Intermittent fasting promotes anxiolytic-like effects unrelated to synaptic mitochondrial function and BDNF support

Area of Science:

• Neuroscience
• Metabolic research
• Behavioral science

Background:

• Anxiety disorders are associated with mitochondrial dysfunction and reduced neurotrophic support.
• Anxiolytic medications often target mitochondria, suggesting metabolic interventions may be beneficial.
• Intermittent fasting (IF) is a non-pharmacological approach that may improve mitochondrial metabolism.

Purpose of the Study:

• To investigate if chronic intermittent fasting (IF) induces anxiolytic-like effects in mice.
• To examine IF's impact on mitochondrial bioenergetics and trophic signaling in the brain.
• To assess behavioral changes and molecular indicators related to anxiety.

Main Methods:

• Male C57BL/6J mice were assigned to either an ad libitum (AL) diet or alternate-day intermittent fasting (IF) for 10 cycles.
• Behavioral tests included the open field, dark/light box, and elevated plus maze.
• Mitochondrial function, hydrogen peroxide production, calcium handling, and protein expression (apoptotic and neurotrophic markers) were analyzed in isolated nerve terminals.

Main Results:

• Intermittent fasting altered food intake patterns but did not affect body weight or general locomotor activity.
• Mice subjected to IF exhibited significantly decreased anxiety-like behavior.
• No significant differences were observed in mitochondrial bioenergetics, oxidative stress, calcium buffering, membrane potential, or levels of apoptotic and neuroplasticity markers between IF and AL groups.

Conclusions:

• Intermittent fasting exerts anxiolytic-like effects in mice.
• These behavioral benefits are not associated with changes in synaptic neuronergetics or neurotrophic protein expression.
• Intermittent fasting shows potential as a nutritional intervention for anxiety-related disorders.