Ultrastructural and histochemical observations in the developing iris musculature in the chick

Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 117-127
Author(s):  
Y. Narayanan ◽  
C. H. Narayanan
Keyword(s):  
Ache Activity ◽  
Neuromuscular Junctions ◽  
Cell Loss ◽  
Ciliary Ganglion ◽  
Cell Degeneration ◽  
Synaptic Terminals ◽  
Time Table ◽  
The Relationship ◽  
Massive Cell ◽  
T System

Irises from chick embryos and from 2- and 3-week-old chicks were studied using ultrastructural and histochemical methods in order to clarify the relationship between cell loss in the ciliary ganglion and the establishment of permanent peripheral connections between the ciliary neurons and the iris muscle. The iris muscle undergoes morphological and biochemical differentiation between 11 and 13 days of incubation. This period coincides with the critical period in the development of the ciliary ganglion when massive cell degeneration occurs. During this period, the iris develops typical sarcomeric structure, with AChE activity in the nuclear envelope, Golgi, and the ‘T’ system. At 15 days of incubation AChE activity is found localized in discrete areas on the muscle fiber, forming specific neuromuscular junctions. Between 13 and 15 days of incubation, there is a shift in the localization of AChE activity in the iris muscle, from the sarcoplasmic structures to the junctional membranes. Few synaptic terminals are observed in the iris musculature prior to 11 days of incubation.There is a marked increase in the number of synaptic terminals between 11 and 13 days of incubation which also coincides with the period of cell loss in the ciliary ganglion. The establishment of neuromuscular junctions at 15 days of incubation corresponds with the period when the number of neurons in the ciliary ganglion has attained the adult level. The time table of the events described above, leads us to conclude that during development only those neurons in the ciliary ganglion which make peripheral contacts survive, and only such contacts differentiate into mature neuromuscular junctions on the iris muscle. This will imply that neurons which are doomed to die, although they may send out fibers to the periphery, do not make peripheral contacts before death.

scholarly journals Acetylcholinesterase from the motor nerve terminal accumulates on the synaptic basal lamina of the myofiber.

1991 ◽  
Vol 115 (3) ◽  
pp. 755-764 ◽  
Author(s):  
L Anglister
Keyword(s):  
Basal Lamina ◽  
Ache Activity ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Synaptic Cleft ◽  
Motor Nerve Terminal ◽  
Nerve Terminals ◽  
Axon Terminals ◽  
Muscle Nerve ◽  
Almost All

Acetylcholinesterase (AChE) in skeletal muscle is concentrated at neuromuscular junctions, where it is found in the synaptic cleft between muscle and nerve, associated with the synaptic portion of the myofiber basal lamina. This raises the question of whether the synaptic enzyme is produced by muscle, nerve, or both. Studies on denervated and regenerating muscles have shown that myofibers can produce synaptic AChE, and that the motor nerve may play an indirect role, inducing myofibers to produce synaptic AChE. The aim of this study was to determine whether some of the AChE which is known to be made and transported by the motor nerve contributes directly to AChE in the synaptic cleft. Frog muscles were surgically damaged in a way that caused degeneration and permanent removal of all myofibers from their basal lamina sheaths. Concomitantly, AChE activity was irreversibly blocked. Motor axons remained intact, and their terminals persisted at almost all the synaptic sites on the basal lamina in the absence of myofibers. 1 mo after the operation, the innervated sheaths were stained for AChE activity. Despite the absence of myofibers, new AChE appeared in an arborized pattern, characteristic of neuromuscular junctions, and its reaction product was concentrated adjacent to the nerve terminals, obscuring synaptic basal lamina. AChE activity did not appear in the absence of nerve terminals. We concluded therefore, that the newly formed AChE at the synaptic sites had been produced by the persisting axon terminals, indicating that the motor nerve is capable of producing some of the synaptic AChE at neuromuscular junctions. The newly formed AChE remained adherent to basal lamina sheaths after degeneration of the terminals, and was solubilized by collagenase, indicating that the AChE provided by nerve had become incorporated into the basal lamina as at normal neuromuscular junctions.

scholarly journals Dynein acts to cluster glutamate receptors and traffic the PIP5 kinase, Skittles, to regulate postsynaptic membrane organization at the neuromuscular junction

