MeSH

Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.

Year introduced: 1978

Toxins, contained in cobra (Naja) venom that block cholinergic receptors; two specific proteins have been described, the small (short, Type I) and the large (long, Type II) which also exist in other Elapid venoms.

Year introduced: 2008(1991)

Toxic proteins produced from the species CLOSTRIDIUM BOTULINUM. The toxins are synthesized as a single peptide chain which is processed into a mature protein consisting of a heavy chain and light chain joined via a disulfide bond. The botulinum toxin light chain is a zinc-dependent protease which is released from the heavy chain upon ENDOCYTOSIS into PRESYNAPTIC NERVE ENDINGS. Once inside the cell the botulinum toxin light chain cleaves specific SNARE proteins which are essential for secretion of ACETYLCHOLINE by SYNAPTIC VESICLES. This inhibition of acetylcholine release results in muscular PARALYSIS.

Year introduced: 1978

Toxic secondary metabolites produced CYANOBACTERIA.

Year introduced: 2022

Peptide neurotoxins from the marine fish-hunting snails of the genus CONUS. They contain 13 to 29 amino acids which are strongly basic and are highly cross-linked by disulfide bonds. There are three types of conotoxins, omega-, alpha-, and mu-. OMEGA-CONOTOXINS inhibit voltage-activated entry of calcium into the presynaptic membrane and therefore the release of ACETYLCHOLINE. Alpha-conotoxins inhibit the postsynaptic acetylcholine receptor. Mu-conotoxins prevent the generation of muscle action potentials. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed)

Year introduced: 2000

Toxins isolated from the venom of Laticauda semifasciata, a sea snake (Hydrophid); immunogenic, basic polypeptides of 62 amino acids, folded by four disulfide bonds, block neuromuscular end-plates irreversibly, thus causing paralysis and severe muscle damage; they are similar to Elapid neurotoxins.

Year introduced: 1991(1973)

Venoms from snakes of the subfamily Crotalinae or pit vipers, found mostly in the Americas. They include the rattlesnake, cottonmouth, fer-de-lance, bushmaster, and American copperhead. Their venoms contain nontoxic proteins, cardio-, hemo-, cyto-, and neurotoxins, and many enzymes, especially phospholipases A. Many of the toxins have been characterized.

Year introduced: 1978

Neurotoxic proteins from the venom of the banded or Formosan krait (Bungarus multicinctus, an elapid snake). alpha-Bungarotoxin blocks nicotinic acetylcholine receptors and has been used to isolate and study them; beta- and gamma-bungarotoxins act presynaptically causing acetylcholine release and depletion. Both alpha and beta forms have been characterized, the alpha being similar to the large, long or Type II neurotoxins from other elapid venoms.

Year introduced: 1974(1973)

A disease caused by potent protein NEUROTOXINS produced by CLOSTRIDIUM BOTULINUM which interfere with the presynaptic release of ACETYLCHOLINE at the NEUROMUSCULAR JUNCTION. Clinical features include abdominal pain, vomiting, acute PARALYSIS (including respiratory paralysis), blurred vision, and DIPLOPIA. Botulism may be classified into several subtypes (e.g., food-borne, infant, wound, and others). (From Adams et al., Principles of Neurology, 6th ed, p1208)

a postsynaptic neurotoxin from the venom of the Stephen's banded snake (Hoplocephalus stephensi); MW 6660 Da; has high sequence homology with other elapid short-chain neurotoxins

Date introduced: November 1, 2006

encodes a group of short-chain alpha neurotoxins in an Australian elapid; amino acid sequence in first source

Date introduced: July 6, 2000

nicotinic receptor antagonist which belongs to a family of naturally occurring marine neurotoxins called lophotoxins; structure given in first source

Date introduced: April 20, 1994

nicotinic receptor antagonist which belongs to a family of naturally occurring marine neurotoxins called lophotoxins; RN refers to (1R*,2S*,4S*(S*),5R*,10R*,12S*,14R*,15R*)-(-)-isomer; structure given in first source

Date introduced: April 20, 1994

has 48 aa residues with 6 half-cystine residues; sequence has homology with type 1 long sea anemone neurotoxins; aa sequence given in first source

Date introduced: October 25, 1993

Polycyclic polyether polyketides most often produced by marine organisms, e.g., DINOFLAGELLATES. Many polyether marine toxins are ionophores and neurotoxins and responsible for seafood poisoning.

Year introduced: 2024

Polycyclic polyketides with distinctive ladder shaped multiple polyether motifs. In STREPTOMYCES polycyclic polyketide backbones are assembled by type I modular polyketide synthases which then are modified by epoxidase and epoxide hydrolase to achieve their stereochemistry. Polyether ionophore antibiotics coordinate alkali metal cations with their multiple oxygen atoms which disturbs sodium/potassium concentration gradient. They are widely used to treat and control COCCIDIOSIS. Structurally related MARINE LADDER POLYETHERS are neurotoxins.

Year introduced: 2024

A super-family of non-enzymatic proteins found in ELAPIDAE VENOMS. They possess a unique tertiary structure resembling a hand with three fingers and have diverse biological activities due to sequence and structural variations; some are ALPHA-NEUROTOXINS that bind NICOTINIC ACETYLCHOLINE RECEPTORS.

Year introduced: 2022

avian CNS disease in which myelin degeneration in the white matter are seen in waterfowls, bald eagles. avian vacuolar myelinopathy is linked to CYANOBACTERIAL NEUROTOXINS (e.g., ETOKTHONOTOXIN; L-BMAA).

Date introduced: March 31, 2021

The longest of all venomous snakes and largest Elapid. It is not a member of the Naja genus, although its hood resembles the hood of Naja species. Its bite can deliver large quantities of neurotoxic and cardiotoxic venom, consisting primarily of ALPHA-NEUROTOXINS. King cobras are indigenous to forests of India and Southeast Asia.

Year introduced: 2018