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Autoimmune autonomic ganglionopathy is a type of immune-mediated autonomic failure that is associated with antibodies against the ganglionic nicotinic acetylcholine receptor present in sympathetic, parasympathetic, and enteric ganglia. Typical symptoms include gastrointestinal dysmotility, orthostatic hypotension, and tonic pupils. [1]
A finding, along with medical history, of ganglionic neuronal acetylcholine receptor and N-type voltage-gated calcium channel autoantibodies in the blood stream would result in a medically acceptable diagnosis of AGID. [3]
Antibodies to GM1 are increased in Guillain–Barré syndrome, dementia and lupus but their function is not clear. [4] There is some evidence to suggest antibodies against GM1 are associated with diarrhea in Guillain–Barré syndrome. [5] GM1 antibodies are also seen in Multifocal Motor Neuropathy (MMN), a rare antibody-mediated inflammatory ...
The exact subunit stoichiometry is not known and it is possible that more than one functional α3β4 receptor assembles in vivo with varying subunit stoichiometries. Ligands which inhibit the α3β4 receptor have been shown to modulate drug-seeking behavior, [ 6 ] making α3β4 a promising target for the development of novel antiaddictive agents.
The disorder occurs when the immune system malfunctions and generates antibodies that attack the body's tissues. The antibodies in MG attack a normal human protein, the nicotinic acetylcholine receptor, or a related protein called MuSK, a muscle-specific kinase. [38] [39] Other, less frequent antibodies are found against LRP4, agrin, and titin ...
Binding of acetylcholine to the N termini of each of the two alpha subunits results in the 15° rotation of all M2 helices. [2] The cytoplasm side of the nAChR receptor has rings of high negative charge that determine the specific cation specificity of the receptor and remove the hydration shell often formed by ions in aqueous solution.
Some have antibodies that bind synaptotagmin, the protein sensor for calcium-regulated vesicle fusion. [6] Many people with LEMS, both with and without VGCC antibodies, have detectable antibodies against the M1 subtype of the acetylcholine receptor; their presence may participate in a lack of compensation for the weak calcium influx. [6]
The nicotinic antagonist hexamethonium, for example, does this by blocking the transmission of outgoing signals across the autonomic ganglia at the postsynaptic nicotinic acetylcholine receptor. Because ganglionic blockers block both the parasympathetic nervous system and sympathetic nervous system, the effect of these drugs depends upon the ...