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Venom black widow spider

Widow spider venom Black widow Nervous system... [Pg.95]

Black Widow spider toxin Black Widow venom... [Pg.69]

Neurotoxin that produces a massive release of transmitters from cholinergic and adrenergic nerve endings resulting in continuous stimulation of muscles. It also induces formation of an ion channel allowing the inward flow of calcium ions into the nerve cell. It is a white powder obtained from the venom of the black widow spider. [Pg.473]

The amount of acetylcholine present in the synapse and the amount of time that it remains there are critical. For example, the venom of the black widow spider is highly neurotoxic. It contains a protein known as a-latrotoxin that elicits the release of massive amounts of acetylcholine at the neuromuscular junction. Too much of a good thing can be a serious problem. [Pg.293]

We noted above that too much acetylcholine in the synapse or at a neuromuscular junction can be a problem black widow spider venom works that way by causing massive release of this neurotransmitter. There is another way to accomplish the same thing inhibit the normal route by which acetylcholine once released is subsequently removed. That route is degradation by acetylcholinesterase, an enzyme that catalyzes... [Pg.294]

Antivenins capable of neutralizing the toxins present in the venom of various poisonous spiders are also available. The major preparations available include Latrodectus mactans antivenin, which contains antibodies raised against the venom of the black widow spider, and... [Pg.408]

Grishin, E. V. (1996). Neurotoxin from black widow spider venom. Structure and function. Advances in Experimental Medicine and Biology 391 231-236. [Pg.145]

Abstract a-Latrotoxin (a-LTX) from black widow spider venom induces exhaustive release of neurotransmitters from vertebrate nerve terminals and endocrine cells. This 130-kDa protein has been employed for many years as a molecular tool to study exocytosis. However, its action is complex in neurons, a-LTX induces massive secretion both in the presence of extracellular Ca2+ (Ca2+e) and in its absence in endocrine cells, it usually requires Ca2+e. To use this toxin for further dissection of secretory mechanisms, one needs an in-depth understanding of its... [Pg.171]

Ceccarelli B, Grohovaz F, Hurlbut WP (1979) Freeze-fracture studies of frog neuromuscular junctions during intense release of neurotransmitter. I. Effects of black widow spider venom and Ca2+-free solutions on the structure of the active zone. J Cell Biol 81 163-77 Ceccarelli B, Hurlbut WP (1980) Ca2+-dependent recycling of synaptic vesicles at the frog neuromuscular junction. J Cell Biol 87 297-303... [Pg.200]

Dudanova I, Sedej S, Ahmad M et al (2006) Important contribution of a-neurexins to Ca2+-triggered exocytosis of secretory granules. J Neurosci 26 10599-613 Fesce R, Segal JR, Ceccarelli B et al (1986) Effects of black widow spider venom and Ca2+ on quantal secretion at the frog neuromuscular junction. J Gen Physiol 88 59-81 Filippov AK, Tertishnikova SM, Alekseev AE et al (1994) Mechanism of a-latrotoxin action as revealed by patch-clamp experiments on Xenopus oocytes injected with rat brain messenger RNA. Neuroscience 61 179-89... [Pg.201]

Finkelstein A, Rubin LL, Tzeng M-C (1976) Black widow spider venom effect of purified toxin on lipid bilayer membranes. Science 193 1009-11 Fredriksson R, Schioth HB (2005) The repertoire of G-protein-coupled receptors in fully sequenced genomes. Mol Pharmacol 67 1414-25... [Pg.201]

Frontali N, Ceccarelli B, Gorio A et al (1976) Purification from black widow spider venom of a protein factor causing the depletion of synaptic vesicles at neuromuscular junctions. J Cell Biol... [Pg.201]

Hlubek MD, Stuenkel EL, Krasnoperov VG et al (2000) Calcium-independent receptor for a-latrotoxin and neurexin la facilitate toxin-induced channel formation evidence that channel formation results from tethering of toxin to membrane. Mol Pharmacol 57 519-28 Hurlbut WP, Ceccarelli B (1979) Use of black widow spider venom to study the release of neurotransmitters. Adv Cytopharmacol 3 87-115 87-115 Hurlbut WP, Chieregatti E, Valtorta F et al (1994) a-Latrotoxin channels in neuroblastoma cells. JMembr Biol 138 91-102... [Pg.201]

Liu J, Wan Q, Lin X et al (2005) a-Latrotoxin modulates the secretory machinery via receptor-mediated activation of protein kinase C. Traffic 6 756-65 Long SB, Campbell EB, Mackinnon R (2005) Crystal structure of a mammalian voltage-dependent Shaker family K+ channel. Science 309 897-903 Longenecker HE, Hurlbut WP, Mauro A et al (1970) Effects of black widow spider venom on the frog neuromuscular junction. Effects on end-plate potential, miniature end-plate potential and nerve terminal spike. Nature 225 701-3... [Pg.203]

