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PubMed1977

Myelination and cholinesterase activity of chick embryo spinal cord.

This work was undertaken to study the myelination and cholinesterase activity of the developing white matter of chick embryo spinal cord from the 6th day of incubation until hatching. Myelination of the white matter was always preceeded by the aggregation of neuroglial cells. The sequence of myelination in the cervical and thoracic segments was from before backwards, whereas in the lumbosacral segments it was from behind forewards. Myelination of the ventral column extended craniocaudally, whereas in the posterior column is extended caudocranially. True cholinesterase activity was encountered in the spinal white matter only before and during the process of myelination and was closely associated with the sites of neuroglial aggregations. No pseudocholinesterase activity could be seen in the white matter before myelination. However, during the period of active myelination, enzymatic activity was seen only at the sites of formed myelin and after myelination of all tracts; the whole white matter reacted positive for the enzyme. The significance of these findings is discussed.

Animals↗
PubMed1983

Development of muscles in the dorsal foreleg of rat embryos. A light microscopic study with the in situ cholinesterase staining technique.

The development of muscles from the dorsal side of the forelegs from 13- to 21-day-old rat embryos was investigated under a light microscope. The muscle blastemata and individual muscles were stained in situ with the cholinesterase technique. The first muscle blastemata are visible on the early day 13. It appears that mainly myotubes are stained. The antebrachial and brachial extensor muscles form separated anlagen which connect on the late day 13 in the proximal region of the extensor carpi ulnaris muscle. The individualization of the muscles in a muscle blastema takes place on days 13 and 14. On day 15 all extensor muscles are visible. However, at this time the inserting points of some of these muscles are not yet visible after staining with alcian blue. On the early day 16 the motor end-plates are conspicuous. Due to the content of unspecific cholinesterase in rat embryos the tendons are also stained on day 16. Muscles and tendons remain stainable until birth. In addition to the muscles also the nerves, especially the epifascial nerves, stain very well with the acetylcholinesterase reaction.

Animals↗
PubMed1975

Suxamethonium sensitivity and segregation of human serum cholinesterase variants at locus, Ch1, among twelve British families.

Sera from 39 individuals with suxamethonium apnoea have been examined. The likelihood of the ChU1ChD1 heterozygotes developing suxamethonium apnoea has been calculated. The results indicate that 1 in 4,000 of normal homozygotes and 1 in 400 of ChU1ChD1 heterozygotes develop suxamethonium apnoea. The period of suxamethonium apnoea in these individuals has been found shorter than that usually seen in ChD1ChD1 homozygotes. An approximate estimate of the frequency of the ChF1 and ChS1 genes has also been calculated. Twelve British families of these suxamethonium apnoea propositi have been examined. The inheritance pattern in all these families was found to be of the Mendelian type. Three of these families have been found to be segregating for the rarer ChF1 gene and two for ChS1 gene, respectively. This present study provides an additional piece of support to the hypothesis that the ChF1 and ChS1 are alleles determining the synthesis of usual and atypical cholinesterase together with the likelihood of ChU1ChD1 heterozygotes having occasional suxamethonium apnoea. In addition, the present report indicates that there may be cholinesterase variants besides dibucaine and fluoride-resistant, 'silent' and C5.

Apnea↗
PubMed1977

Plasma cholinesterase polymorphism in Down's syndrome.

The plasma cholinesterase variants in 80 patients having Down's syndrome have been examined and compared with a random control sample of individuals domiciled in the same area. Neither a change in frequency of known C5+ variant nor any new variant has been found in the electrophoretic studies. A highly significant increase in frequency of the fluoride resistant gene as well as a significant decrease in frequency of the atypical gene has been found in the Down's syndrome individuals. This altered distribution of the rare phenotype of plasma cholinesterase in mental illness may lead to a useful diagnostic acid in genetic counselling.

Cholinesterases↗
PubMed1992

Urinary cholinesterase activity is increased in insulin-dependent diabetics: further evidence of diabetic tubular dysfunction.

