Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The relationship between Km and assay temperature was examined in three tropical and two temperate Drosophila species, and in the cosmopolitan species, D. melanogaster, for isocitrate dehydrogenase and acetylcholinesterase. 2. For both enzymes Km patterns were similar among species from the same habitat, and different between habitats. No such parallelism was seen with respect to thermal inactivation. 3. The Q10 values in general reflected temperature dependent changes in Km, but exceptions were noted.
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PMID:Adaptation of Drosophila enzymes to temperature--I. Acetylcholinesterase and NADP-dependent isocitrate-dehydrogenase. 31 70

1. Acetylcholine (ACh), 7.5 x 10(-5) M, and carbachol, 5 x 10(-6) M (CCh) depressed the frequency of miniature endplate potentials (m.e.p.ps) in the frog (Rana temporaria) sartorius neuromuscular junction with active acetylcholinesterase to about 50-55% of the controls. 2. A similar depression was produced by the nicotinic agonists, nicotine, suberyldicholine and tetramethylammonium. 3. The muscarinic agonists, oxotremorine, methylfurmethide and methacholine were without effect on m.e.p.p. frequency. The muscarinic antagonist, atropine and the nicotinic antagonist, (+)-tubocurarine, had no effect on the depression of m.e.p.p. frequency evoked by CCh. 4. The ganglionic blockers, benzhexonium and IEM-1119, were also without effect on the CCh-evoked depression of m.e.p.p. frequency. 5. Pretreatment of muscles with anticholinesterases did not prevent the CCh-induced drop in m.e.p.p. frequency. 6. The effect of CCh was proportionally the same as in the controls in preparations where the m.e.p.p. frequency was changed by elevation of K+ and in the presence of theophylline, noradrenaline, dibutyryl adenosine 3':5'-cyclic monophosphate (db cyclic AMP) and db cyclic GMP. 7. An inhibitor of Na+,K(+)-ATPase, ouabain, 5 x 10(-5) mol l-1, prevented or reversed the depression of m.e.p.p. frequency by CCh. However, the depression was present in a nominally K(+)-free medium. Insulin and adrenaline, which are considered to be Na+,K(+)-ATPase activators, were without effect on depression of m.e.p.p. frequency. 8. The depression of m.e.p.p. frequency by 5 x 10(-6) M CCh was the same at temperatures between 5 and 30 degrees C with a Q10 near to 1.0. When threshold amounts of CCh were used (6 x 10-7 and 3 x 10-7 M), the depression was less at higher temperatures.9. The receptive structures responsible for the CCh (or ACh)-evoked depression of m.e.p.p. frequency differ pharmacologically from muscarinic, nicotinic ganglionic and neuromuscular junction ACh-receptors as well as from the synaptic cholinesterase, in contrast to previous reports (Duncan & Publicover, 1979).The low temperature-dependence points to the possibility that physical rather than biochemical processes are limiting in this presynaptic effect of cholinomimetics.
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PMID:Depression of miniature endplate potential frequency by acetylcholine and its analogues in frog. 166 83

1. The effect of temperature (5-35 degrees C) on the decay and growth phases of miniature end-plate currents (MEPCs) was investigated in extraocular muscle from freshwater carp acclimated to either high (28 degrees C) or low (8 degrees C) temperature. 2. The temperature dependence of the time constant of decay (TD) was found to follow an Arrhenius relationship; the relationship between logTD and reciprocal of absolute temperature (1/K) being linear in both groups. The TD of MEPCs recorded from cold-acclimated carp was not statistically significant from that of the warm group. 3. TD was moderately temperature-dependent. Regression gave a Q10 of 1.78 for the warm-acclimated carp, corresponding to an activation energy, Ea, of 41.15 +/- 2.17 kJ mol-1. For the cold-acclimated carp, the Q10 was 1.79, and Ea was 41.43 +/- 2.46 kJ mol-1. 4. Growth time (TG) was less susceptible than TD to temperature change. The relationship between growth time (taken as the time for MEPCs to rise from 20 to 80% of maximum) and temperature was linear for the cold-acclimated group, with a Q10 of 1.34 and Ea of 20.94 +/- 4.75 kJ mol-1. The data for the warm group, were, in contrast, best fitted by two linear regressions meeting at 15.1 degrees C. At temperatures below 15.1 degrees C Q10 was 3.16 and Ea was 82.20 +/- 15.47 kJ mol-1; above 15 degrees C, Q10 was 1.22 and Ea was 14.15 +/- 12.24 kJ mol-1. 5. The acetylcholinesterase inhibitor neostigmine increased TD by approximately twofold and raised TG to approximately 1.4 times control values. These effects were observed across the temperature range scanned for both groups. 6. The results are discussed with reference to the documented effects of temperature and temperature acclimation on membrane lipids and proteins.
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PMID:The temperature dependence of the time course of growth and decay of miniature end-plate currents in carp extraocular muscle following thermal acclimation. 253 39

