Jon Lindstrom

TL;DR: In the present study, three different monoclonal antibodies raised against the α7 subunit were used to map its distribution throughout the central nervous system of the rat.

TL;DR: MAbs have proven to be excellent probes for these proteins, and have been used to show that neuronal nicotinic AChRs of chickens, rats, and cattle are macromolecules approximately 10 S in size and composed of only 2 kinds of subunits: an ACh-binding subunit and a structural subunit.

TL;DR: Peroxidase-conjugated α-bungarotoxin (P-BGT) was used for the ultrastructural localization of the acetylcholine receptor in end-plates in external intercostal muscles of four patients with myasthenia gravis, in forelimb digit extensor muscles of rats with advanced chronic experimental autoimmune myasthensia Gravis, and in suitable human and rat controls.

TL;DR: The net effect of the mutation is to reduce AChR function, which could result in the hyperexcitability characteristic of epilepsy if the mutant AChRs were part of an inhibitory circuit, e.g., presynaptically regulating the release of GABA.

TL;DR: In the present study, acute EAMG, induced either by passive transfer of syngeneic antibodies or by active immmunization, was inhibited in rats depleted of complement by treatment with cobra venom factor (CoF), implying that redistribution, accelerated degradation, and impairment of the ionophore function of AChR, effects of antibodies described in vitro on extrajunctional A chR, do not play a significant role in vivo in impairing neuromuscular transmission in an