We measured the cholinesterase activity in morning urines from 63 insulin-dependent diabetics and 27 controls. The total esterase (TotE) activity (Ellman's method) has been divided into aliesterase (AliE), pseudocholinesterase and acetylcholinesterase by means of two inhibitors, eserine and quinidine. Diabetics were divided in 2 groups according to the urinary albumin/creatinine ratio (mg/mmol, < 2 in group 1, > 2 in group 2). The urinary cholinesterase behavior was correlated with that of a known tubular lysosomal hydrolase, N-acetyl-beta-D-glucosaminidase (NAG). Compared to normals, in addition to a significant increase in urinary NAG in diabetes (in group 2 more than in group 1), TotE and AliE were also significantly raised (+36% and 109% of the controls, in group 1 as much as in group 2).

Adolescent↗
PubMed2005

Cortical activation during cholinesterase-inhibitor treatment in Alzheimer disease: preliminary findings from a pharmaco-fMRI study.

OBJECTIVE: Cholinesterase inhibitors improve cognitive functioning in Alzheimer disease (AD). The authors studied, with functional magnetic resonance imaging (fMRI), the neural mechanism by which this cholinergic enhancement improves memory encoding in AD over longer time periods. METHODS: Brain activation was measured in 10 patients with AD and 10 healthy elderly comparison subjects with fMRI while they were encoding novel faces. Patients were scanned again after a 10-week open treatment with the cholinesterase-inhibitor donepezil. RESULTS: Neuropsychologically-tested memory performance improved during the treatment phase in the patients. During the encoding of novel faces, elderly comparison subjects showed more activation in the right fusiform gyrus than the group of AD patients. After a 10-week treatment with donepezil, the fusiform gyrus was also activated in patients, similar to the comparison group. CONCLUSIONS: The right fusiform gyrus is associated with the processing of faces. Cholinergic enhancement augments selective attention by increased selectivity of perceptual responses in patients with AD. This mechanism may contribute to a more efficient processing of the attended stimulus and thus be a mechanism underlying clinical improvement of cognitive functioning. These promising preliminary findings need to be confirmed in a larger, controlled trial in which both fMRI and attention measures serve as outcomes.

Aged↗
PubMed2000

Orbital and dorsolateral frontal perfusion defect associated with behavioral response to cholinesterase inhibitor therapy in Alzheimer's disease.

The authors retrospectively explored the behavioral and functional imaging profile of Alzheimer's disease (AD) patients who respond to cholinesterase inhibitor therapy by using the Neuropsychiatric Inventory (NPI) and baseline [99mTc]HMPAO SPECT. Thirty AD patients were divided into three groups (Responders, Nonresponders, and Unchanged) based on their behavioral response to donepezil. Responders had significantly (P < or = 0.01) more pretreatment irritability, disinhibition (P < or = 0.05), and euphoria (P = 0.05) than Nonresponders and significantly lower lateral orbital frontal (P < 0.00001) and dorsolateral frontal (P < or = 0.0005) perfusion bilaterally. A pretreatment orbitofrontal syndrome may predict behavioral response to cholinesterase inhibitor therapy in AD.

Aged↗
PubMed1984

A BASIC program for serum cholinesterase phenotyping using a microcomputer.

We have modified a BASIC program for serum cholinesterase phenotyping using a microcomputer. This program accepts the reaction-rate result of total and inhibitor assays of activity, allows the patient to be identified and prints out a full account of the fitting process thus allowing adequate documentation. We believe that this modification enhances the usefulness of the program to laboratories engaged in the routine determination of serum cholinesterase phenotyping.

Cholinesterases↗
PubMed1977

The plasma cholinesterase variants in mentally ill patients.

The distribution of the plasma cholinesterase variants found in 1,374 mentally ill patients differs from that of a random control sample. The patients are more likely to have a rare phenotype than an individual from the normal population. None of the diagnostic groups have been shown to differ in the distribution of the E1a gene, but there is strong statistical evidence that Group IV (psychosis) patients have a higher frequency of the E1f gene than the other groups. The overall frequency of the electrophoretic variant C5 + did not differ significantly from that observed in a Caucasian population, with the exception of the increase observed in Group IV c2. Twenty-eight unrelated patients with Huntington's chorea were found to have a significantly altered incidence of the C5 + variant and six patients from this group were found to have the rare E1f gene. Our results indicate that the plasma cholinesterase variants may provide some insight into the inheritance of Huntington's chorea.

