Structure and diversity of insect nicotinic acetylcholine receptors
A final consideration is the potential influence of repeated exposure to suxamethonium, however we are not aware of any direct action of suxamethonium upon acetylcholine receptor
Detection of autoantibodies to the neuromuscular nicotinic acetylcholine receptor
(ACHR) has proved useful in assisting in the diagnosis of MG; however, the complexity of this disease, combined with the variety of antibodies associated with MG, has led to multiple attempts to correlate disease severity with antibody detection and concentration.
These agents have a positively charged quaternary ammonium group that binds to the negatively charged acetylcholine receptor
These receptors are collectively known as neuronal nicotinic acetylcholine receptors
(nAChRs) because they primarily interact with the brain chemical (i.
Solubilization and characterization of atrial muscarinic acetylcholine receptors
in sucrose monolaurate.
MG is caused by T cell dependent antibodies that bind to and deplete acetylcholine receptors
(AChR) at neuromuscular junctions causing muscle weakness by interfering with neuromuscular transmission and junction architecture.
The scientists from University of California, San Diego studied the properties of the peptide called catestatin that binds nicotinic acetylcholine receptors
found in the nervous system, and developed a pharmacophore model of its active centers.
Inhibition of nicotinic acetylcholine receptors
by telithromycin may cause exacerbation of myasthenia gravis, visual disturbances and hepatic toxicity; the pyridine moiety in telithromycin could be linked to nicotinic acetylcholine receptor
NMBAs either depolarize the per-and post-synaptic membrane receptors or compete with acetylcholine for binding of the acetylcholine receptors
at the neuromuscular junction.
Whether the molecule in its current form binds too many types of acetylcholine receptors
, whether it activates other neurological systems or whether suicide risk is simply elevated among people giving up cigarettes is unknown.
Twenty-four articles discuss topics including: allosteric modulation of G protein-coupled receptors, AMP-activated protein kinase as a drug target, aldo-keto reductases and bioactivation/detoxication, current and future pharmacological treatments for obesity, acute effects of estrogen on neuronal physiology, new insights into the mechanism of action of amphetamines, and nicotinic acetylcholine receptors
and nicotinic cholinergic mechanisms of the central nervous system, among others.