Disease relevance of tetraethylammonium

• Secretory responses of intact glomus cells in thin slices of rat carotid body to hypoxia and tetraethylammonium [1].
• Furthermore, a potassium channel antagonist, tetraethylammonium ion (TEA [3 mmol/L]) and a G(i) or G(o) protein inhibitor, pertussis toxin (100 ng/mL) also blocked the flow-induced increase in cGMP [2].
• Serotonin decreases the duration of action potentials recorded from tetraethylammonium-treated bullfrog dorsal root ganglion cells [3].
• The mechanisms of verapamil and tetraethylammonium (TEA) inhibition of voltage-gated K+ channels in LNCaP human prostate cancer cells were studied in whole-cell and outside/inside-out patch-clamp configurations [4].
• 1 The chick biventer cervicis muscle immersed in methohexitone (8.8 x 10(-5) M) responded to tetraethylammonium with contractures which were dose-related [5].

Psychiatry related information on tetraethylammonium

• It has been proposed that the lack of intracellular calcium concentration ([Ca2+]i) increase induced by the potassium channel blocker tetraethylammonium (TEA) in skin fibroblast cell lines identifies patients with both sporadic and familial Alzheimer's disease (AD) [6].

High impact information on tetraethylammonium

• Broadening the presynaptic action potential with the potassium-channel blocker tetraethylammonium, which increases Ca2+ entry, further enhances the rate of replenishment [7].
• 3H-thymidine incorporation by T lymphocytes following PHA stimulation is inhibited by the 'classical' K+ channel blockers tetraethylammonium and 4-aminopyridine, and also by quinine, at doses found to block the K+ channel in voltage-clamped T lymphocytes, suggesting that K+ channels may play a part in mitogenesis [8].
• Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented [9].
• The channels encoded by KAT1 are highly selective for K+ over other monovalent cations, are blocked by tetraethylammonium and barium, and have a single channel conductance of 28 +/- 7 picosiemens with 118 millimolar K+ in the bathing solution [10].
• Tetraethylammonium ion (TEA+) and charybdotoxin (CTX), at concentrations that block calcium-activated potassium channels in smooth muscle cells isolated from cerebral arteries, depolarized and constricted pressurized cerebral arteries with myogenic tone [11].

Chemical compound and disease context of tetraethylammonium

• Moreover, hypoxia inhibited a K(+) current in rabbit PASM cells in the presence of charybdotoxin and capsaicin, which preserve Kv3.1b while blocking most other Kv channels, but not in the presence of millimolar tetraethylammonium ions, which abolish Kv3.1b current [12].
• Transport of D-glucose, p-aminohippurate and tetraethylammonium has been studied using renal brush border membrane vesicles isolated from rats with uranyl nitrate-induced acute renal failure (ARF) [13].
• 3 The contractures produced by tetraethylammonium in the presence of methohexitone were not reduced by exposure to botulinum toxin which eliminated all response of the muscle to indirect stimulation [5].
• Exposure to 20 mM tetraethylammonium and 1 mM 3,4-diaminopyridine increased the amplitude of the hypoxia-induced depolarization, suggesting that activation of K channels may normally limit the amplitude of the hypoxia response [14].
• Contractions of the nictitating membrane and postganglionic action potentials evoked by electrical stimulation of the vagal artificial preganglionic trunk in the cross-anastomosed ganglion were blocked by treatment with tetraethylammonium and also with atropine [15].

Biological context of tetraethylammonium

• The most prominent activities came from a set of potassium channels with the properties of activation by positive but not negative voltages, high selectivity for potassium over sodium ion, unit conductance of 20 picosiemens, inhibition by tetraethylammonium or barium ions, and bursting kinetics [16].
• We demonstrated enhanced presynaptic function during long-term potentiation (LTP) induced either chemically (with tetraethylammonium), or by high-frequency (200-Hz) electrical stimulation [17].
• The aromatic binding site for tetraethylammonium ion on potassium channels [18].
• The subunit stoichiometry of the mammalian K+ channel KV1.1 (RCK1) was examined by linking together the coding sequences of 2-5 K+ channel subunits in a single open reading frame and tagging the expression of individual subunits with a mutation (Y379K or Y379R) that altered the sensitivity of the channel to block by external tetraethylammonium ion [19].
• Supporting this contention, the K+ channel blocker tetraethylammonium (20 mM) inhibits the increased K+ permeability that follows treatment of swollen sperm (and of sperm in seawater) with 2.5 pM speract [20].

