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Neurotoxicology
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Sean D. McCann, Trevonne M. Thompson
Tetrodotoxin (TTX) is found in several animal species including puffer fish, the blue-ringed octopus, the moon snail, and several species of starfish, crabs, worms, toads, and newts. TTX is a sodium channel blocker that interferes with neurotransmission leading to paralysis. TTX is produced by symbiotic bacteria and used as a defense mechanism against predators. Exposure to small amounts of TTX will cause a tingling sensation, which is considered a desirable effect in fugu, a dish in Japanese cuisine prepared from puffer fish. Expert care must be taken to avoid contamination of the meat with excess TTX, as respiratory paralysis can result. The sale of puffer fish is severely restricted in United States. The treatment of TTX poisoning is supportive care, including intubation if necessary.
Hormesis
Published in T. D. Luckey, Radiation Hormesis, 2020
Biologic examples of hormesis include the stimulation by dietary antibiotics, other drugs, mercury, lead, and selenium.134,518,547,922 Tetrodotoxin is an interesting example which is 100,000 times more toxic than plutonium.546 Tetrodotoxin is a natural halucinogen found in Fugu, the puffer fish treasured for centuries in Japan. A small amount of tetrodotoxin produces euphoria; too much produces severe paralysis. In fact, overdoses are thought to kill dozens of Japanese each year. It is also the principle ingredient of the mixture used in creating zombies by Haiti witch doctors.215
Asphyxia due to Metabolic Poisons
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Tetrodotoxin is the toxin in puffer fish and can produce lethal poisoning at extremely low concentrations. It is also found in some other fish and aquatic animals such as certain species of octopus, newt and snail. Tetrodotoxin can also be produced by some bacteria including the Pseudomonas genus. The most prominent and serious effect is respiratory depression, which is due mainly to interference with the action potential generation in striated muscles, causing paralysis. Experimentally it was shown that, after i.v. tetrodotoxin administration, the phrenic nerve continued to elicit action potential for a substantial time after the diaphragm action potential stopped and diaphragm had ceased to contract [5]. Subsequent studies have shown that tetrodotoxin is a sodium channel blocker of excitable tissues (nerves and muscles) in mammals, whereas the animals producing this toxin are protected due to a substitution of the aromatic amino acid chain in the domain I of the sodium channels with non-aromatic amino acids [20].
Abnormal larval neuromuscular junction morphology and physiology in Drosophila prickle isoform mutants with known axonal transport defects and adult seizure behavior
Published in Journal of Neurogenetics, 2022
Atsushi Ueda, Tristan C. D. G. O’Harrow, Xiaomin Xing, Salleh Ehaideb, J. Robert Manak, Chun-Fang Wu
To enable analysis of presynaptic terminal excitability, we also performed electrotonic stimulation on the NMJ (Ganetzky & Wu, 1982, 1983; Wu et al., 1978). Briefly, tetrodotoxin (TTX, 3 µM) was applied to block Na+ channels. To achieve direct electrotonic stimulation of the terminal, a longer duration (2-ms) stimulus was applied near the hemisegment entry point by drawing in the segmental nerve to the suction pipette, so as to effectively control different levels of depolarization with passive electrotonic spreading to the terminal. In this manner, synaptic terminal CaV channels were directly triggered by local depolarization, independent from invasion of axonal Na+ action potentials (Wu et al., 1978). For the generation of plateau EJPs, multiple K+ channel types in presynaptic terminals, including Shaker (Kv1; Jan, Jan, & Dennis, 1977), Shab (Kv2; Ueda & Wu, 2006) and eag ( Kv10; Ganetzky & Wu, 1982, 1983) were blocked by application of 4-aminopyridine (4-AP) and tetraethylammonium (TEA) to allow the development of full-blown regenerative Ca2+-action potentials that sustain prolonged transmitter release (Lee, Ueda, & Wu, 2014; Ueda & Wu, 2009).
Cucumis sativus extract elicits chloride secretion by stimulation of the intestinal TMEM16A ion channel
Published in Pharmaceutical Biology, 2021
Tultul Saha, Joydeep Aoun, Paramita Sarkar, Andrea J. Bourdelais, Daniel G. Baden, Normand Leblanc, John M. Hamlyn, Owen M. Woodward, Kazi Mirajul Hoque
Monolayers were considered polarised and appropriately mounted in an Ussing chamber when resistance was equal to or greater than 1,500 Ω.cm2. The T84 cells grown on Snapwell inserts were mounted in an Ussing chamber for short circuit current (Isc) measurements, which were done at 37 °C with both sides of the monolayer immersed in an oxygenated HCO3-free solution containing (in mM) 140 NaCl, 5 KCl, 1 MgSO4, 2 CaCl2, 10 HEPES, and 10 glucose, pH 7.4. Fluid (5 mL) in each half of the chamber was connected via KCl agar bridges to voltage and current electrodes and clamped at 0 mV using a VCC MC6 multi-channel voltage-current clamp amplifier (Physiologic Instruments). Tetrodotoxin (TTX, 0.5 µM) was used to eliminate the possible neuronal influence on short circuit currents (Isc) and amiloride (10 µM) was used to inhibit epithelial sodium channels (ENaC) (Sheikh et al. 2013). The change in Isc induced by the treatment was expressed as the difference from the baseline to the steady state. The effects of CCE on apical membrane Cl- conductance (ICl) were assessed in T84 cell monolayers after permeabilization of the basolateral membrane with 50 µg/mL nystatin and the establishment of a basolateral to apical Cl- concentration gradient according to our previously published protocol (Hoque et al. 2010).
Attenuation of Retinal Endothelial Vasodilator Function in a Rat Model of Retinopathy of Prematurity
Published in Current Eye Research, 2019
Ayuki Nakano, Asami Mori, Shiho Arima, Daiki Asano, Akane Morita, Kenji Sakamoto, Tohru Nagamitsu, Tsutomu Nakahara
Our results suggest that abnormalities in the vasodilator function of retinal blood vessels persist at the young adult stages. The resolution of the morphological abnormalities in retinal vasculature is commonly reported in ROP patients. However, in patients with a history of ROP, significant abnormalities in visual function have been shown to persist. By assessing retinal cross-sections stained with hematoxylin and eosin, we did not observe any visible structural changes in the retinal layers in ROP rats compared with control rats (unpublished observations). However, the impaired retinal vasodilator function would increase the risk of making local retinal hemodynamics unstable, inducing local ischemia and affecting neuronal function in the retina.26 Therefore, additional research is needed to examine whether the retinal vasodilator function is altered in patients with a history of ROP. In addition, the data presented here were obtained from rats treated with tetrodotoxin and methoxamine. Therefore, the vascular function should be evaluated under normal physiological conditions using conscious rats.