The Importance of Axonal Transport and Endoplasmic Reticulum in the Function of Cholinergic Synapse in Normal and Pathological Conditions

Koenig, Herbert L.; Giamberardino, L. Di; Couraud, Jean-Yves; Chrétien, M; Souyri, F.

doi:10.1016/s0079-6123(08)64619-1

Cited by 22 publications

(8 citation statements)

References 33 publications

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“…The existence of a proximo-distal gradient of AChE activity along the nerves is well established (Lubinska et al, 1963). The exponential mode of this decay, which means that the quantity decreases at a rate proportional to itself, is not unexpected (Droz et al, 1979;Munoz-Martinez et al, 1981). It is consistent with the well accepted concept that aliquots are continually removed from the AChE transported along the axons for incorporation into the axolemma or release (Brimijoin et al, 1978).…”

Section: Ache In the Sciatic-tibia1 Nerve Trunksupporting

confidence: 72%

“…Studies of axonal transport have established that the molecular forms of AChE are selectively distributed among several specific axonal compartments in which they are subjected to different types of transport (ortho-and retrograde, fast and slow, etc.) (Lubinska, 1975;Brimijoin, 1979;Droz et al, 1979;Couraud and Di Giamberardino, 1980). Direct and simple correlations cannot be established between these compartments revealed by dynamic analyses of the axoplasmic flow and the two com-partments derived from our static measurements.…”

Section: Ache In the Sciatic-tibia1 Nerve Trunkmentioning

confidence: 99%

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Decreased G₄ (10S) Acetylcholinesterase Content in Motor Nerves to Fast Muscles of Dystrophic 129/ReJ Mice: Lack of a Specific Compartment of Nerve Acetylcholinesterase?

Gisiger

Stephens

1984

Journal of Neurochemistry

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Acetylcholinesterase (AChE; EC 3.1.1.7) activity and the distribution of its molecular forms were studied in the nervous system of normal and dystrophic 129/ReJ mice, including the sciatic-tibial nerve trunk and motor nerves to slow- and fast-twitch muscles. In normal mice, motor nerves to the slow-twitch soleus exhibited a low AChE activity together with a low level of G4 (10S form) as compared with nerves of the predominantly fast-twitch plantaris and extensor digitorum longus. In contrast, in dystrophic mice, the AChE activity as well as the G4 content of nerves to the fast-twitch muscles were low, displaying an AChE content similar to that of the nerve of the soleus muscle. In the sciatic-tibial nerve trunk, the AChE activity decreased along the nerve in an exponential mode, at rates that were similar in both conditions. However, in dystrophic mice, the AChE activity was reduced throughout the nerve length by a constant value of approximately 180 nmol/h/mg protein. Further analyses indicated that AChE in this nerve trunk was distributed among two compartments, a decaying and a constant one. The decay involved exclusively the globular forms. The activity of A12 (16S form) remained constant along the nerve and was similar in both normal and dystrophic mice. In addition, according to the equation describing the decay of AChE, the reduction in enzymatic activity observed in the dystrophic mice affected mainly G4 in the constant compartment. Brain, spinal cord, sympathetic ganglia, and serum, which were also examined, showed no remarkable differences between the two conditions in their G4 content. The AChE abnormalities that we found in nervous tissues of 129/ReJ dystrophic mice were confined to the motor system.

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Section: Ache In the Sciatic-tibia1 Nerve Trunksupporting

confidence: 72%

Section: Ache In the Sciatic-tibia1 Nerve Trunkmentioning

confidence: 99%

Decreased G₄ (10S) Acetylcholinesterase Content in Motor Nerves to Fast Muscles of Dystrophic 129/ReJ Mice: Lack of a Specific Compartment of Nerve Acetylcholinesterase?

Gisiger

Stephens

1984

Journal of Neurochemistry

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“…However this may be, it might be further evidence for a basic impairment of axonal membrane maintenance and synthesis. Certainly the autoradiographic evidence of Griffin et al (1977) and of Droz et al (1979) that there is a failure of transported proteins to be incorporated into axon membrane would favour such a general conclusion. Of relevance to this idea is the lack of relationship of the metabolic lesion to the axonal terminals as shown by the observation of Cavanagh & Gysbers (1980 that acrylamide given to rats after a nerve injury (ligation) is followed by a retrograde degeneration proximal to the injury point, the degree of which is dose-dependent.…”

Section: T H E D I S T a L F I L A M E N T A N D M E M B R A N E A C mentioning

confidence: 99%

The Pathokinetics of Acrylamide Intoxication: A Reassessment of the Problem

Cavanagh

1982

Neuropathology Appl Neurobio

105

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Acrylamide was given intraperitoneally to rats (30 mg/kg/day, five times/week) for 3 weeks, and the nervous and muscle tissues were examined by conventional methods over 5 weeks. Three striking cellular changes were observed. 1 Scattered degeneration of many Purkinje cells from 5 days onwards. 2 Widespread swelling and argyrophilia of nerve terminals from 10 days in both PNS and CNS. Motor and sensory endings were equally affected in all muscles examined. Synaptic and preterminal swelling also occurred in spinal cord, brain stem, and in certain cerebellar terminals. Degeneration occasionally followed this change, particularly in sensory nerve fibres, but not necessarily. 3 Chromatolysis in spinal ganglion cells and occasionally in anterior horn cells from 7 days onwards before the onset of axonal degeneration. This unique sequence of events is discussed in the light of the metabolic and other changes described by earlier authors.