2021 ◽  
Author(s):  
Amanda L. Neisch ◽  
Thomas Pengo ◽  
Adam W. Avery ◽  
Min-Gang Li ◽  
Thomas S. Hays
Keyword(s):  
Neuromuscular Junctions ◽  
Cytoplasmic Dynein ◽  
Postsynaptic Membrane ◽  
Independent Function ◽  
Protein Levels ◽  
Cluster Organization ◽  
Synaptic Terminals ◽  
Cargo Transport ◽  
Spectrin Cytoskeleton ◽  
Phosphatidylinositol 4

Cytoplasmic dynein is essential in motoneurons for retrograde cargo transport that sustains neuronal connectivity. Little, however, is known about dynein's function on the postsynaptic side of the circuit. Here we report distinct postsynaptic roles for dynein at neuromuscular junctions (NMJs). Intriguingly, we show that dynein punctae accumulate postsynaptically at glutamatergic synaptic terminals. Moreover, Skittles, a phosphatidylinositol 4-phosphate 5-kinase that produces PI(4,5)P2 to organize the spectrin cytoskeleton, also localizes specifically to glutamatergic synaptic terminals. Depletion of postsynaptic dynein disrupts the accumulation of Skittles, PI(4,5)P2 phospholipid, and organization of the spectrin cytoskeleton at the postsynaptic membrane. Coincidental with dynein depletion, we observe an increase in the clusters size of ionotropic glutamate receptor (iGluR), and an increase in the amplitude and frequency of mEJPs. However, PI(4,5)P2 levels do not affect iGluR clustering and dynein does not affect the protein levels of iGluR subunits at the NMJ, suggesting a separate, transport independent function for dynein in iGluR cluster organization. As dynein punctae closely associate with iGluR clusters, we propose that dynein physically tethers iGluR clusters at the postsynaptic membrane to ensure proper synaptic transmission.

Linking Mathematical Literacy to ICT

2011 ◽  
pp. 202-210
Author(s):  
Tshele Moloi
Keyword(s):  
Everyday Life ◽  
Mathematical Literacy ◽  
Mathematical Skills ◽  
Time Table ◽  
The Relationship ◽  
Financial Issues

Finally, there is need to indicate the relationship between mathematics/mathematical literacy and ICTs. In this chapter, the two are seen as inseparable. In everyday life, a person is continually faced with challenges that call for mathematical skills, such as financial issues (hire-purchase, mortgage bonds, and investments), understand house plans, read a map, follow time table, et cetera; with the usage of ICT these can be done very fast and accurately. It is of utmost importance that a person must have a sense and knowledge of Mathematics, so as to detect mistakes committed by the usage of ICT.

Cell cycle kinetics in the alveolar epithelium

1997 ◽  
Vol 272 (6) ◽  
pp. L1031-L1045 ◽  
Author(s):  
B. D. Uhal
Keyword(s):  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelium ◽  
Cell Loss ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Pathological Conditions ◽  
Type Ii Cell ◽  
The Relationship

The type II alveolar epithelial cell has important metabolic and biosynthetic functions but also serves as the stem cell of the alveolar epithelium. Much of the evidence underlying this premise was obtained before 1980 and provided the basis for a working model that has not been reconsidered for more than fifteen years. With the exceptions to be discussed below, little evidence has accumulated in the interim to suggest that the model requires significant alteration. Important questions remain unanswered, however, and some components of the model need to be supplemented, particularly in light of recent investigations that have provided insights not possible in earlier work. In particular, in vitro studies have suggested that the relationship between the parent type II cell and its progeny may not be as straightforward as originally thought. In addition, the rate of epithelial cell loss was recognized long ago to be an important factor in the regulation of this system, but its kinetics and mechanisms have received little attention. These and other unresolved issues are critical to our understanding of the homeostasis of the alveolar epithelium under normal and pathological conditions.