Miniature end-plate currents (MEPC) were recorded in voltage-clamped end-plates of the rat diaphragm. A positive correlation between the amplitude and half-decay time of individual MEPC was found in control, after acetylcholinesterase (AChE) inhibition the correlation increased: correlation coefficients--0.29 and 0.49, respectively (28 degrees C). Addition of curare after the AChE inhibition caused a decrease in the amplitude and duration of MEPC, but had no effect on the correlation between these parameters. Cooling down to 18 degrees C led to the essential reduction of this correlation in control as well as after the AChE inhibition. Effect of the prolongation of the half-decay time due to the AChE inhibition was more significant at 28 degrees C than at 18 degrees C. The Q10 value for duration of the rising MEPC phase (about 2) was less than that for the half-decay time (about 3). The role of factors determining the MEPC duration is discussed. The results are explained by the postsynaptic potentiation in terms of the cooperative action of agonists on cholinoreceptors and of peculiarities of the acetylcholine diffusion from the synaptic cleft.
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PMID:[Postsynaptic potentiation of miniature currents of muscle fiber endplates in the rat diaphragm. The effect of an acetylcholinesterase inhibitor, temperature and curare]. 282 14

The decay time-constants of the 2nd and 1st nerve-evoked paired end-plate currents (epc) were recorded in transversely cut muscle preparations of frog. After the inhibition of synaptic acetylcholinesterase by prostigmine (3 X 10(-6) mol/l) the decay of the 2nd epc was 39 +/- 8% slower than the decay of the 1st epc (the interstimulus interval being 100 ms) due to postsynaptic potentiation (PSP). It was found that PSP does not depend on the membrane potential level in the range of-30-120 mV. A drop in temperature from 22 degrees to 12 degrees resulted in several effects: an increase in the decay time constant of epc and meps; a slight decrease in mepc amplitude; a fall of epc quantal content. The comparison of paired epc of equal quantal content showed that PSP was more pronounced at lower temperature. The temperature coefficient (Q10) for the ratio of decay time constants of the 2nd and the 1st epc was 2.0 +/- 0.2. Evidently, the trace of preceding activity of the transmitter does not depend on the membrane potential level but becomes stronger with a fall of the temperature.
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PMID:[Effect of changes in membrane potential and temperature on the post-synaptic potential on the neuromuscular junction of the frog]. 302 Apr 53

Excitatory postsynaptic currents (EPSCs), miniature excitatory postsynaptic currents (MEPSCs), and acetylcholine-induced current fluctuations (noise) have been studied in voltage-clamped bullfrog parasympathetic ganglion cells of the atrial septum. EPSCs were also recorded from voltage-clamped sympathetic B cells and, in general, it was found that the basic properties of the EPSCs are similar in both parasympathetic and sympathetic B cells. For parasympathetic cells, the EPSC reached a peak amplitude of several nanoamperes within 3 msec and decayed exponentially. For 31 cells voltage-clamped to -50 mV (22 to 23 degrees C), peak amplitude was -4.3 +/- 1.4 nA (mean +/- SD) and the decay time constant, tau, was 5.6 +/- 1.0 msec. tau was independent of EPSC amplitude at a set voltage but increased with hyperpolarization, the coefficient of voltage dependence being -0.0070 +/- 0.0025 mV-1 in 13 cells (21 to 23 degrees C). The EPSC amplitude-voltage relationship was linear between -30 and -90 mV. The reversal potential, determined by interpolation, was -4.0 +/- 6.7 mV (n = 11). The EPSC tau had a Q10 equal to 2.9. Blocking the acetylcholinesterase with methane sulfonyl fluoride (MSF) pretreatment prolonged EPSC decay but decreased EPSC amplitude. In addition, EPSC decay after MSF treatment deviated from a single exponential function. MEPSCs exhibited decay characteristics very similar to those of EPSCs recorded at the same voltage and temperature. Acetylcholine-induced current fluctuations were well described by a single Lorentzian function with the estimated mean channel open time (tau noise) very similar to the EPSC decay time constant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of fast excitatory postsynaptic currents in bullfrog parasympathetic ganglion cells. 631 74

