Effect Of Tetramethylammonium Research Articles

Effect of tetramethylammonium hydroxide/isopropyl alcohol wet etching on geometry and surface roughness of silicon nanowires fabricated by AFM lithography.

The optimization of etchant parameters in wet etching plays an important role in the fabrication of semiconductor devices. Wet etching of tetramethylammonium hydroxide (TMAH)/isopropyl alcohol (IPA) on silicon nanowires fabricated by AFM lithography is studied herein. TMAH (25 wt %) with different IPA concentrations (0, 10, 20, and 30 vol %) and etching time durations (30, 40, and 50 s) were investigated. The relationships between etching depth and width, and etching rate and surface roughness of silicon nanowires were characterized in detail using atomic force microscopy (AFM). The obtained results indicate that increased IPA concentration in TMAH produced greater width of the silicon nanowires with a smooth surface. It was also observed that the use of a longer etching time causes more unmasked silicon layers to be removed. Importantly, throughout this study, wet etching with optimized parameters can be applied in the design of the devices with excellent performance for many applications.

PFG NMR Investigations of TPA−TMA−Silica Mixtures

Pulsed-field gradient (PFG) NMR studies of tetrapropylammonium (TPA)-tetramethylammonium (TMA)-silica mixtures are presented, and the effect of TMA as a foreign ion on the TPA-silica nanoparticle interactions before and after heating has been studied. Dynamic light scattering (DLS) results suggest that silica nanoparticles in these TPA-TMA systems grow via a ripening mechanism for the first 24 h of heating. PFG NMR of mixtures before heating show that TMA can effectively displace TPA from the nanoparticle surface. The binding isotherms of TPA at room temperature obtained via PFG NMR can be described by Langmuir isotherms, and indicate a decrease in the adsorbed amount of TPA upon addition of TMA. PFG NMR also shows a systematic increase in the self-diffusion coefficient of TPA in both the mixed TPA-TMA systems and pure TPA systems with heating time, indicating an increased amount of TPA in solution upon heating. By contrast, a much smaller amount of TMA is observed to desorb from the nanoparticles upon heating. These results point to the desorption of TPA from the nanoparticles being a kinetically controlled process. The apparent desorption rate constants were calculated from fitting the desorbed amount of TPA with time via a pseudosecond-order kinetic model. This analysis show the rate of TPA desorption in TPA-TMA mixtures increases with increasing TMA content, whereas for pure TPA mixtures the rate of TPA desorption is much less sensitive to the TPA concentration.

EFFECTS OF NICOTINE, DIMETHYLPHENYLPIPERAZINIUM AND TETRAMETHYLAMMONIUM ON SMOOTH MUSCLES FROM FELINE AND HUMAN GASTRIC CORPUS

Both excitatory and inhibitory intrinsic neurons could be found within the gastric wall, both of them receiving innervation from vagal fibres and being sensitive to nicotine. The effects of three nicotine receptor agonists, nicotine, tetramethylammonium (TMA) and 1,1-dimethyl-4-phenylpiperazinium (DMPP), on contractile activity of preparations isolated from feline and human gastric corpus wall were investigated. While DMPP (3.5×10−8to 5.9×10−4m) did not affect either spontaneous contractions or basal tension of isolated preparations from both species, TMA produced concentration-dependent tonic contractions of both circular and longitudinal isolated preparations from human (3.66×10−5to 5.10×10−3m) and feline (6.1×10−7to 2.1×10−3m) stomach. On the other hand, nicotine (4.1×10−8to 7.0×10−4m) produced concentration-dependent relaxation of only circular isolated preparations from feline gastric corpus. The effect of nicotine was sensitive to mecamylamine, and not to pancuronium, while the effect of TMA was sensitive to both mecamylamine and pancuronium. Although in our experiments DMPP had no effect, its excitatory action on gastric intrinsic neurons through the hexamethonium-insensitive pathway had already been described. The results of our study suggest that two different types of ganglion nicotine receptor exist together within the wall of feline stomach: (1) type NN1which is involved in relaxation and is sensitive only to nicotine and mecamylamine, and not to DMPP, TMA and pancuronium; (2) and type NN2which is involved in contraction of gastric muscle and sensitive to DMPP, TMA, mecamylamine and pancuronium, and not to nicotine.

Effect of tetramethylammonium, choline and edrophonium on insect acetylcholinesterase: test of a kinetic model

Cholinesterases display a non-Michaelian behaviour with respect to substrate concentration. With the insect enzyme, there is an activation at low substrate concentrations and an inhibition at high concentrations. Previous studies allow us to propose a kinetic model involving a secondary non-productive binding site for the substrate. Unexpectedly, this secondary site has a very high affinity for the substrate when the enzyme is free. On the contrary, when the catalytic site of the enzyme is occupied a strong decrease of this affinity was observed. Moreover, a substrate molecule bound to the peripheral site results in a global decrease of the acylation and/or the deacylation step. Kinetic studies with three reversible inhibitors, tetramethylammonium, edrophonium and choline supported the kinetic model and enable its further refinement.