Anatomical context of tetraethylammonium

• The proportionality between the permeability to tetraethylammonium ions and the junctional conductance, measured here with exceptionally fine time resolution, indicates that a common gap junctional pathway mediates both electrical and chemical fluxes between cells, and that closure of single gap junction channels by voltage is all or none [21].
• The electrophysiological properties of glial cells were examined in primary culture in the presence of tetraethylammonium and Ba2+, a treatment that reduces K+ permeability of the membrane and enhances currents through voltage-dependent Ca2+ channels [22].
• Intracellular injection of tetraethylammonium ions into one giant interneuron increases the duration of the action potential of the injected cell to 30 milliseconds and reduces the rise time and amplitude of the postsynaptic response recorded in the other giant interneuron [23].
• Gallamine triethiodide (flaxedil): tetraethylammonium- and pancuronium-like effects in myelinated nerve fibers [24].
• The permeability of gap junctions to tetraethylammonium ions was measured in isolated pairs of blastomeres from Rana pipiens L. and compared to the junctional conductance [21].

Associations of tetraethylammonium with other chemical compounds

• When mutated to cysteine, residues in this region render minK susceptible to covalent blockade by methanethiosulfonate ethylsulfonate and alter reversible inhibition by tetraethylammonium [25].
• Reversible block of the expressed insect AChR by mecamylamine, d-tubocurarine, tetraethylammonium, bicuculline and strychnine has also been observed [26].
• Acetylcholine caused shortening of action potentials in neurons treated with tetraethylammonium to partially block K+ channels [27].
• The potassium dependence of macroscopic conductance in RCK4 channels was related by site-directed mutagenesis to that lysine residue in the extracellular loop between the transmembrane segments S5 and S6 of RCK4 protein that confers resistance to extracellular blockage by tetraethylammonium [28].
• The results indicated that prolonged activation of PKC by preincubation with phorbol esters attenuated PKA-mediated actions of 5-HT, including increases in sensory neuron excitability and spike broadening in the presence of tetraethylammonium (TEA) and nifedipine [29].

Gene context of tetraethylammonium

• SLC22A4 codes for an integral membrane protein, OCTN1, that has been presumed to carry organic cations like tetraethylammonium across the plasma membrane [30].
• Absence of Oct2 in itself had little effect on the pharmacokinetics of tetraethylammonium (TEA), but in Oct1/2(-/-) mice, renal secretion of this compound was completely abolished, leaving only glomerular filtration as a TEA clearance mechanism [31].
• Here, we determined the specificity, potency, and binding site of tetraethylammonium (TEA) to block Aquaporin water permeability [32].
• KCNQ5 currents were insensitive to the K(+) channel blocker tetraethylammonium but were strongly inhibited by the selective M-current blocker linopirdine [33].
• When expressed heterologously in HeLa cells, OCTN2 mediates the transport of tetraethylammonium, a prototypical organic cation, in a pH-dependent manner [34].

Analytical, diagnostic and therapeutic context of tetraethylammonium

• The permeability to tetraethylammonium ions was determined by injecting one cell of a pair with tetraethylammonium and monitoring its changing concentration in the prejunctional and postjunctional cells with ion-selective electrodes [21].
• Application of internal tetraethylammonium (an open channel blocker) induced Off charge immobilization for large depolarizations, suggesting that the internal tetraethylammonium-binding site becomes available upon depolarization [35].
• The remaining three human and all seven pig coronary arteries showed propagation of such drug-induced contraction after treatment with 10 mM tetraethylammonium (TEA) [36].
• Because EP was depressed by vascular perfusion of Ba2+, an inhibitor of inwardly rectifying K+ (Kir) channels, but not by either 4-aminopyridine or tetraethylammonium, we examined the expression of Kir channel subunits in cochlear stria vascularis, the tissue that is supposed to play the central role in the generation of positive EP [37].
• Increased extracellular K+ concentrations or K(+)-channel blockers, such as quinine, tetraethylammonium, or barium chloride, inhibited the LPS-stimulated release of TNF alpha, as well as the accumulation of cell-associated TNF alpha as found by enzyme-linked immunosorbent assay analysis, but did not inhibit TNF alpha mRNA accumulation [38].

References