The Plasticity of Autonomic Ganglia

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 292

Special Issue Editor


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Guest Editor
Departamento de Biología Celular and Fisiología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico
Interests: acetylcholine; GABA; co-transmission; neuroplasticity; transmitter segregation; synapse; gLTP; binge-eating disorders; dysautonomia; heart disease

Special Issue Information

Dear Colleagues,

The autonomic ganglia, long regarded as passive relay centers within the autonomic nervous system, are now understood to possess remarkable plasticity. Far from being static structures, these ganglia exhibit dynamic changes in response to the development, homeostatic requirements, injury, disease, and aging. This Special Issue, titled “Plasticity of Autonomic Ganglia”, presents a selection of original research articles and reviews that explore the cellular, molecular, and functional mechanisms underlying this adaptability.

Contributions to this Special Issue examine a wide spectrum of topics, including ganglionic long-term potentiation (gLTP), synaptic remodeling, neurotransmitter switching, neuroimmune interactions, and the role of trophic factors in ganglionic plasticity. Studies span multiple model systems and methodologies, reflecting the interdisciplinary nature of this relevant field. Importantly, several articles address how plastic changes in autonomic ganglia contribute to pathological conditions such as stress, hypertension, heart failure, metabolic syndrome, and binge-eating disorders offering new perspectives on therapeutic targets.

By compiling these diverse yet complementary studies, this Special Issue aims to provide a comprehensive overview of current progress and to stimulate further investigation into the plastic nature of autonomic ganglia. We hope it serves as a valuable resource for neuroscientists, physiologists, and clinicians interested in the complex regulation of autonomic function.

Dr. Miguel Angel Morales
Guest Editor

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Keywords

  • acetylcholine
  • GABA
  • co-transmission
  • neuroplasticity
  • transmitter segregation
  • synapse
  • gLTP
  • binge-eating disorders
  • dysautonomia
  • heart disease

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Published Papers (1 paper)

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Research

13 pages, 1352 KB  
Article
Long-Term Potentiation and Neurotransmitter Expression Change in Dysautonomia Linked to Binge Eating Disorder: Protective Role of Exercise
by Fernanda Veladiz-Gracia, Diana Elinos, Constanza González-Sierra, Angel Rubio-Galicia, Fredy Cifuentes and Miguel Angel Morales
Biology 2025, 14(10), 1410; https://doi.org/10.3390/biology14101410 - 14 Oct 2025
Viewed by 200
Abstract
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue The Plasticity of Autonomic Ganglia)
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