Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Research was conducted upon 28 patients with a diagnosis of endogenous depression after their pharmacological treatment with imipramine or chlorimipramine. The investigation considered the interrelationship between psychophysiological parameters (heart rate, respiration rhythm, postural muscular tension) and the indices of the cholinergic and adrenergic systems (kinetic parameters of choline transport in the blood; Vmax, the activity of plasmic pseudocholinesterase, Che; blood acetylcholinesterase AChE, monoaminoxidase in blood platelets, MAO; and dopamine beta hydroxylase DBH). The results indicate that during relapse of endogenous depression there occurs an imbalance in the cholinergic-adrenergic systems which may be the result of some somatic symptoms typically found in the depression syndrome. The appearance, after pharmacotherapy, of a correlation between the indices of the activity of the cholinergic system with the respiratory rhythm suggest that the part played by the cholinergic mechanism in the regulation of autonomic processes normalizes itself during the course of successful therapy. The appearance of characteristic correlations between the activity of the cholinergic and adrenergic systems and the psychophysiological parameters in the presence of relatively low psychological stress seems to accompany successful treatment with imipramine and chlorimipramine.
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PMID:[Psychophysiological characteristics and metabolic indices of neurotransmitter metabolism in patients ill with endogenous depression]. 130 98

The investigations were conducted on two groups of students of the Baku Naval School (15 subjects in each group). It was shown that in the presence of traditional nutrition containing mainly meat and grain products and characterized by insufficient content of animal protein and milk products, the psychoemotional and mental stress by the end of the examination session, as compared to the period of the current studies, resulted in a significant growth of acetylcholine-like substances, alpha- and gamma-globulins, a tendency to an increased acetylcholinesterase concentration in their blood, most manifest on the day of passing the 3d examination, and a tendency to elevated cholinesterase activity on the day of passing the 4th examination; a significant decrease of protein content and albumin levels. Due to nutrition correction (mainly by the protein component) shifts in the content of protein and albumin levels, alpha- and gamma-globulins, acetylcholine-like substances in the blood were recorded by the end of the examination session, and were appreciably close to the values in the period of the current studies.
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PMID:[The effect of qualitatively different nutrition on various indicators of the functional status of the parasympathetic nervous system and blood proteins in students during an examination period]. 262 48

Mental stress may induce myocardial ischemia and ventricular arrhythmia in patients with coronary artery disease, and cholinergic stimulation is a potential protective mechanism. The purpose of this study was to determine the effect of pyridostigmine bromide (PYR), a reversible cholinesterase inhibitor, on the cardiac responses to a mental stress challenge. Twelve healthy young volunteers were submitted to a mental stress test (arithmetic test) 2 hours after the oral administration of either placebo or PYR (45 mg) on two separate days, following a randomized crossover double-blind protocol. Heart rate was reduced after both placebo and PYR (p < 0.05), but the cardiac responses to the mental stress were lower with PYR (p < 0.05): mean RR interval (mean +/- SE)-placebo: 730 +/- 19 msec; PYR: 769 +/- 21 msec; Peak systolic pressure-placebo: 129 +/- 4 mmHg; PYR: 124 +/- 3 mmHg; Peak diastolic pressure-placebo: 92 +/- 3 mmHg; PYR: 89 +/- 4 mmHg; Mean rate-pressure product-placebo: 10,496 +/- 412 bpm x mmHg; PYR: 9,746 +/- 383 bpm x mmHg. In conclusion, 45 mg of pyridostigmine blunted the pressor and chronotropic responses to mental stress in healthy young subjects.
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PMID:Cholinergic stimulation with pyridostigmine blunts the cardiac responses to mental stress. 1021 43

Cholinergic hyperexcitation can be induced by both acute psychological stress and exposure to acetylcholinesterase inhibitors. Both factors are known risk factors for delayed neurodeterioration processes such as Alzheimer's disease and Parkinson's disease. Recent publications on the involvement of cholinergic pathways in these and other neurodeterioration syndromes are reviewed.
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PMID:Tracking cholinergic pathways from psychological and chemical stressors to variable neurodeterioration paradigms. 1067 58