Excitatory postsynaptic currents (EPSCs) have been studied in voltage-clamped bullfrog sympathetic ganglion B cells. The EPSC was small, rose to a peak within 1-3 ms, and then decayed exponentially over most of its time-course. For 36 cells at --50 mV (21-23 degrees C), peak EPSC size was --6.5 +/- 3.5 nA (mean +/- SD), and the mean decay time constant tau was 5.3 +/- 0.9 ms. tau showed a small negative voltage dependence, which appeared independent of temperature, over the range --90 to --30 mV; the coefficient of voltage dependence was --0.0039 +/-0.0014 mV-1 (n = 29). The peak current-voltage relationship was linear between --120 and --30 mV but often deviated from linearity at more positive potentials. The reversal potential determined by interpolation was approximately --5 mV. EPSC decay tau had a Q10 = 3. The commonly used cholinesterase inhibitors, neostigmine and physostigmine, exhibited complex actions at the ganglia. Neostigmine (1 X 10(-5)M) produced a time-dependent slowing of EPSC decay without consistent change in EPSC size. In addition, the decay phase often deviated from a single exponential function, although it retained its negative voltage dependence. With 1 x 10(-6) M physostigmine, EPSC decay was slowed by the decay phase remained exponential. At higher concentrations of physostigmine, EPSC decay was markedly prolonged and was composed of at least two decay components. High concentrations of atropine (10(-5) to 10(-4) M) produced complex alterations in EPSC decay, creating two or more exponential components; one decay component was faster and the other was slower than that observed in untreated cells. These results suggest that the time-course of ganglionic EPSC decay is primarily determined by the kinetics of the receptor-channel complex rather than hydrolysis or diffusion of transmitter away from the postsynaptic receptors.
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PMID:Voltage clamp study of fast excitatory synaptic currents in bullfrog sympathetic ganglion cells. 696 7

Electric organs of skate (Raja species) dissociate to form populations of individual electrocytes when incubated in saline solutions containing collagenase. The rate of dissociation was highly temperature dependent, with an apparent Q10 of > 6 in the range of 6 degrees-26 degrees C. The number of electrocytes per organ was relatively constant and independent of electric organ size, whereas mean cell diameters increased with organ size. The activities of two cholinergic marker enzymes, choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), in extracts of whole fresh organs were much less than those reported for the electric ray Torpedo, suggesting a lower volume of terminals in the organ. Electrocytes prepared from collagenase-treated organs had good resting potentials and generated postsynaptic evoked potentials. Spontaneous and electrode pressure-evoked miniature endplate potentials (MEPPs) were readily recorded from isolated electrocytes. Incubation periods of more than 4 days in collagenase at 6 degrees C produced electrocytes with good resting potentials and very low MEPP frequencies, indicating denervation. Detachment of terminals and decreased MEPP frequencies were concurrent. The time course of denervation was followed with the appearance of ChAT and AChE activities in a small particulate fraction derived from washed electrocytes. Peak activities of both enzymes were seen at 4 days of incubation at 16 degrees C, but after 20 h at 16 degrees C. Electrocytes from 4-day, 6 degrees C incubations showed detached, mitochondria-rich nerve terminals and dissociated Schwann cells. In unfixed preparations examined with Nomarski optics, isolated nerve terminals were recognized and distinguished from nucleated Schwann cells. Electron micrographs show that isolated terminals were similar to attached terminals just before they dissociated. The MEPP frequencies and evoked potentials were normal at terminals just before dissociation. We conclude that the transmitter release process was normal in detached terminals and in terminals free of Schwann cells.
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PMID:Detached, purified nerve terminals from skate electric organ for biochemical and physiological studies. 885 32

The present work addresses the 'dual temperature' model for the estimation of Gibb's free energy change (delta G), enthalpy change (delta H), heat of activation (delta H.) entropy change (delta S), temperature coefficient (Q 10) and activation energy (Ea) of chicken brain acetylcholinesterase (AChE) inhibited by cyclophosphamide monohydrate (CP). In this investigation, the PZ factor (number of sterically and energy wise favorable collisions occurring between CP and AChE) has also been studied. The inhibitor has considerably increased all energetics parameters except delta S and Q10. These results are in general agreement with the data from the other reported studies. The significance of the use of CP in cancer therapy and various aspects of thermodynamic parameters have also been discussed.
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PMID:Dual temperature model for the estimation of energetics parameters for acetylcholinesterase inhibition by cyclophosphamide. 935 76

The present study determines the energy parameters, such as the Gibb's free energy change (deltaG), enthalpy change (deltaH), heat of activation (deltaH*), entropy change (deltaS), temperature coefficient (Q10) and activation energy (Ea), of human retinal acetylcholinesterase (AChE, EC 3.1.1.7) inhibition by tacrine. The stereo-frequency collisions factor (PZ, the number of sterically and energetically favorable collisions occurring between tacrine and AChE) was also studied in this investigation. Tacrine significantly increased the value of deltaG, deltaH, deltaH*, Q10, Ea and PZ factor, and decreased the value of deltaS for AChE. Since there is no known report on the inhibition of human retinal AChE by tacrine, these results were compared with the reported values for the energy parameters of camel retinal and chicken brain AChE inhibition by an anti-cancer drug, cyclophosphamide. The uniqueness of this approach lies in the development of the 'dual substrate and dual temperature' model, which may open up a new, more efficient avenue for the study of various enzyme catalyzed reactions.
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PMID:Thermodynamic analysis of human retinal acetylcholinesterase inhibition using an anti-Alzheimer's drug, tacrine, through the development of a dual substrate and temperature model. 1094 43


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