Mee CJ, Tomlinson SR, Perestenko PV et al (2004) Latrophilin is required for toxicity of black widow spider venom in Caenorhabditis elegans. Biochem J 378 185-91 Meiri H, Erulkar SD, Lerman T et al (1981) The action of the sodium ionophore, monensin, or transmitter release at the frog neuromuscular junction. Brain Res 204 204-8 Meldolesi J, Huttner WB, Tsien RY et al (1984) Free cytoplasmic Ca2+ and neurotransmitter release studies on PCI 2 cells and synaptosomes exposed to a-latrotoxin. Proc Natl Acad Sci US A 81 6204... [Pg.203]

Misler S, Falke LC (1987) Dependence on multivalent cations of quantal release of transmitter induced by black widow spider venom. Am J Physiol 253 C469-76 Misler S, Hurlbut WP (1979) Action of black widow spider venom on quantized release of acetylcholine at the frog neuromuscular junction dependence upon external Mg2+. Proc Nad Acad Sci U S A 76 991-5... [Pg.203]

Silva AM, Liu-Gentry J, Dickey AS et al (2005) a-Latrotoxin increases spontaneous and depolarization-evoked exocytosis from pancreatic islet P-cells. J Physiol 565 783-99 Siu R, Fladd C, Rotin D (2006) N-cadherin is an in vivo substrate for PTPo and partidpates in PTPo-mediated inhibition of axon growth. Mol Cell Biol 27 208-19 Smith DS, Russell FE (1966) Structure of the venom gland of the black widow spider Latrodectus mactans. A preliminary light and electron microscopic study. In Russell FE, Saunders PR (eds) Animal Toxins, Oxford, Pergamon, pp 1-15... [Pg.205]

Tse FW, Tse A (1999) a-Latrotoxin stimulates inward current, rise in cytosolic calcium concentration, and exocytosis in pituitary gonadotropes. Endocrinology 140 3025-33 Tzeng MC, Cohen RS, Siekevitz P (1978) Release of neurotransmitters and depletion of synaptic vesicles in cerebral cortex slices by a-latrotoxin from black widow spider venom. Proc Natl Acad Sci U S A 75 4016-20... [Pg.205]

Tzeng MC, Siekevitz P (1979) The binding interaction between a-latrotoxin from black widow spider venom and a dog cerebral cortex synaptosomal membrane preparation. J Neurochem... [Pg.206]

Vicentini LM, Meldolesi J (1984) a Latrotoxin of black widow spider venom binds to a specific receptor coupled to phosphoinositide breakdown in PC 12 cells. Biochem Biophys Res Commun 121 538-44... [Pg.206]

Volkova TM, Pluzhnikov KA, Woll PG et al (1995) Low-molecular-weight components from black-widow spider venom. Toxicon 33 483-9... [Pg.206]

Wanke E, Ferroni A, Gattanini P et al (1986) a-Latrotoxin of the black widow spider venom opens a small, non-closing cation channel. Biochem Biophys Res Commun 134 320-5 Watanabe O, Meldolesi J (1983) The effects of a-latrotoxin of black widow spider venom on synaptosome ultrastructure. A morphometric analysis correlating its effects on transmitter release. J Neurocytol 12 517-31... [Pg.206]

There are about 30,000 species of spiders, virtually all of which produce venom. Fortunately, most lack dangerous quantities of venom or the means to deliver it. Nevertheless, about 200 species of spiders are significantly poisonous to humans. Many of these have colorful common names, such as tarantula, trap-door spider, black widow, giant crab spider, poison lady, and deadly spider. Space permits only a brief discussion of spider venoms here. [Pg.408]

Release of acetylcholine When an action potential propagated by the action of voltage-sensitive sodium channels arrives at a nerve ending, voltage-sensitive calcium channels in the presynaptic membrane open, causing an increase in the concentration of intracellular calcium. Elevated calcium levels promote the fusion of synaptic vesicles with the cell membrane and release of acetylcholine into the synapse. This release is blocked by botulinum toxin. By contrast, black widow spider venom causes all of the cellular acetylcholine stored in synaptic vesicles to spill into the synaptic gap. [Pg.47]

Hurlbut, W.P., Ceccarelli, B. (1979). Use of black widow spider venom to study the release of neurotransmitters. Adv. Cyto-pharmacol. 3 87-115. [Pg.476]

Phylum Arthropoda is the largest phylum in the animal kingdom. Most of the species are nontoxic. However, Class Arachnida contains spiders. Arach-nidism means envenomation from a spider. Most spiders are venomous however, the black widow, brown recluse, and hobo spiders are responsible for a significant number of toxicity events in humans, so these will be discussed in more detail. [Pg.140]

Lactrodectus mactans (lactrodectism is produced by a bite from the female spider). The female is larger than the male. It is noted for a black color that is shiny, with a rounded abdomen and a red hourglass mark on the ventral surface. The black widow spider produces neurotoxic venom. Alpha latrotoxin is the protein of the neurotoxin. [Pg.140]


See other pages where Venom black widow spider is mentioned: [Pg.490]    [Pg.255]    [Pg.635]    [Pg.159]    [Pg.209]    [Pg.75]    [Pg.1776]    [Pg.214]    [Pg.118]    [Pg.172]    [Pg.201]    [Pg.201]    [Pg.202]    [Pg.203]    [Pg.204]    [Pg.490]    [Pg.162]    [Pg.468]    [Pg.199]   
See also in sourсe #XX -- [ Pg.293 ]




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