Male infertility is often attributed to stress. However, the protein or proteins that mediate stress-related infertility are not yet known. Overexpression of the "readthrough" variant of acetylcholinesterase (AChE-R) is involved in the cellular stress response in a variety of mammalian tissues. Here, we report testicular overexpression of AChE-R in heads, but not tails, of postmeiotic spermatozoa from mice subjected to a transient psychological stress compared with age-matched control mice. Transgenic mice overexpressing AChE-R displayed reduced sperm counts, decreased seminal gland weight, and impaired sperm motility compared with age-matched nontransgenic controls. AChE-R was prominent in meiotic phase spermatocytes and in tails, but not heads, of testicular spermatozoa from AChE-R transgenic mice. Head-localized AChE-R was characteristic of human sperm from fertile donors. In contrast, sperm head AChE-R staining was conspicuously reduced in samples from human couples for whom the cause of infertility could not be determined, similar to the pattern found in transgenic mice. These findings indicate AChE-R involvement in impaired sperm quality, which suggests that it is a molecular marker for stress-related infertility.
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PMID:Modified testicular expression of stress-associated "readthrough" acetylcholinesterase predicts male infertility. 1151 15

Mentally or emotionally stressful situations occur throughout our lives and cause physiological haemodynamic responses. In patients with coronary artery disease, such events can also induce myocardial ischaemia and ventricular arrhythmias, increasing mortality rates. The purpose of the present study was to determine the acute effects of the oral administration of pyridostigmine, a reversible cholinesterase inhibitor and thus an indirect cholinomimetic drug, on echocardiographic variables during mental stress in healthy subjects. A total of 18 healthy young volunteers were subjected to mental stress tests (mental arithmetic and the Stroop colour-word test) 2 h after the oral administration of either placebo or pyridostigmine bromide (45 mg), using a balanced-randomized, double-blind, crossover protocol. During mental stress, heart rate (pyridostigmine, 64+/-1 beats/min; placebo, 70+/-1 beats/min; P =0.0003) and diastolic blood pressure (pyridostigmine, 66+/-2 mmHg; placebo, 79+/-3 mmHg; P =0.01) were lower in the pyridostigmine group, but systolic pressure was not (pyridostigmine, 124+/-3 mmHg; placebo, 123+/-3 mmHg; P =0.40). There were no detectable abnormalities in the left ventricular wall motion score during mental stress, but left ventricular outflow tract mean velocity (pyridostigmine, 0.68+/-0.02 m/s; placebo, 0.64+/-0.02 m/s; P <0.05) and mitral inflow velocity deceleration (placebo, 4.05+/-0.18 m/s(2); pyridostigmine, 4.41+/-0.16 m/s(2); P <0.05) were higher in the pyridostigmine group. In conclusion, cholinergic stimulation with pyridostigmine seems to increase left ventricular diastolic function during mental stress in healthy subjects.
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PMID:Cardiac function during mental stress: cholinergic modulation with pyridostigmine in healthy subjects. 1262 98

The mammalian acetylcholinesterase (ACHE) gene gives rise to diverse enzymatically active proteins with three different carboxyl termini. In the brain, the normally rare readthrough AChE-R monomer accumulates under embryonic development and in adults following psychological stress, head injury, or exposure to AChEs. In the prenatal developing cortex, its unique C-terminal peptide ARP associates with radial glial fibers supporting neuronal migration. In contrast, the major synaptic AChE-S variant appears in the migrating neurons themselves. Moreover, antisense suppression of AChE-R attenuates neuronal migration, allowing increased proliferation of neuronal progenitors. In the adult brain, neuronal AChE-R is either secreted or accumulates intraneuronally, where it interacts through ARP with the scaffold protein RACK1 and activated PKC-betaII. This associates with increased PKC-betaII activity, which shuttles to submembranal clusters (e.g., in hyperactivated hippocampal neurons). Cleavage yields the AChE-R-specific C-terminal peptide, including immunopositive ARP. Importantly, intrahippocampal injection of synthetic ARP was followed by its efficient neuronal penetration and retrograde transport into cortical and basal nuclei neurons. Moreover, ARP-injected mice presented increased stress-induced contextual fear, inhibitable by antisense suppression of AChE-R mRNA. Together, our findings point at the cleavable ARP peptide as a key regulator of neuronal development and plasticity and suggest its use as a drug target and/or research and therapeutic tool.
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PMID:ARP, the cleavable C-terminal peptide of "readthrough" acetylcholinesterase, promotes neuronal development and plasticity. 1669 Oct 12

