Related Experiment Video
Updated: Aug 11, 2026

Subcutaneous Administration of Muscarinic Antagonists and Triple-Immunostaining of the Levator Auris Longus Muscle in Mice
Published on: September 8, 2011
Experimental myasthenia gravis is inhibited by receptor-antireceptor complexes
Abstract:
Experimental autoimmune myasthenia gravis (EAMG) induced in rabbits by immunisation with purified nicotinic acetylcholine receptor from Torpedo marmorata is a highly reproducible model for the human disease. Pretreatment of experimental animals with immune complexes containing receptor and anti-receptor antibodies suppressed the subsequent induction of EAMG. Animals were protected from the normal severe paralysis. Moreover, antibody levels were reduced by synthesis of antibody rapidly terminated. Possible mechanisms are discussed.
Related Concept Videos
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Indirect-Acting Cholinergic Agonists: Pharmacological Actions
At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...
Myasthenia Gravis: Overview and Treatment
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Myasthenia Gravis: Diagnostic Tests
The edrophonium test is a diagnostic tool for myasthenia gravis. It involves...
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Myasthenia Gravis ll: Pathophysiology

