Related Research Articles
Acetylcholine (ACh) is an organic compound that functions in the brain and body of many types of animals as a neurotransmitter. Its name is derived from its chemical structure: it is an ester of acetic acid and choline. Parts in the body that use or are affected by acetylcholine are referred to as cholinergic.
An acetylcholine receptor or a cholinergic receptor is an integral membrane protein that responds to the binding of acetylcholine, a neurotransmitter.
Suxamethonium chloride, also known as suxamethonium or succinylcholine, or simply sux in medical abbreviation, is a medication used to cause short-term paralysis as part of general anesthesia. This is done to help with tracheal intubation or electroconvulsive therapy. It is administered by injection, either into a vein or into a muscle. When used in a vein, onset of action is generally within one minute and effects last for up to 10 minutes.
An anesthetic or anaesthetic is a drug used to induce anesthesia — in other words, to result in a temporary loss of sensation or awareness. They may be divided into two broad classes: general anesthetics, which result in a reversible loss of consciousness, and local anesthetics, which cause a reversible loss of sensation for a limited region of the body without necessarily affecting consciousness.
Nicotinic acetylcholine receptors, or nAChRs, are receptor polypeptides that respond to the neurotransmitter acetylcholine. Nicotinic receptors also respond to drugs such as the agonist nicotine. They are found in the central and peripheral nervous system, muscle, and many other tissues of many organisms. At the neuromuscular junction they are the primary receptor in muscle for motor nerve-muscle communication that controls muscle contraction. In the peripheral nervous system: (1) they transmit outgoing signals from the presynaptic to the postsynaptic cells within the sympathetic and parasympathetic nervous system, and (2) they are the receptors found on skeletal muscle that receive acetylcholine released to signal for muscular contraction. In the immune system, nAChRs regulate inflammatory processes and signal through distinct intracellular pathways. In insects, the cholinergic system is limited to the central nervous system.
Muscarinic acetylcholine receptors (mAChRs) are acetylcholine receptors that form G protein-coupled receptor complexes in the cell membranes of certain neurons and other cells. They play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibers. They are mainly found in the parasympathetic nervous system, but also have a role in the sympathetic nervous system in the control of sweat glands.
End plate potentials (EPPs) are the voltages which cause depolarization of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction. They are called "end plates" because the postsynaptic terminals of muscle fibers have a large, saucer-like appearance. When an action potential reaches the axon terminal of a motor neuron, vesicles carrying neurotransmitters are exocytosed and the contents are released into the neuromuscular junction. These neurotransmitters bind to receptors on the postsynaptic membrane and lead to its depolarization. In the absence of an action potential, acetylcholine vesicles spontaneously leak into the neuromuscular junction and cause very small depolarizations in the postsynaptic membrane. This small response (~0.4mV) is called a miniature end plate potential (MEPP) and is generated by one acetylcholine-containing vesicle. It represents the smallest possible depolarization which can be induced in a muscle.
Tubocurarine is a toxic benzylisoquinoline alkaloid historically known for its use as an arrow poison. In the mid-1900s, it was used in conjunction with an anesthetic to provide skeletal muscle relaxation during surgery or mechanical ventilation. Safer alternatives, such as cisatracurium and rocuronium, have largely replaced it as an adjunct for clinical anesthesia and it is now rarely used.
Neuromuscular-blocking drugs, or Neuromuscular blocking agents (NMBAs), block transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. This is accomplished via their action on the post-synaptic acetylcholine (Nm) receptors.
Mivacurium chloride is a short-duration non-depolarizing neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation.
α-Bungarotoxin is one of the bungarotoxins, components of the venom of the elapid Taiwanese banded krait snake. It is a type of α-neurotoxin, a neurotoxic protein that is known to bind competitively and in a relatively irreversible manner to the nicotinic acetylcholine receptor found at the neuromuscular junction, causing paralysis, respiratory failure, and death in the victim. It has also been shown to play an antagonistic role in the binding of the α7 nicotinic acetylcholine receptor in the brain, and as such has numerous applications in neuroscience research.
Desformylflustrabromine (dFBr) is a NMT derivative indole alkaloid which was first isolated from the marine bryozoan Flustra foliacea.
A nicotinic agonist is a drug that mimics the action of acetylcholine (ACh) at nicotinic acetylcholine receptors (nAChRs). The nAChR is named for its affinity for nicotine.
Bungarotoxins are toxins found in the venom of snakes and kraits. Bites from these animals can result in severe symptoms including bleeding or hemorrhage, paralysis and tissue damage that can result in amputation. The paralytic effects of venom are particularly dangerous as they can impair breathing. These symptoms are the result of bungarotoxin presence in the venom. In actuality, venom contains several distinct bungarotoxins, each varying in which receptors they act on and how powerful they are.
α-Cobratoxin is a substance of the venom of certain Naja cobras. It is a nicotinic acetylcholine receptor (nAChR) antagonist which causes paralysis by preventing the binding of acetylcholine to the nAChR.
Neuronal acetylcholine receptor subunit alpha-1, also known as nAChRα1, is a protein that in humans is encoded by the CHRNA1 gene. The protein encoded by this gene is a subunit of certain nicotinic acetylcholine receptors (nAchR).
