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)

The inducible cholinesterase of Pseudomonas aeruginosa strain K (ATCC 25102) degraded propionylcholine, acetylthiocholine, acetylcholine and acetyl-beta-methylcholine at a high rate and butyrylcholine and succinylcholine at very low rates. The localization of the enzyme in the periplasmic space was indicated by a similar rate of acetylcholine degradation by intact cells or their extracts, by release of cholinesterase together with alkaline phosphatase into the culture medium during cell growth in a low phosphate-containing medium, by liberation of cholinesterase and alkaline phosphatase during lysozyme-induced conversion of cells to spheroplasts and by freezing and thawing. Threatment of cells with diazo-7-amino-1,3-naphthalenedisulphonic acid, which inactivates surface-located enzymes, abolished most of the cholinesterase and 5'-nucleotidase activities.
J Gen Microbiol 1980 Mar
PMID:Localization of cholinesterase in Pseudomonas aeruginosa strain K. 677 68

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.
J Gen Physiol 1980 Jan
PMID:Voltage clamp study of fast excitatory synaptic currents in bullfrog sympathetic ganglion cells. 696 7

Young adult mice were inoculated in the hind limb with rabies virus or Sindbis virus. Rabies 1820B virus antigen was detected in leg sections by immuno-fluorescence at 1 h post-inoculation at sites comparable in form and distribution to cholinesterase-positive sites, which represent motor end-plates (MEPs). Sites which were rabies virus antigen-positive by immunofluorescence were also cholinesterase- positive on double-stained slides. Rabies CVS virus detected by autoradiography was similarly distributed at 6 h post-inoculation. Uptake of rabies virus at motor nerve endings was confirmed by the detection of rabies antigen by immunofluorescence in ventral horn cells in the spinal cord at 20 h post-inoculation before involvement of dorsal root ganglia. Rabies virus antigen could not be detected at MEPs if the virus had been inactivated by beta propiolactone or mixed with antibody prior to injection or if the sciatic nerve had been cut 7 days earlier, similarly treated groups of mice survived for the observation period of 6 weeks. Rabies virus antigen was found at MEPs in mice given antibody 24 h before virus injection, but virus antigen was not found in the spinal cord, and mice similarly treated survived. Sindbis virus strain Ar86, which like rabies virus is neurotropic in adult mice, was also found at MEPs and in peripheral nerves by autoradiography at 6 h post-inoculation. In contrast to results with rabies virus-infected mice, stimulation of the sciatic nerve for the first hour post-inoculation prevented mortality. Sindbis virus strain Ar339, which is not neurotropic in adult mice, could not be detected at MEP's by immunofluorescence or autoradiography and mice injected with virus survived. The results presented here suggest that rabies virus and perhaps other neurotropic viruses can use the motor axon terminal at the neuromuscular junction as a site of entry into the nervous system.
J Gen Virol 1981 Oct
PMID:Entry of rabies virus into the peripheral nerves of mice. 703 Nov 82

Within the substantia nigra acetylcholinesterase is released independently of cholinergic transmission: this release could be related to some aspects of motor control. To investigate this possibility, acetylcholinesterase release was continuously monitored in relation to specific movements evoked by central electrical stimulation. Increased intensities of stimulation of the subthalamic nucleus in awake guinea-pigs produced a behavioural response, ranging from a decrease in spontaneous movement, to chewing, to both chewing and circling movements. Enhancement of acetylcholinesterase release occurred only when large scale movements (circling as well as chewing) were evoked by subthalamic stimulation: however, a similar protocol of stimulation during ketamine-induced anaesthesia did not produce any comparable movements nor any concomitant change in the release of acetylcholinesterase. Perfusion of the glutamate agonist N-methyl-D-aspartate (NMDA) into the substantia nigra also induced an increase in release of acetylcholinesterase from the substantia nigra of conscious animals, whereas (S)-alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) did not significantly enhance acetylcholinesterase levels. It is concluded that AChE release in the substantia nigra can occur as a result of activation of glutamatergic subthalamic afferents, and that this activation may also be associated with changes in movement.
J Neural Transm Gen Sect 1994
PMID:The subthalamo-nigral pathway regulates movement and concomitant acetylcholinesterase release from the substantia nigra. 753 13

1. Effect of REM sleep (REMs) deprivation treatment on clozapine response in the forced swimming test was investigated. 2. Clozapine significantly increased the swimming activity in REMs-deprived mice at a dose of 5 mg/kg (i.p.) which did not affect the activities in the control groups. 3. Physostigmine (0.3 mg/kg, i.p.), an acetylcholinesterase inhibitor, blocked the increasing effect of 5 mg/kg clozapine on swimming activity in REMs-deprived animals. 4. These results suggest that the REMs deprivation treatment-induced enhancement of effect of clozapine on swimming activity is mediated by the functional change of central cholinergic system following the treatment.
Gen Pharmacol 1995 Oct
PMID:REM sleep deprivation treatment enhances the effect of clozapine in the forced swimming test. 759 Jan 10

