Antibody-mediated impairment and homeostatic plasticity of autonomic ganglionic synaptic transmission
Open accessAbstract
Antibodies against ganglionic acetylcholine receptors (AChR) are implicated as the cause of autoimmune autonomic ganglionopathy (AAG). To characterize ganglionic neurotransmission in an animal model of AAG, evoked and spontaneous excitatory post-synaptic potentials (EPSP) were recorded from neurons in isolated mouse superior cervical ganglia (SCG). In vitro exposure of ganglia to IgG from AAG patients progressively inhibited synaptic transmission. After passive transfer of antibody to mice, evoked EPSP amplitude decreased, and some neurons showed no synaptic responses. EPSP amplitude recovered by day 7 despite persistence of ganglionic AChR antibody in the mouse serum. There was a more persistent (at least 14-day) reduction in miniature EPSP amplitude consistent with antibody-mediated reduction in post-synaptic AChR. Although the quantal size was reduced, a progressive increase in the frequency of spontaneous synaptic events occurred, suggesting a compensatory increase in presynaptic efficacy. The quantal size returned to baseline by 21 days while the frequency remained increased for at least four weeks. Ganglionic AChR antibodies cause an impairment of autonomic ganglionic synaptic transmission. Homeostatic plasticity in autonomic neurotransmission could help explain the spontaneous clinical recovery seen in some AAG patients and may also play an important role in regulating normal autonomic reflexes.
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Anti-gAChR antibodies may impair autonomic ganglionic synaptic transmission, and antibodies that interfere with ganglionic transmission may contribute to dysautonomia in patients with POTS.
“Anti-gAChR antibodies may impair autonomic ganglionic synaptic transmission, and antibodies that interfere with ganglionic transmission may contribute to dysautonomia in patients with POTS.18”
From Autoimmune postural orthostatic tachycardia syndrome (2018) · cites this paper as [18]
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Autoimmune postural orthostatic tachycardia syndrome
Watari, M., Nakane, S., Mukaino, A., Nakajima, M., Mori, Y., Maeda, Y., Masuda, T., Takamatsu, K., Kouzaki, Y., Higuchi, O., et al. (2018) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.524 · Cited by 94 · see citing works
“The prevalence of anti-gAChR antibodies in this study was higher than that in previous study.17 Anti-gAChR antibodies may impair autonomic ganglionic synaptic transmission, and antibodies that interfere with ganglionic transmission may contribute to dysautonomia in patients with POTS.18 Although POTS is pathophysiolog…”
BackgroundInfluential
- Authors
- Wang, Z., Low, P. A., & Vernino, S.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Mayo Clinic (US)
- Corresponding author
- Vernino, Steven
- Venue
- Experimental Neurology
- Publisher
- Elsevier BV
- Published
- 2010-03
- Volume
- 222
- Issue
- 1
- Pages
- 114-119
- ISSN
- 0014-4886 (ISSN-L)
- PMC
- PMC2829424
- OpenAlex
- W2024843700
- Cited by
- 34
- References
- 24
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 2 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 2 · 2013: 3
- FWCI
- 1.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Johns Hopkins University
- University of Texas Southwestern Medical Center
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (P50NS 32352, P50NS032352)
- Topics
- Health Sciences › Medicine › Neurology › Myasthenia Gravis and Thymoma
- Health Sciences › Medicine › Neurology › Autoimmune Neurological Disorders and Treatments
- Health Sciences › Medicine › Neurology › Peripheral Neuropathies and Disorders
- Keywords
- autoimmune autonomic ganglionopathy, acetylcholine receptor antibodies, superior cervical ganglion, synaptic transmission, homeostatic plasticity, excitatory postsynaptic potentials, quantal size, passive antibody transfer, autonomic reflexes
- MeSH terms
- Adult, Animals, Autonomic Nervous System Diseases, Electric Stimulation, Female, Ganglia, Autonomic, Humans, Immunoglobulin G, Male, Mice, Inbred C57BL, Middle Aged, Neuronal Plasticity, Neurons, Receptors, Nicotinic, Time Factors, Microscopy, Immunoelectron, Superior Cervical Ganglion, Excitatory Postsynaptic Potentials, Mice, Young Adult, In Vitro Techniques
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