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)

Complete heart block was produced in eight dogs by the selective perfusion of physostigmine or neostigm into the atrioventricular (AV) node artery. A characteristic escape AV junctional rhythm emerged in each dog. After reversal of the cholinesterase paralysis with atropine, in each dog partial heart block was produced by an incision into the AV nodal region. In three of these eight dogs, a second incision placed slightly more anteriorly produced complete AV block which was followed by the emergence of an escape AV junctional rhythm similar to the one produced pharmacologically. Hearts of these three dogs were examined histologically with serial sections to determine the exact location of the incisions and their relationship to the AV node and His bundle. In each dog the incision that produced complete heart block passed directly through the junction of AV node with His bundle. In this region previous studies had demonstrated numerous P cells, which are thought to be the site of origin of normal cardiac automaticity. In each of the three hearts there were abundant P cells in continuity with the His bundle distal to the cut producing heart block. Significance of these findings is discussed relative to the locus of action of acetylcholine within the AV junction, the site of origin of AV junctional rhythm, and sme aspects of the experimental and therapeutic production of heart block.
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PMID:Correlative electrophysiological and anatomical studies concerning the site of origin of escape rhythm during complete atrioventricular block in the dog. 44 92

The regional distribution of acetylcholinesterase in the right atrium was determined by quantitative chemical measurements on hearts obtained from 14 infant and 9 adult humans of autopsy, and 9 adult dogs after termination of acute animal experiments. The atrium and interatrial septum were dissected, and the appendage was cut along its fold from the ventricular border to the superior vena cava. The atrium was cut into 20 consecutive sections. Homogenates (10% w/v) were prepared, centrifuged, and the supernatants were used for the enzyme assay by the method of Ellman. The acetylcholinesterase concentration [AChE] was mapped by section, or the sections were grouped into areas and mapped. The results show that: 1) in the dog, [AChE] is significantly higher in the nodal regions as compared to the appendicular areas, which contain the lowest [AChE]; 2) in the human, the [AChE] distribution pattern is qualitatively similar between the adult and infant, and in contrast to the dog, the appendicular areas contain the highest [AChE]; 3) for all areas studied, human infant [AChE] levels are significantly higher than human adult levels for corresponding areas. It is concluded that there is a distinct species difference between the regional distribution of the [AChE] in human and canine right atrium. Also, within humans, there is an age-related difference in the quantitative [AChE] levels. These species and age-related differences may reflect a varying pattern of distribution of the vagus nerve between the two species studied.
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PMID:Regional distribution of acetylcholinesterase in the right atria of humans and dogs. 51 86

In the stage 4 chick blastoderm, an area located 0.6 mm posterior to Hensen's node, the post-nodal piece (PNP), consists of an undifferentiated population of cells, since the explants when cultivated in vitro in a variety of media do not develop into any histologically identifiable structures. However, addition of a specific low molecular weight RNA isolated from the 16-day-old chick embryonic heart promotes the appearance of a distinct mode of morphological and biochemical changes that is similar to that of embryonic cardiogenic process. The RNA-induced changes in the PNP also include a marked increase in acetylcholinesterase activity. The increase in enzymatic activity can be measured biochemically, as well as visualized histochemically.
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PMID:Acetylcholinesterase differentiation during myogenesis in early chick embryonic cells caused by an inducer RNA. 65 37

The problem of development of the innervation of the rat atrioventricular node has been investigated by electron microscopy. Nerve bundles appear in relation to the node as early as the second postnatal day and vesiculated axons are seen throughout the entire node by the fourth day. Intimate contacts between nodal cells, axons and terminal varicosities are frequently observed. Use of the 5-hydroxydopamine tracer technique has enabled the identification of both cholinergic and adrenergic axons. It is concluded that the node has a dual innervation although cholinergic endings far outnumber those classified as adrenergic on the sixth postnatal day. These results are quite different to earlier findings made at the light microscope level and the discrepancies are discussed with respect to the histochemical techniques used. The suggestion that nodal differentiation is induced by nerves is considered in relation to the differences in cholinesterase activity exhibited by nodal cells during normal development and following neonatal sympathectomy.
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PMID:The development of innervation in the rat atrioventricular node. 83 26