Bipolar Disorder↗
PubMed2005

Amyloid, cholinesterase, melatonin, and metals and their roles in aging and neurodegenerative diseases.

The aging brain shows selective neurochemical changes involving several neural cell populations. Increased brain metal levels have been associated with normal aging and a variety of diseases, including Alzheimer's disease (AD). Melatonin levels are decreased in aging, particularly in AD subjects. The loss of melatonin, which is synthesized by the pineal gland, together with the degeneration of cholinergic neurons of the basal forebrain and the deposition of aggregated proteins, such as the amyloid beta peptides (Abeta), are believed to contribute to the development of cognitive symptoms of dementia. Aging and its variants, such as AD, should be viewed as the result of multiple "hits," including alterations in the levels of Abeta, metals, cholinesterase enzymes, and neuronal gene expression. Herein, we present evidence in support of this theory, based on several studies. We discuss melatonin's neuroprotective function, which plays an important role in aging, prolongation of life span, and health in the aged individual. It interacts with metals and, in some cases, neutralizes their toxic effects. Dietary supplementation of melatonin restores its age-related loss. In mice, an elevated brain melatonin significantly reduced levels of potentially toxic Abeta peptides. Thus, compensation of melatonin loss in aging by dietary supplementation could well be beneficial in terms of reducing metal-induced toxicity, lipid peroxidation, and losses in cholinergic signaling. We propose that certain cholinesterase inhibitors and the NMDA partial antagonist memantine, which are FDA-approved drugs for AD and useful to boost central nervous system functioning, can be made more effective by their combination with melatonin or other neuroprotectants. Herein, we highlight studies elucidating the role of the amyloid pathway, metals, melatonin, and the cholinergic system in the context of aging and AD. Finally, melatonin is present in edible plants and walnuts, and consuming foodstuffs containing melatonin would be beneficial by enhancing the antioxidative capacity of the organisms.

Aging↗
PubMed2000

A post-ischaemic single administration of galanthamine, a cholinesterase inhibitor, improves learning ability in rats.

Transient forebrain ischaemia is widely observed in clinical practice. We have examined the effect of a single administration of the cholinesterase inhibitor galanthamine (2mg kg(-1) i.p.) 25 min after reperfusion in male Sprague-Dawley rats (180 +/- 20 g) after a 20-min common carotid artery occlusion. Twenty-four-hours post-ischaemia there was no difference in motor co-ordination or muscle tonus of the rats treated with or without galanthamine as assessed by the rota-rod test. Learning ability was examined using the shuttle-box test, evaluating the latency time and the number of errors for six days in succession. The performance of the ischaemic saline-injected rats was significantly impaired on days 4, 5, 6 (latency time) compared with the non-ischaemic rats and with the ischaemic animals administered galanthamine (P < 0.05). Similar results were obtained when counting the number of errors (failure to cross the cage during conditioned or unconditioned stimulus). The monitoring of body temperature during the first 12-h post-ischaemia did not show any significant difference between the groups. The data showed a beneficial effect of galanthamine on the recovery of learning ability when administered once only post-ischaemia. This suggests a direct effect on the early pathologic mechanisms of CNS damage. Cholinesterase inhibitors may prove useful in the early clinical treatment of ischaemic conditions.

Animals↗
PubMed2000

Effect of Rhazya stricta Decne on monoamine oxidase and cholinesterase activity and brain biogenic amine levels in rats.

