# Long-Term Potentiation and Neurotransmitter Expression Change in Dysautonomia Linked to Binge Eating Disorder: Protective Role of Exercise

## TL;DR

The study shows that binge eating disorder causes autonomic nervous system changes, which can be prevented by exercise.

## Contribution

The study identifies dysautonomia in a rat model of binge eating disorder and shows that exercise prevents these changes.

## Key findings

- Binge eating disorder in rats caused impaired long-term potentiation in sympathetic ganglia.
- Binge eating increased GABA expression and altered neurotransmitter distribution.
- Exercise prevented the onset of binge eating and its associated autonomic changes.

## Abstract

The autonomic nervous system is the branch of the nervous system that controls internal organs, keeping them in stable balance known as homeostasis. It can adapt its structure and function to meet new demands, a property known as plasticity. When it fails, a condition called dysautonomia occurs, which can arise on its own or be linked to diseases such as binge eating disorder. This disorder involves the repeated, compulsive eating of large amounts of high-calorie food in a short time. In our study, we recreated this disorder in rats to understand how it affects autonomic function and whether exercise has a positive effect. We studied possible changes in neuroplasticity in sympathetic ganglia, particularly in long-term potentiation of nerve transmission and in expression of neurotransmitters. Binge eating was induced through cycles of food restriction and free feeding, combined with access to tasty high-caloric food and frustration stress. We found neuroplasticity changes, including reduced potentiation, increase in one neurotransmitter, and altered neurotransmitter distribution. Exercise prevented the development of binge eating and avoided these nerve changes. Data could help to diagnose binge eating disorder as a form of dysautonomia, improve understanding of its symptoms and body-wide effects, and support exercise as a protective, non-drug intervention.

The autonomic nervous system (ANS) regulates internal organ function to maintain homeostasis. Dysautonomias are ANS disorders involving reduced or excessive sympathetic or parasympathetic activity and can be associated with metabolic syndrome and eating disorders such as binge eating disorder (BED). The ANS exhibits synaptic plasticity phenomena, including long-term potentiation (LTP) and neurotransmitter expression changes, which may influence autonomic function. BED is defined as recurrent, compulsive intake of large amounts of high-calorie food in a short time. Here, we examined dysautonomia in a rat BED model induced by cycles of food restriction and access to highly caloric food, and assessed whether exercise prevents these alterations. After confirming BED induction, we characterized LTP in the superior cervical ganglion (SCG) and analyzed acetylcholine (ACh) and GABA expression and their co-localization/segregation. BED rats exhibited impaired LTP and increased GABA expression. Voluntary aerobic exercise prevented BED onset and the associated changes in LTP and GABA. We propose that BED-associated dysautonomia proceeds at least in the ganglionic sympathetic cholinergic transmission, with reduced sympathetic activity. These results may contribute to a better understanding of the autonomic disorder associated with BED and support exercise as a protective intervention.