Tetraethylammonium Block of the BNC1 Channel

The brain Na + channel-1 (BNC1, also known as MDEG1 or ASIC2) is a member of the DEG/ENaC cation channel family. Mutation of a specific residue (Gly430) that lies N-terminal to the second membrane-spanning domain activates BNC1 and converts it from a Na +-selective channel to one permeable to both Na + and K +. Because all K + channels are blocked by tetraethylammonium (TEA), we asked if TEA would inhibit BNC1 with a mutation at residue 430. External TEA blocked BNC1 when residue 430 was a Val or a Thr. Block was steeply voltage-dependent and was reduced when current was outward, suggesting multi-ion block within the channel pore. Block was dependent on the size of the quaternary ammonium; the smaller tetramethylammonium blocked with similar properties, whereas the larger tetrapropylammonium had little effect. When residue 430 was Phe, the effects of tetramethylammonium and tetrapropylammonium were not altered. In contrast, block by TEA was much less voltage-dependent, suggesting that the Phe mutation introduced a new TEA binding site located ∼30% of the way across the electric field. These results provide insight into the structure and function of BNC1 and suggest that TEA may be a useful tool to probe function of this channel family.

Tetramethylammonium activation of muscarinic receptors in cardiac ventricular myocytes.

Replacement of extracellular Na+ with tetramethylammonium (TMA) reduces the magnitude of the Cl- current activated by beta-adrenergic receptor stimulation in guinea pig ventricular myocytes. However, the effects of replacing Na+ appear to be associated with the presence of TMA, rather than the absence of Na+. Direct addition of TMA to extracellular solutions, without changing the Na+ concentration, was able to inhibit the Cl- current activated by isoproterenol (Iso) in a concentration-dependent manner. The concentration of TMA that caused half-maximal inhibition was 327 microM when the Cl- current was activated by 1 microM Iso and 29 microM when the Cl- current was activated by 0.03 microM Iso. The effect of TMA was also blocked by atropine, suggesting that TMA exerts its effect through stimulation of the muscarinic receptors. Furthermore, TMA inhibited the Iso-activated Ca2+ current, as would be expected for an effect involving muscarinic receptor stimulation. The response to complete Na+ replacement with TMA could not be overcome by increasing the concentration of Iso 1,000-fold, and direct addition of TMA was able to antagonize the Cl- current activated independently of the beta-adrenergic receptor, using forskolin and histamine. These results are consistent with the hypothesis that TMA does not exert its effects through a competitive mechanism at the beta-adrenergic receptor. It is concluded that TMA is able to antagonize adenosine 3',5'-cyclic monophosphate-dependent activation of ion channels in the heart through activation of muscarinic receptors.

The effect of tetramethylammonium on single sodium channel currents

Voltage-dependent Na conductance of rat myotubes was studied by patch recordings of single-channels. The patches were excised from the cell with the patch electrode, and the cytoplasmic surface was bathed in either CsF or tetramethylammonium (TMA)-F. Inward currents were examined from -20 to -50 mV. In this range Cs and TMA both appeared to be nearly impermeant, but TMA blocked the channel in a voltage-dependent manner. A first-order blocking site was located a maximum of 89% of the way through the membrane field from the cytoplasmic surface.

Effects of tea on hippocampal neurons

The effects of the potassium channel blockers, tetraethylammonium (TEA) and tetramethylammonium (TMA) on behavior of hippocampal CA1 neurons were studied in the in vitro slice preparation. Intracellular injections of TEA produced marked spike broadening, increased input resistance, and a prolongation of a putative slow calcium-activated afterhyperpolarization (AHP). Little effect was seen on synaptic potentials. Bursting activity induced by TEA in hippocampal neurons was qualitatively different from the epileptiform bursting induced by raising extracellular potassium concentrations or by including penicillin in the bathing medium. Effects of TMA were qualitatively similar to those of TEA, but much slower and less dramatic. The results suggested that there are at least two different potassium channels in the membranes of hippocampal CA1 neurons, and that both were important in determining normal neuronal activity. TEA appeared to preferentially block a fast, voltage-dependent potassium conductance ( g k ); however, it also modified the slow, calcium-activated g k . Although cell bursting activity may have resulted from blockade of a g k produced by TEA treatment, the epileptiform bursts produced by penicillin exposure appeared to be independent of this mechanism.

Spin-labeled TMA analogs as probes to study the anionic site of acetylcholinesterase

1. 1. Spin-labeled analogs of tetramethylammonium (TMA) were synthesized to study the “topography” of the anionic site of the elective eel AChE. 2. 2. These compounds competitively inhibited the enzyme in a reversible manner. 3. 3. The effect of TMA, of tetraethylammonium (TEA) and of gallamine [1, 2, 3 Tris-(2-triethylammonium ethoxy)benzene triiodide] and the inhibition of AChE by the spin-labeled probes I and II has been studied using acetylthiocholine (ATCh) as substrate. 4. 4. Neither TEA nor gallamine antagonized the binding of spin-labeled I and II. On the other hand, TMA inhibited the binding of I and II.

Effect of tetramethylammonium and potassium chloride on adrenal 17-hydroxycorticosteroid secretion in unanesthetized dogs.

Adrenal 17-hydroxycorticosteroid (17-OHCS) secretion was followed after injection of tetramethylammonium or potassium chloride. In unanesthetized dogs the adrenal venous blood was collected by a modification of the method of Satake and his co-workers and was analyzed for 17-OHCS by the method of Nelson and Samuels. The 17-OHCS secretion rate before injection was 0.03-0.29μg/kg/min. After injection of tetramethylammonium it increased markedly in all of 3 dogs and attained to 1.10-1.43μg/kg/min. After injection of potassium chloride it increased definitely in 2 of 3 dogs and attained to 1.14-1.73μg/kg/min.