Novel and diverse functions of glial cells are currently the focus of much attention [A. Volterra and J. Meldolesi (2005) Nature Rev. 6, 626-640]. Here we present evidence that rat astroglia release acetylcholinesterase (AChE) as part of their response to hypoxic damage. Exposure of astroglia to tert-butyl hydroperoxide, and hence oxidative stress, subsequently leads to a switching in mRNA from the classical membrane-bound T-AChE to a preferential increase in the splice variant for a soluble form, R-AChE, This change in expression is reflected in increased perinuclear and reduced cytoplasmic AChE staining of the insulted glial cells, with a concomitant and marked increase in extracellular secretion that peaks at 1 h post-treatment. An analogous increase in R-AChE, over a similar time scale, occurs in response to psychological stress [D. Kaufer et al. (1998) Nature 93, 373-377], as well as to head injury and stroke [E. Shohami et al. (1999) J. Neurotrauma 6, 365-76]. The data presented here suggest that glial cells may be key chemical intermediaries in such situations and, perhaps more generally in pathological conditions involving oxidative stress, such as neurodegeneration.
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PMID:Astroglia up-regulate transcription and secretion of 'readthrough' acetylcholinesterase following oxidative stress. 1690 48

Mental stress causes physiological autonomic adjustments that may trigger myocardial ischemia and ventricular dysfunction in patients with coronary artery disease. Thus, it was hypothetized that cholinergic stimulation may counteract the ventricular dysfunction provoked by mental stress in coronary disease. Six patients with coronary disease underwent a randomized, double-blind, cross-over, and placebo-controlled protocol in which they received placebo or a single dose of pyridostigmine bromide (45 mg p.o.), a reversible cholinesterase inhibitor, and thus, a cholinomimetic agent 2 h before a standard mental stress task (Stroop color-word test), while hemodynamic and echocardiographic variables were continuously monitored. There were no signs of myocardial ischemia on ECG during mental stress under PYR or placebo. Heart rate and blood pressure increased during mental stress (P<0.01) similarly with placebo and PYR (P>0.05). There were no ventricular wall motion abnormalities during mental stress with either placebo or PYR, but mental stress decreased ejection fraction (pre 63+/-2%, stress 57+/-2%; P=0.004) and impaired the indices of diastolic ventricular function. On the other hand, PYR prevented the fall in ejection fraction (pre 62+/-2%, stress 64+/-2%; P=0.13) and in the indices of diastolic function (P>0.05). In conclusion, cholinergic stimulation with pyridostigmine prevented the impairment in myocardial function during mental stress in patients with coronary artery disease.
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PMID:Cholinergic stimulation with pyridostigmine prevents the impairment in ventricular function during mental stress in coronary artery disease patients. 1739 49

The organophosphorus agent sarin is a potent inhibitor of acetylcholinesterase. Experiments tested the influence of exposure to low doses of sarin along with psychological stress on delayed behavioral and endocrine changes in mice. Motor activity, acoustic startle response (ASR), pre-pulse inhibition (PPI) of ASR, activity of cholinesterase in blood and catecholamine levels in adrenals were evaluated after low dose sarin exposure (3 x 0.4 LD50 subcutaneously) combined with chronic intermittent stress in C57BL/6J mice. While sarin alone produced depression of motor activity, no interaction of the stress with sarin exposure was observed. Cholinesterase activity was significantly reduced 24 h after exposure to sarin; however, the basal activity was re-established 3 weeks later. The combination of low dose sarin exposure and stress produced delayed behavioral change manifested as excessive grooming together with endocrine alterations in adrenals 7 weeks after exposure. The size of the adrenals in the combined exposure group was increased and the concentration of catecholamines was significantly decreased. In conclusion, these findings indicate that sarin in low doses is more dangerous when combined with shaker stress inducing delayed behavioral and endocrine changes.
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PMID:Delayed behavioral and endocrine effects of sarin and stress exposure in mice. 1750


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