The effects of two different diets [diet 1 (D1), high protein-low carbohydrate; diet 2 (D2), low protein-high carbohydrate] on brain and pituitary gonadotropin-releasing hormone (GnRH) contents, as well as circulating steroids and vitellogenin, were studied over the reproductive period of the sea bass. Salmon GnRH was measured using a newly developed competitive enzyme immunoassay with an enzymatic tracer made of sGnRH covalently coupled to acetylcholinesterase from the electric organ of the eel Electrophorus electricus. The pituitary GnRH content of animals of both sexes fed D1 was significantly reduced at the time of spawning compared with the pre- and postspawning stages, whereas fish fed D2 did not exhibit such changes. In the brain only minor differences in the GnRH content were observed between the two diets. It is concluded that GnRH release rather than synthesis is affected in fish fed a low protein-high carbohydrate regimen. Plasma sex steroids and vitellogenin were not greatly affected by the diet.
Gen Comp Endocrinol 1994 Sep
PMID:An enzyme immunoassay for salmon gonadotropin-releasing hormone and its application to the study of the effects of diet on brain and pituitary GnRH in the sea bass, Dicentrarchus labrax. 782 83

1. The effects of acute oral administration of carbaryl (10-80 mg/kg), a carbamate insecticide, on some experimental models for detecting dopaminergic activity were examined in rats. Also, serum biochemical variables following carbaryl treatments were determined. 2. Carbaryl (20 and 40 mg/kg) significantly increased the number of apomorphine-induced yawns and at dose of 80 mg/kg it prolonged the duration time of haloperidol-induced catalepsy. Pretreatment with carbaryl failed to affect apomorphine-induced stereotypes. 3. Carbaryl significantly reduced blood cholinesterase activity and elevated blood glucose levels and SGOT and SGPT activities. 4. These results indicate that low oral doses of carbaryl can cause behavioral and toxicological effects in rats.
Gen Pharmacol 1994 Oct
PMID:Effects of carbaryl on some dopaminergic behaviors in rats. 787 55

1. Habituation was regarded as a difference between exploratory activity measured first (session 1) and that measured second (session 2) in a novel environment. 2. Scopolamine (1.0 mg/kg) significantly increased the horizontal activity in sessions 1 and 2 when administered prior to session 1, resulting in the impairment of habituation. 3. Haloperidol (0.2 mg/kg) inhibited scopolamine-induced hypermotility in session 1, but it did not inhibit the scopolamine-induced impairment of habituation in session 2. 4. The direct cholinergic agonist oxotremorine (0.03 mg/kg), unlike the cholinesterase inhibitor physostigmine, significantly inhibited the scopolamine-induced impairment of habituation in the horizontal and vertical activities. 5. These results suggest that the direct stimulation of cholinergic receptors is more effective for scopolamine-induced amnesia than the indirect stimulation of cholinergic receptors by cholinesterase inhibitors in the habituation task.
Gen Pharmacol 1994 May
PMID:Characterization of the effects of scopolamine on the habituation of exploratory activity: differential effects of oxotremorine and physostigmine. 792 87

1. The present study was performed to investigate the effect of ketamine on the contractile responses induced by the H2-receptor antagonist ranitidine and the anticholinesterase agent physostigmine on the isolated guinea pig ileum. 2. The contractile responses induced by ranitidine and physostigmine on the guinea pig ileum were significantly prevented, in a concentration-dependent manner, by ketamine, while the ones induced by acetylcholine were not modified. The contractile responses induced by acetylcholine were inhibited by exogenous acetylcholinesterase. Ranitidine and physostigmine inhibited the above reduction, and this effect was significantly prevented by ketamine in a concentration-dependent manner. 3. These findings show that ketamine inhibits the contractile effect of ranitidine and physostigmine on the guinea pig ileum. This inhibition caused by ketamine seems to be associated with the protection of acetylcholinesterase against the inhibition by ranitidine and physostigmine.
Gen Pharmacol 1994 Jul
PMID:Ketamine inhibits the anticholinesterase activity of ranitidine and physostigmine. 795 21

1. Experiments were designed to study the effects of ageing on muscarine and NK2 receptor mechanisms in the three different regions of rabbit airway. 2. The pD2 value of acetylcholine changed with age in three different regions while that of carbamylcholine, which is resistant to acetylcholinesterase, did not. 3. The pD2 values of neurokinin A and the activity of protease, a degradative enzyme, changed with age. However, by the pretreatment with phosphoramidon, a protease inhibitor, the regional difference and age related change of the pD2 value of neurokinin A disappeared. 4. In conclusion, the observations about age related changes and regional differences of pD2 value of acetylcholine and neurokinin A were due to the difference of their degradative enzyme activities.
Gen Pharmacol 1994 Jul
PMID:Effects of ageing on regional differences in the contractile responses to acetylcholine and neurokinin A in rabbit airway. 795 29


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