ArticleExperimental neurology2010
Antibody-mediated impairment and homeostatic plasticity of autonomic ganglionic synaptic transmission.
Article in Experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Plasticity in thoracic paravertebral sympathetic postganglionic neurons after high spinal cord transection.bioRxiv : the preprint server for biology · 2025Article
- The Presence of Ganglionic Acetylcholine Receptor Antibodies in Sera from Patients with Functional Gastrointestinal Disorders: A Preliminary Study.Journal of personalized medicine · 2024Article
- Article
- ACh Transfers: Homeostatic Plasticity of Cholinergic Synapses.Cellular and molecular neurobiology · 2023Review
- A novel murine model of autoimmune dysautonomia by α3 nicotinic acetylcholine receptor immunization.Frontiers in neuroscience · 2022Article
- Association between neurosarcoidosis with autonomic dysfunction and anti-ganglionic acetylcholine receptor antibodies.Journal of neurology · 2021Article
- Detecting gastrointestinal manifestations in patients with systemic sclerosis using anti-gAChR antibodies.Arthritis research & therapy · 2020Article
- Postural Tachycardia Syndrome in Children and Adolescents: Pathophysiology and Clinical Management.Frontiers in pediatrics · 2020Review
- The role of the nAChR subunits α5, β2, and β4 on synaptic transmission in the mouse superior cervical ganglion.Physiological reports · 2019Article
- Anti-ganglionic AChR antibodies in Japanese patients with motility disorders.Journal of gastroenterology · 2018Article
- Autoimmune postural orthostatic tachycardia syndrome.Annals of clinical and translational neurology · 2018Article
- Orthostatic Circulatory Disorders: From Nosology to Nuts and Bolts.American journal of hypertension · 2016Review
- Article
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Authors and funding
3 authors.
Funding
Abstract
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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