The effect of treatment with the medicinal plant Rhayva stricta Decne, on monoamine oxidase (MAO) and cholinesterase activity, and on the concentration of brain biogenic amines was studied in rats. R. stricta extract, at doses of 0.2 and 0.5 g kg(-1), significantly (P < 0.05-0.01) increased the hepatic and cerebral activity of MAO by 36-127%. The higher doses used (2.0 and 8.0 g kg(-1)) produced smaller (10-26%) and statistically insignificant increases in MAO activity in liver and brain. Cholinesterase activity in blood, liver and brain was not significantly influenced by treatment with R. stricta. The concentrations of the measured biogenic amines (noradrenaline, adrenaline, 5-hydroxytryptamine and dopamine) were significantly lowered in rats treated with R. stricta. The observed increase in MAO activity may be responsible for the lowered biogenic amines levels and may, in part, be responsible for the pharmacological effects of R. stricta extract in rats.

Animals↗
PubMed1983

Contrast media and enzyme inhibition. I. Cholinesterase.

Cholinergic mechanisms, activated by the inhibition of the acetylcholine hydrolysing enzyme cholinesterase, may be responsible for many of the adverse effects of intravascular radiological contrast media. The relative cholinesterase-inhibiting activities of several conventional and new contrast media have been measured and significant differences are found. Some of the possible implications of these differences are discussed.

Animals↗
PubMed2001

Developmental neurotoxicity of chlorpyrifos modeled in vitro: comparative effects of metabolites and other cholinesterase inhibitors on DNA synthesis in PC12 and C6 cells.

The widely used organophosphate pesticide chlorpyrifos is a suspected neuroteratogen. In the current study, we compared the effects of chlorpyrifos and its major metabolites in two in vitro models, neuronotypic PC12 cells and gliotypic C6 cells. Chlorpyrifos inhibited DNA synthesis in both cell lines but had a greater effect on gliotypic cells. Chlorpyrifos oxon, the active metabolite that inhibits cholinesterase, also decreased DNA synthesis in PC12 and C6 cells with a preferential effect on the latter. Trichloropyridinol, the major catabolic product of chlorpyrifos, had a much smaller, but nevertheless statistically significant, effect that was equivalent in both cell lines. Diazinon, another organophosphate pesticide, also inhibited DNA synthesis with preference toward C6 cells, but was less effective than was chlorpyrifos. Physostigmine, a non-organophosphate cholinesterase inhibitor, was less effective than either chlorpyrifos or diazinon, but still caused significant inhibition of DNA synthesis in C6 cells. We also found that the addition of sera protected the cells from the adverse effects of chlorpyrifos and that the effect could be reproduced by addition of albumin. These results indicate that chlorpyrifos and other organophosphates such as diazinon have immediate, direct effects on neural cell replication, preferentially for gliotypic cells. In light of the protective effect of serum proteins, the fact that the fetus and newborn possess lower concentrations of these proteins suggests that greater neurotoxic effects may occur at blood levels of chlorpyrifos that are nontoxic to adults.

Animals↗
PubMed1999

Cholinesterases in neural development: new findings and toxicologic implications.

Developing animals are more sensitive than adults to acute cholinergic toxicity from anticholinesterases, including organophosphorus pesticides, when administered in a laboratory setting. It is also possible that these agents adversely affect the process of neural development itself, leading to permanent deficits in the architecture of the central and peripheral nervous systems. Recent observations indicate that organophosphorus exposure can affect DNA synthesis and cell survival in neonatal rat brain. New evidence that acetylcholinesterase may have a direct role in neuronal differentiation provides additional grounds for interest in the developmental toxicity of anticholinesterases. For example, correlative anatomic studies show that transient bursts of acetylcholinesterase expression often coincide with periods of axonal outgrowth in maturing avian, rodent, and primate brain. Some selective cholinesterase inhibitors effectively suppress neurite outgrowth in model systems like differentiating neuroblastoma cells and explanted sensory ganglia. When enzyme expression is altered by genetic engineering, acetylcholinesterase levels on the outer surface of transfected neurons correlate with ability to extend neurites. Certain of these "morphogenic" effects may depend on protein-protein interactions rather than catalytic acetylcholinesterase activity. Nonetheless, it remains possible that some pesticides interfere with important developmental functions of the cholinesterase enzyme family.

Acetylcholinesterase↗