The conduction velocity and histological structure of motoneurons innervating normal and hypertrophied rat plantaris muscles were investigated. Hypertrophy was produced by ablation of synergist muscles. Single motor units were obtained by ventral root dissection and conduction velocities measured. The structure of neurons was investigated following retrograde labeling with horseradish peroxidase. A combined silver, gold and cholinesterase staining method was developed to study the motor endplate. In addition, the peripheral nerve was fixed, embedded in Araldite, and sectioned for determination of axonal size and myelin thickness. Conduction velocity of motor axons decreased following hypertrophy of the skeletal muscle (control CV = 75.8 +/- 8.9 m s-1, n = 94, hypertrophy CV = 69.0 +/- 12.3 m s-1, n = 84). However, no alteration in the size of motor axons or myelin thickness could account for this alteration in conduction velocity. Mean motoneuronal soma size decreased following muscle hypertrophy (soma diameter: control 36.1 +/- 4.6 microns, n = 283, hypertrophy 32.9 +/- 4.5 microns, n = 294). The complexity of the motor endplate increased following hypertrophy with an increased occurrence of nodal sprouts. In addition, the area of cholinesterase staining increased following hypertrophy (control 588.1 +/- 297.2 microns 2, n = 269, hypertrophy 857.7 +/- 357.0 microns 2, n = 269). This study found that both the morphological and physiological parameters of motoneurons innervating a hypertrophied muscle were shifted toward those of normal rat slow motor units.
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PMID:Functional and structural changes of rat plantaris motoneurons following compensatory hypertrophy of the muscle. 199 79

The mechanisms responsible for slowing cardiac impulse conduction through the atrioventricular (AV) node are not well understood but include anatomical architecture, presence of cells with diverse electrophysiological characteristics, and modulation by autonomic nervous system. The present study was designed to determine the site of vagally induced slowing of conduction through the AV node. We attempted to correlate the electrophysiological response of AV nodal cells to postganglionic vagal stimulation applied in different regions of the node with the morphological findings and patterns of acetylcholinesterase-positive staining of nodal tissue. This multifaceted approach revealed that vagal stimulation produced localized hyperpolarization of the cells from the N region of the AV node, which correlated with the strong acetylcholinesterase positive staining of the central nodal area. In contrast, the density of the acetylcholinesterase staining decreased toward both the AN and His bundle regions, whereas vagal stimulation had a negligible effect on the cells from these regions. These results suggest that vagal-induced depression of AV nodal conduction is produced by release of acetylcholine predominantly around the midnodal region and the depressive action of acetylcholine is concentrated on the cells occupying the same region (i.e., the N cells). Thus, there appears to be a close juxtaposition of nerve elements and effector cells in the midnodal region of the AV node. This unique combination of available neuromediator and responding cells with hyperpolarization and depressed action potential determines the midnodal region as the focus of vagal effect on AV nodal conduction.
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PMID:Morphological and electrophysiological correlates of atrioventricular nodal response to increased vagal activity. 239 13

The localization and distribution of neuropeptide Y-like immunoreactivity in the guinea-pig heart were studied by use of immunohistochemical methods. A widespread distribution of immunoreactive processes was observed in all regions of the heart. They occur either singly or together with several other immunoreactive processes and are most often aligned parallel to the myocardial bundles. A dense network of processes is present in the region of both the sinuatrial and atrioventricular nodes and single fibers are occasionally observed to be closely associated with nodal ganglion cells. Positive cell bodies were not seen within the heart. All small, medium and large coronary vessels are surrounded by a dense network of immunoreactive processes. A rich innervation at the media-adventitia junction of the aorta, pulmonary trunk, superior and inferior vena cava was also observed. Comparison of adjacent sections stained with antisera directed to avian pancreatic polypeptide, carboxyl-terminal hexapeptide of pancreatic polypeptide or neuropeptide Y demonstrated a very similar immunoreactive pattern, suggesting that these antisera are reacting with the same or a closely related substance. Likewise, the same immunoreactive patterns were observed in adjacent sections incubated in antiserum to neuropeptide Y or tyrosine hydroxylase, and analysis of elution-restained sections demonstrated that the same processes contain both neuropeptide Y- and tyrosine hydroxylase-like immunoreactivity. Neuropeptide Y- and tyrosine hydroxylase-like immunoreactivity was reduced by the same magnitude after treatment with the sympathetic neurotoxin 6-hydroxydopamine, but it was not affected by the primary sensory neurotoxin capsaicin. Furthermore, the pattern of neuropeptide Y- and tyrosine hydroxylase-like immunoreactivity did not match the staining patterns observed with antisera to vasoactive intestinal polypeptide or substance P or with the acetylcholinesterase staining pattern. In conclusion, neuropeptide Y-like immunoreactivity in the heart and great vessels coexists with that for catecholamines and is likely to originate from sympathetic ganglia.
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PMID:Distribution and colocalization of neuropeptide Y- and tyrosine hydroxylase-like immunoreactivity in the guinea-pig heart. 241 9

