The acetylcholinesterase activity of the denervated rat diaphragm

Crone, H.D.; Freeman, Shirley E.

doi:10.1111/j.1471-4159.1972.tb01442.x

Cited by 31 publications

(10 citation statements)

References 9 publications

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“…I~( seems very unlikely that such a selective outfow of enzyme results from a passive diffusion consecutive to either modification of the membrane permeability or cell death. This selective release of the 10 S form, considered together with the localization in the endoplasmic reticulum of most of this form [4,5,14,15], clearly suggests an active secretion of the enzyme. It probably represents a physiological event occurring in vivo, although it is likely that the rate of enzymatic release is different from that observed in vitro.…”

Section: Discussionmentioning

confidence: 77%

A specific form of acetylcholinesterase is secreted by rat sympathetic ganglia

Gisiger

1977

FEBS Letters

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Section: Discussionmentioning

confidence: 77%

A specific form of acetylcholinesterase is secreted by rat sympathetic ganglia

Gisiger

1977

FEBS Letters

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“…Many previous studies have established that denervation leads to a marked decline in the AChE activity of mammalian skeletal muscle, especially in endplate regions (Guth et al, 1964;Crone and Freeman, 1972; for review, see Guth, 1%8). The (McLaughlin and Bosmann, 1970;Fernandez et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

Effects of Acute and Chronic Denervation on Release of Acetylcholinesterase and Its Molecular Forms in Rat Diaphragms

Carter¹,

Brimijoin²

1981

Journal of Neurochemistry

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Hemidiaphragms were removed from rats at various times after intrathoracic transection of the left phrenic nerve and were incubated in organ baths containing 1.5 ml of oxygenated, buffered physiologic saline solution, with added glucose and bovine serum albumin. After incubation, the acetylcholinesterase (AChE: EC 3.1.1.7) activities of the bath fluid and of the muscle were determined. Innervated left hemidiaphragms were found to release 107 units of AChE over a 3-h period, corresponding to 1.9% of their total AChE activity. Denervation led to a rapid loss of AChE from the muscle coincident with a transient increase in the outpouring of enzyme activity into the bath fluid. Thus, 1 day after nerve transection the left hemidiaphragm contained only 68% of the control amounts of AChE activity, but released 140% as much as control. After 3 or 4 days of denervation, the AChE activity of the diaphragm stabilized at 35% of the control value. Release also fell below control by this time, but not as far. One week after denervation the release, 69 units per 3 hr, correspond to 3.3% of the reduced content of AChE activity in the muscle, indicating that denervation caused an increase in the proportion of AChE released. Sucrose density gradient ultracentrifugation showed that 10S AChE accounted for more than 80% of the released enzyme activity at all times. The results did not rule out the possibility, however, that the released enzyme originally stemmed from 4S or 16S AChE in the diaphragms.

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“…This is unexpected since it has been reported that denervation results in a fall of cholinesterase activity, not only of the NMJ region but also of the nerve-free part of skeletal muscle (Brzin & Majcen-Tkacev, 1963;Guth, Albers & Brown, 1964;Eranko & Teriiviiinen, 1967;Crone & Freeman, 1972;Miledi et al 1982). A decrease in cholinesterase activity has also been reported in skeletal muscles after disuse due to pharmacological blockade of the motor nerve (Drachman, 1972;Butler, Drachman & Goldberg, 1978).…”

Section: Acetylcholinesterasementioning

confidence: 79%

Release and synthesis of acetylcholine at ectopic neuromuscular junctions in the rat.

Kempen

Molenaar

Slater

1994

The Journal of Physiology

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1. The ability of axons in the superficial fibular nerve to synthesize and release acetylcholine (ACh) has been studied before and after the formation of ectopic neuromuscular junctions (NMJs) with denervated soleus muscles of adult rats. 2. The central end of the severed fibular nerve was transplanted to the surface of the soleus muscle. After 3.5‐5 weeks the soleus muscle was denervated in one group of rats by cutting the tibial nerve, allowing the formation of functional ectopic NMJs within a few days. In other rats the tibial nerve remained intact, preventing the formation of functional ectopic NMJs. 3. A month later the content of ACh, the levels of activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), and the amount of ACh released by depolarization by exposure to 50 mM KCl were measured in segments of isolated muscles that (i) contained normal or ectopic NMJs, (ii) were free of nerve or (iii) contained nerve that had not made NMJs. 4. Regions of muscles with ectopic nerve growth in which new NMJs had not formed contained substantial amounts of ACh and ChAT but no AChE. No detectable release of ACh could be evoked from these regions. 5. In muscles in which ectopic NMJs had formed after cutting the tibial nerve, the amounts of ACh and ChAT were about one‐fifth of those in the regions of innervation of control muscles. ACh release could be evoked from the region of ectopic nerve growth in amounts nearly as great as those released from NMJs in normal and contralateral control muscles. 6. We conclude that the ability of the terminal parts of mature motor axons to synthesize and store ACh is largely independent of functional contact with muscle fibres. By contrast, the ability to release ACh in substantial amounts only develops when NMJs are formed. The possible significance of this situation for the development of synapses is discussed.

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The acetylcholinesterase activity of the denervated rat diaphragm

Cited by 31 publications

References 9 publications

A specific form of acetylcholinesterase is secreted by rat sympathetic ganglia

A specific form of acetylcholinesterase is secreted by rat sympathetic ganglia

Effects of Acute and Chronic Denervation on Release of Acetylcholinesterase and Its Molecular Forms in Rat Diaphragms

Release and synthesis of acetylcholine at ectopic neuromuscular junctions in the rat.

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