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“…Partial accounts of these results were given elsewhere (Couraud and Di Giamberardino, 1977;Droz and Couraud, 1978; Droz et al, 1979).…”

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confidence: 99%

Axonal Transport of the Molecular Forms of Acetylcholinesterase in Chick Sciatic Nerve

Couraud¹,

Giamberardino²

1980

Journal of Neurochemistry

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Acetylcholinesterase (AChE) polymorphism was studied in the sciatic nerve of 4-week-old Leghorn chicks, by sucrose gradient sedimentation analysis. Four main AChE molecular forms were found with sedimentation coefficients of 5S, 7.5S, 11.5S and 20S respectively. Axonal transport of each of these forms was investigated on the basis of the enzyme accumulation kinetics measured on both sides of nerve transections and of the enzyme redistribution kinetics in nerve segments isolated in vivo. After nerve transection, 11.5S and 20S forms accumulated faster in the anterograde than in the retrograde direction and also much faster than 5S and 7.5S forms in the anterograde direction. Retrograde accumulations of 5S and 7.5S were faint or negligible. In addition, 1 h after nerve cutting, the accumulation rates for 11.5S and 20S forms (but not for 5S and 7.5S) fell, in both directions, to about one-third of their initial values, probably owing to reversal of axonal transport at the axotomy site. Local protein synthesis inhibition by cycloheximide did not affect the accumulation of 11.5S and 20S in front of a transection, at least during the first hours, but reduced that of 5S and 7.5S by about 40%. In isolated nerve segments in vivo, the rapidly mobile fraction of AChE was estimated to constitute 23% of the total enzyme activity present in the nerve, 14% of it moving in an anterograde and 9% in a retrograde direction. A small amount of 11.5S molecules (approx. 20%) was in rapid transit (two-thirds in the anterograde and one-third in the retrograde direction), whereas almost all the 20S--about 90%--migrated rapidly (two-thirds forwards and one-third backwards). Anterograde velocities of 408 +/- 94 and 411 +/- 161 mm/day respectively were estimated for the 11.5S and 20S forms. Their respective retrograde velocities were 175 +/- 85 and 145 +/- 107 mm/day. Assuming that the totality of 5S and 7.5S molecules are moving in the anterograde direction, their accumulation rates were consistent with the average anterograde velocities of 2.9 +/- 1.3 and 5.1 +/- 1.4 mm/day, respectively.

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The Importance of Axonal Transport and Endoplasmic Reticulum in the Function of Cholinergic Synapse in Normal and Pathological Conditions

Cited by 22 publications

References 33 publications

Decreased G₄ (10S) Acetylcholinesterase Content in Motor Nerves to Fast Muscles of Dystrophic 129/ReJ Mice: Lack of a Specific Compartment of Nerve Acetylcholinesterase?

Decreased G₄ (10S) Acetylcholinesterase Content in Motor Nerves to Fast Muscles of Dystrophic 129/ReJ Mice: Lack of a Specific Compartment of Nerve Acetylcholinesterase?

The Pathokinetics of Acrylamide Intoxication: A Reassessment of the Problem

Axonal Transport of the Molecular Forms of Acetylcholinesterase in Chick Sciatic Nerve

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The Importance of Axonal Transport and Endoplasmic Reticulum in the Function of Cholinergic Synapse in Normal and Pathological Conditions

Cited by 22 publications

References 33 publications

Decreased G4 (10S) Acetylcholinesterase Content in Motor Nerves to Fast Muscles of Dystrophic 129/ReJ Mice: Lack of a Specific Compartment of Nerve Acetylcholinesterase?

Decreased G4 (10S) Acetylcholinesterase Content in Motor Nerves to Fast Muscles of Dystrophic 129/ReJ Mice: Lack of a Specific Compartment of Nerve Acetylcholinesterase?

The Pathokinetics of Acrylamide Intoxication: A Reassessment of the Problem

Axonal Transport of the Molecular Forms of Acetylcholinesterase in Chick Sciatic Nerve

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Decreased G₄ (10S) Acetylcholinesterase Content in Motor Nerves to Fast Muscles of Dystrophic 129/ReJ Mice: Lack of a Specific Compartment of Nerve Acetylcholinesterase?

Decreased G₄ (10S) Acetylcholinesterase Content in Motor Nerves to Fast Muscles of Dystrophic 129/ReJ Mice: Lack of a Specific Compartment of Nerve Acetylcholinesterase?