The change in sinus period elicited by vagal stimulation depends on the rate of acetylcholine (ACh) release from the nerve endings, the rate of ACh degradation in the nodal tissue, and the responsiveness of the sinus node to ACh. Vagal stimulation in anesthetized dogs prolonged sinus period. After cessation of vagal stimulation, the sinus period returned to the prestimulation period. We developed a mathematical model to analyze the dynamics of ACh degradation in the neuroeffector junction and the dependence of sinus period on the concentration of ACh. From the in vitro reaction kinetics of acetylcholinesterase, we derived an analytical expression for the rate of ACh degradation in the intact animal. Our model represents the electrical behavior of the sinus node by the electrical activity of one pacemaker cell with six membrane ionic currents. This model predicts the decline in sinus period of the intact anesthetized dog as acetylcholinesterase degrades ACh in the neuroeffector junction. The half-life of ACh after cessation of vagal stimulation was estimated to be 2.7 s. We conclude that following termination of vagal stimulation, the sinus node of the intact animal responds to ACh as if the sinus node were one oscillator.
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PMID:Mathematical model of dependence of heart rate on tissue concentration of acetylcholine. 291 85

Experiments were performed to determine the degree of overlap in the distribution of muscarinic receptors and cholinergic innervation of the rat heart. Localization of muscarinic receptors was determined by autoradiography with [3H]quinuclidinyl benzilate. Adjacent sections were stained for acetylcholinesterase to determine innervation. The distribution of muscarinic receptors and cholinergic innervation overlapped in cardiac parasympathetic ganglia, nodal tissue, His bundle-Purkinje system, vena cava and pulmonary veins. Cholinergic innervation to the right atrium was greater than to the left atrium while muscarinic receptor density was equal in the two atria. Innervation of the ventricles was confined primarily to the base of the right ventricle. A low density of muscarinic receptors was observed throughout the ventricles. Neither cholinergic innervation nor muscarinic receptors were detected in the pulmonary trunk, ascending aorta or cardiac valves. Muscarinic receptors and cholinergic innervation in the nodal regions, ventricular conduction system and myocardium probably mediate negative chronotropic, dromotropic and inotropic effects of vagal nerve stimulation. Muscarinic receptors at sites not containing cholinergic innervation may be associated with noradrenergic nerves of the myocardium.
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PMID:Distribution of muscarinic receptors and acetylcholinesterase in the rat heart. 359 49

Sartorius muscles of the frog Rana pipiens were used to study the incidence of motor nerve sprouting in normal unoperated muscles, in experimental muscles contralateral to axotomy of the sartorius nerve, and in sham-operated control muscles. Muscles were stained with either a combination of nitroblue tetrazolium nerve terminal stain and cholinesterase stain or with a combination of silver nerve terminal stain and cholinesterase stain. Each endplate that could be clearly seen was classified into one or more of the following categories: normal endplates without sprouts, three types of terminal sprouts, preterminal sprouts, nodal sprouts, sprouts of unknown origin and destination, and doubly innervated gutters. A quantitative study of 318 endplates from nine unoperated muscles, 779 endplates from 45 experimental muscles, and 694 endplates from 41 control muscles showed that all muscles had a high incidence of motor nerve sprouting and other forms of remodelling (20-28% of all endplates). There were, however, no significant differences between experimental, control, and unoperated muscles when results obtained with the same stains were compared. Results obtained with the two different stains were only slightly different. We conclude that sprouting is a very common but highly variable feature of normal frog neuromuscular junctions, and in the sartorius, contralateral axotomy does not alter this ongoing remodelling.
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PMID:Motor axon sprouting in frog sartorius muscles is not altered by contralateral axotomy. 387 65


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