The alpha-7 nicotinic receptor, also known as the α7 receptor, is a type of nicotinic acetylcholine receptor implicated in long-term memory, consisting entirely of α7 subunits. As with other nicotinic acetylcholine receptors, functional α7 receptors are pentameric [i.e., (α7)5 stoichiometry].
Philanthotoxins are components of the venom of the Egyptian solitary wasp Philanthus triangulum, commonly known as the European beewolf. Philanthotoxins are polyamine toxins, a group of toxins isolated from the venom of wasps and spiders which immediately but reversibly paralyze their prey. δ-philanthotoxin, also known as PhTX-433, is the most active philanthotoxin that can be refined from the venom. PhTX-433 functions by non-selectively blocking excitatory neurotransmitter ion channels, including nicotinic acetylcholine receptors (nAChRs) and ionotropic glutamate receptors (iGluRs). Synthetic analogues, including PhTX-343 and PhTX-12, have been developed to improve selectivity. While the IC50 values of philanthotoxins varies between analogues and receptor subunit composition, the IC50 value of PhTX-433 at the iGluR AMPA receptor naturally expressed in locust leg muscle is 18 μM and the IC50 value at rat nAChRs is 1 μM.
Histrionicotoxins are a group of related toxins found in the skin of poison frogs from the family Dendrobatidae, notably Oophaga histrionica, which are native to Colombia. It is likely that, as with other poison frog alkaloids, histrionicotoxins are not manufactured by the amphibians, but absorbed from insects in their diet and stored in glands in their skin. They are notably less toxic than other alkaloids found in poison frogs, yet their distinct structure acts as a neurotoxin by non-competitive inhibition of nicotinic acetylcholine receptors.
The alpha-3 beta-4 nicotinic receptor, also known as the α3β4 receptor and the ganglion-type nicotinic receptor, is a type of nicotinic acetylcholine receptor, consisting of α3 and β4 subunits. It is located in the autonomic ganglia and adrenal medulla, where activation yields post- and/or presynaptic excitation, mainly by increased Na+ and K+ permeability.
References
- ↑ Rang HP, Dale MM, Ritter JM, Moore PK, et al. (2003). Pharmacology (5th ed.). Churchill Livingstone. p. 138. ISBN 978-0-443-07145-4.
- ↑ Akk, Gustav; Steinbach, Joe Henry (2003-08-15). "Activation and block of mouse muscle-type nicotinic receptors by tetraethylammonium". The Journal of Physiology. 551 (Pt 1): 155–168. doi:10.1113/jphysiol.2003.043885. ISSN 0022-3751. PMC 2343137 . PMID 12824448.
- 1 2 Alberola-Die A, Fernández-Ballester G, González-Ros JM, Ivorra I, Morales A (2016-02-15). "Muscle-Type Nicotinic Receptor Blockade by Diethylamine, the Hydrophilic Moiety of Lidocaine". Frontiers in Molecular Neuroscience. 9: 12. doi: 10.3389/fnmol.2016.00012 . PMC 4753328 . PMID 26912995.
- ↑ Alberola-Die A, Fernández-Ballester G, González-Ros JM, Ivorra I, Morales A (2016-11-24). "Muscle-Type Nicotinic Receptor Modulation by 2,6-Dimethylaniline, a Molecule Resembling the Hydrophobic Moiety of Lidocaine". Frontiers in Molecular Neuroscience. 9: 127. doi: 10.3389/fnmol.2016.00127 . PMC 5121239 . PMID 27932949.
- 1 2 Cobo, Raúl; Nikolaeva-Koleva, Magdalena; Alberola-Die, Armando; Fernández-Ballester, Gregorio; González-Ros, José Manuel; Ivorra, Isabel; Morales, Andrés (15 July 2020). "Mechanisms of Blockade of the Muscle-Type Nicotinic Receptor by Benzocaine, a Permanently Uncharged Local Anesthetic". Neuroscience. 439: 62–79. doi:10.1016/j.neuroscience.2019.05.043. hdl: 10045/107949 . ISSN 1873-7544. PMID 31158437. S2CID 171092620.
- 1 2 Cobo, Raúl; Nikolaeva, Magdalena; Alberola-Die, Armando; Fernández-Ballester, Gregorio; González-Ros, José M.; Ivorra, Isabel; Morales, Andrés (2018-08-08). "Mechanisms Underlying the Strong Inhibition of Muscle-Type Nicotinic Receptors by Tetracaine". Frontiers in Molecular Neuroscience. 11: 193. doi: 10.3389/fnmol.2018.00193 . ISSN 1662-5099. PMC 6092513 . PMID 30135641.
- ↑ Marshall CG, Ogden DC, Colquhoun D (September 1990). "The actions of suxamethonium (succinyldicholine) as an agonist and channel blocker at the nicotinic receptor of frog muscle". The Journal of Physiology. 428: 155–74. doi:10.1113/jphysiol.1990.sp018205. PMC 1181640 . PMID 2133043.
- ↑ "Acetylcholine". Neurosci.pharm, MBC 3320. Archived from the original on 2007-12-27.