Cisplatin-Induced Hyperactivity in the Dorsal Cochlear Nucleus and Its Relation to Outer Hair Cell Loss: Relevance to Tinnitus

2002 ◽  
Vol 88 (2) ◽  
pp. 699-714 ◽  
Author(s):  
James A. Kaltenbach ◽  
John D. Rachel ◽  
T. Alecia Mathog ◽  
Jinsheng Zhang ◽  
Pamela R. Falzarano ◽  
...  
Keyword(s):  
Cochlear Nucleus ◽  
Outer Hair Cell ◽  
Cell Loss ◽  
Outer Hair Cells ◽  
Dorsal Cochlear Nucleus ◽  
Spontaneous Neural Activity ◽  
Electrophysiological Recordings ◽  
Significant Damage ◽  
Basal Half ◽  
The Relationship

Cisplatin causes both acute and chronic forms of tinnitus as well as increases in spontaneous neural activity (hyperactivity) in the dorsal cochlear nucleus (DCN) of hamsters. It has been hypothesized that the induction of hyperactivity in the DCN may be a consequence of cisplatin's effects on cochlear outer hair cells (OHCs); however, systematic studies testing this hypothesis have yet to appear in the literature. In the present investigation, the relationship between hyperactivity and OHC loss, induced by cisplatin, was examined in detail. Hamsters received five treatments of cisplatin at doses ranging from 1.5 to 3 mg · kg−1 · day−1, every other day. Beginning 1 mo after initiation of treatment, electrophysiological recordings were carried out on the surface of the DCN to measure spontaneous multiunit activity along a set of coordinates spanning the medial-lateral (tonotopic) axis of the DCN. After recordings, cochleas were removed and studied histologically using a scanning electron microscope. The results revealed that cisplatin-treated animals with little or no loss of OHCs displayed levels of activity similar to those seen in saline-treated controls. In contrast, the majority (75%) of cisplatin-treated animals with severe OHC loss displayed well-developed hyperactivity in the DCN. The induced hyperactivity was seen mainly in the medial (high-frequency) half of the DCN of treated animals. This pattern was consistent with the observation that OHC loss was distributed mainly in the basal half of the cochlea. In several of the animals with severe OHC loss and hyperactivity, there was no significant damage to IHC stereocilia nor any observable irregularities of the reticular lamina that might have interfered with normal IHC function. Hyperactivity was also observed in the DCN of animals showing severe losses of OHCs accompanied by damage to IHCs, although the degree of hyperactivity in these animals was less than in animals with severe OHC loss but intact IHCs. These results support the view that loss of OHC function may be a trigger of tinnitus-related hyperactivity in the DCN and suggest that this hyperactivity may be somewhat offset by damage to IHCs.

scholarly journals Basal lamina directs acetylcholinesterase accumulation at synaptic sites in regenerating muscle.

1985 ◽  
Vol 101 (3) ◽  
pp. 735-743 ◽  
Author(s):  
L Anglister ◽  
U J McMahan
Keyword(s):  
Plasma Membrane ◽  
Neuromuscular Junction ◽  
Basal Lamina ◽  
Acetylcholine Receptors ◽  
Skeletal Muscles ◽  
Ache Activity ◽  
Neuromuscular Junctions ◽  
Muscle Fibers ◽  
Synaptic Cleft

In skeletal muscles that have been damaged in ways which spare the basal lamina sheaths of the muscle fibers, new myofibers develop within the sheaths and neuromuscular junctions form at the original synaptic sites on them. At the regenerated neuromuscular junctions, as at the original ones, the muscle fibers are characterized by junctional folds and accumulations of acetylcholine receptors and acetylcholinesterase (AChE). The formation of junctional folds and the accumulation of acetylcholine receptors is known to be directed by components of the synaptic portion of the myofiber basal lamina. The aim of this study was to determine whether or not the synaptic basal lamina contains molecules that direct the accumulation of AChE. We crushed frog muscles in a way that caused disintegration and phagocytosis of all cells at the neuromuscular junction, and at the same time, we irreversibly blocked AChE activity. New muscle fibers were allowed to regenerate within the basal lamina sheaths of the original muscle fibers but reinnervation of the muscles was deliberately prevented. We then stained for AChE activity and searched the surface of the new muscle fibers for deposits of enzyme they had produced. Despite the absence of innervation, AChE preferentially accumulated at points where the plasma membrane of the new muscle fibers was apposed to the regions of the basal lamina that had occupied the synaptic cleft at the neuromuscular junctions. We therefore conclude that molecules stably attached to the synaptic portion of myofiber basal lamina direct the accumulation of AChE at the original synaptic sites in regenerating muscle. Additional studies revealed that the AChE was solubilized by collagenase and that it remained adherent to basal lamina sheaths after degeneration of the new myofibers, indicating that it had become incorporated into the basal lamina, as at normal neuromuscular junctions.

