of America (PNAS).
Motivational deficits, including loss of motivation, are often seen in mental disorders such as depression, addiction and ADHD. However, the brain mechanisms behind these problems remain largely unclear.
The research team, led by Hiroyuki Mizoguchi, associate professor, and Kiyofumi Yamada, professor emeritus, at Nagoya University's Graduate School of Medicine, focused on orexin neurons. These neurons regulate essential physiological functions such as sleep, appetite and energy expenditure. Although recent studies suggest that orexin neurons also influence motivation, their exact role has remained unclear.
[...] suppressing orexin neurons impaired motivation, but artificially exciting them beyond natural levels did not enhance it. The researchers say this asymmetry suggests orexin neurons are necessary for sustaining motivated behavior, though simply raising their activity may not be sufficient to increase it. Further studies are needed to determine what governs this effect, such as the duration or pattern of orexin neuron activity.
Mizoguchi concluded, "Our study demonstrated significant changes in orexin neuron activity depending on expected rewards and the effort required, suggesting a potential mechanism for translating expectations into sustained action."
Future research will investigate the input and output circuits connected to orexin neurons. A deeper understanding of orexin function may inform new approaches to addressing motivational deficits, including loss of motivation or challenges in sustaining goal-directed behavior. (MORE - missing details, no ads)
EXCERPTS: What enables us to sustain effort toward goals, even when the task becomes increasingly difficult? A recent study by researchers at Nagoya University in Japan revealed the underlying brain mechanism, showing that orexin neurons play a crucial role in driving and regulating motivated behavior. The findings were published in Proceedings of the National Academy of Sciences of the United States of America (PNAS).
Motivational deficits, including loss of motivation, are often seen in mental disorders such as depression, addiction and ADHD. However, the brain mechanisms behind these problems remain largely unclear.
The research team, led by Hiroyuki Mizoguchi, associate professor, and Kiyofumi Yamada, professor emeritus, at Nagoya University's Graduate School of Medicine, focused on orexin neurons. These neurons regulate essential physiological functions such as sleep, appetite and energy expenditure. Although recent studies suggest that orexin neurons also influence motivation, their exact role has remained unclear.
[...] suppressing orexin neurons impaired motivation, but artificially exciting them beyond natural levels did not enhance it. The researchers say this asymmetry suggests orexin neurons are necessary for sustaining motivated behavior, though simply raising their activity may not be sufficient to increase it. Further studies are needed to determine what governs this effect, such as the duration or pattern of orexin neuron activity.
Mizoguchi concluded, "Our study demonstrated significant changes in orexin neuron activity depending on expected rewards and the effort required, suggesting a potential mechanism for translating expectations into sustained action."
Future research will investigate the input and output circuits connected to orexin neurons. A deeper understanding of orexin function may inform new approaches to addressing motivational deficits, including loss of motivation or challenges in sustaining goal-directed behavior. (MORE - missing details, no ads)