scholarly journals Acetylcholinesterase Activity Measurement and Clinical Features of Delirium

2016 ◽  
Vol 43 (1-2) ◽  
pp. 29-37 ◽  
Author(s):  
Thomas A. Jackson ◽  
Hannah C. Moorey ◽  
Bart Sheehan ◽  
Alasdair M.J. Maclullich ◽  
John R. Gladman ◽  
...  
Keyword(s):  
Clinical Features ◽  
Ache Activity ◽  
Colorimetric Assay ◽  
Acetylcholinesterase Activity ◽  
Activity Measurement ◽  
Hospitalised Patients ◽  
Hospital Patients ◽  
The Mean ◽  
Hypoactive Delirium ◽  
The Relationship

Aims: Cholinergic deficiency is commonly implicated in the pathophysiology of delirium. We aimed to investigate the relationship between directly measured serum acetylcholinesterase (AChE) activity and (1) clinical features of delirium and (2) outcomes among older hospital patients with delirium. Methods: Hospitalised patients with delirium were recruited, and delirium motor subtype, severity and duration of delirium were measured. Serum AChE activity was measured using a colorimetric assay. Results: The mean AChE activity for the whole sample was 2.46 μmol/μL/min (standard deviation 1.75). Higher AChE activity was associated with increased likelihood of hypoactive delirium rather than the hyperactive or mixed subtype (odds ratio 1.98, 95% confidence interval 1.10-3.59). Conclusion: Higher AChE activity was associated with hypoactive delirium but did not predict outcomes. Simple enhancement of cholinergic neurotransmission may not be sufficient to treat delirium.

Effects of dichlorvos, maldison and pirimiphos-methyl on food consumption, egg production, egg and tissue residues, and plasma acetylcholinesterase inhibition in layer strain hens

1984 ◽  
Vol 24 (124) ◽  
pp. 83 ◽  
Author(s):  
RAE Pym ◽  
G Singh ◽  
WS Gilbert ◽  
JP Armstrong ◽  
BV McCleary
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Ache Activity ◽  
Egg Production ◽  
Acetylcholinesterase Inhibition ◽  
Ache Inhibition ◽  
Laying Performance ◽  
Maximum Residue Limits ◽  
Pirimiphos Methyl ◽  
The Relationship

In three experiments laying performance was studied in hens given graded levels of maldison, dichlorvos and pirimiphos-methyl either separately or combined in the feed over a four-week test period. Results conclusively demonstrated interaction between dichlorvos and maldison as measured by depressed food consumption and egg production. Combining the three insecticides at levels which when given separately had no effect, severely depressed food consumption and egg production. After four weeks on treatment, birds receiving pirimiphos-methyl at 50 �g/g of diet had residues of 0.08-0.17 �g/g in fat and 0-0.06 �g/g in muscle, and residues of 0-0.07 �g/g maldison were recovered in the fat of birds receiving it at 100 �g/g of diet. No residues of any insecticide were detected in eggs and no dichlorvos residues were detected in any tissues. Plasma acetylcholinesterase (AChE) levels were reduced by 70% with dichlorvos at 30 �g/g, by 30% with maldison at 100 �g/g and by 90% with pirimiphos-methyl at 50 �g/g. There was no indication of potentiation between insecticides as measured by plasma AChE inhibition, and effects upon food consumption and egg production appeared unrelated to plasma AChE activity. The relationship between food consumption and egg production was similar in groups receiving dichlorvos-maldison mixtures and in those receiving graded levels of untreated food, indicating that the insecticides' effect upon egg production was mediated via a reduced food intake. Maximum residue limits for pesticides in feeds should be based on a total index which takes account of interaction between the different pesticides present.

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