Resting Release of Acetylcholine at the Motor Endplate

1986 ◽  
pp. 481-487
Author(s):  
P. C. Molenaar ◽  
R. L. Polak
Keyword(s):  
Motor Endplate ◽  
Release Of Acetylcholine

Human motor endplate remodeling after traumatic nerve injury

2020 ◽  
pp. 1-8
Author(s):  
Ranjan Gupta ◽  
Justin P. Chan ◽  
Jennifer Uong ◽  
Winnie A. Palispis ◽  
David J. Wright ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Surgical Intervention ◽  
Linear Regression Analysis ◽  
Motor Endplate ◽  
Nerve Injuries ◽  
Denervated Muscle ◽  
Sequence Of Events ◽  
Human Motor ◽  
Denervated Muscles

OBJECTIVECurrent management of traumatic peripheral nerve injuries is variable with operative decisions based on assumptions that irreversible degeneration of the human motor endplate (MEP) follows prolonged denervation and precludes reinnervation. However, the mechanism and time course of MEP changes after human peripheral nerve injury have not been investigated. Consequently, there are no objective measures by which to determine the probability of spontaneous recovery and the optimal timing of surgical intervention. To improve guidance for such decisions, the aim of this study was to characterize morphological changes at the human MEP following traumatic nerve injury.METHODSA prospective cohort (here analyzed retrospectively) of 18 patients with traumatic brachial plexus and axillary nerve injuries underwent biopsy of denervated muscles from the upper extremity from 3 days to 6 years after injury. Muscle specimens were processed for H & E staining and immunohistochemistry, with visualization via confocal and two-photon excitation microscopy.RESULTSImmunohistochemical analysis demonstrated varying degrees of fragmentation and acetylcholine receptor dispersion in denervated muscles. Comparison of denervated muscles at different times postinjury revealed progressively increasing degeneration. Linear regression analysis of 3D reconstructions revealed significant linear decreases in MEP volume (R = −0.92, R2 = 0.85, p = 0.001) and surface area (R = −0.75, R2 = 0.56, p = 0.032) as deltoid muscle denervation time increased. Surprisingly, innervated and structurally intact MEPs persisted in denervated muscle specimens from multiple patients 6 or more months after nerve injury, including 2 patients who had presented > 3 years after nerve injury.CONCLUSIONSThis study details novel and critically important data about the morphology and temporal sequence of events involved in human MEP degradation after traumatic nerve injuries. Surprisingly, human MEPs not only persisted, but also retained their structures beyond the assumed 6-month window for therapeutic surgical intervention based on previous clinical studies. Preoperative muscle biopsy in patients being considered for nerve transfer may be a useful prognostic tool to determine MEP viability in denervated muscle, with surviving MEPs also being targets for adjuvant therapy.

scholarly journals Globular and asymmetric acetylcholinesterase in frog muscle basal lamina sheaths.

1986 ◽  
Vol 102 (3) ◽  
pp. 762-768 ◽  
Author(s):  
M Nicolet ◽  
M Pinçon-Raymond ◽  
F Rieger
Keyword(s):  
Basal Lamina ◽  
Acetylcholine Receptors ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Motor Endplate ◽  
Molecular Forms ◽  
Nonionic Detergent ◽  
Plasmic Membrane ◽  
Triton X

After denervation in vivo, the frog cutaneus pectoris muscle can be led to degenerate by sectioning the muscle fibers on both sides of the region rich in motor endplate, leaving, 2 wk later, a muscle bridge containing the basal lamina (BL) sheaths of the muscle fibers (28). This preparation still contains various tissue remnants and some acetylcholine receptor-containing membranes. A further mild extraction by Triton X-100, a nonionic detergent, gives a pure BL sheath preparation, devoid of acetylcholine receptors. At the electron microscope level, this latter preparation is essentially composed of the muscle BL with no attached plasmic membrane and cellular component originating from Schwann cells or macrophages. Acetylcholinesterase is still present in high amounts in this BL sheath preparation. In both preparations, five major molecular forms (18, 14, 11, 6, and 3.5 S) can be identified that have either an asymmetric or a globular character. Their relative amount is found to be very similar in the BL and in the motor endplate-rich region of control muscle. Thus, observations show that all acetylcholinesterase forms can be accumulated in frog muscle BL.

scholarly journals Human facial muscles: Dimensions, motor endplate distribution, and presence of muscle fibers with multiple motor endplates

1997 ◽  
Vol 249 (2) ◽  
pp. 276-284 ◽  
Author(s):  
Wolfgang Happak ◽  
Ji Liu ◽  
Georg Burggasser ◽  
Amanda Flowers ◽  
Helmut Gruber ◽  
...  
Keyword(s):  
Muscle Fibers ◽  
Motor Endplate ◽  
Motor Endplates ◽  
Facial Muscles

The Motor Endplate.

1964 ◽  
Vol 11 (6) ◽  
pp. 684-685
Author(s):  
W. L. Nastuk
Keyword(s):  
Motor Endplate

Amitriptyline and imipramine inhibit the release of acetylcholine from parasympathetic nerve terminals in the rat iris

1984 ◽  
Vol 62 (7) ◽  
pp. 857-859 ◽  
Author(s):  
J. S. Richardson ◽  
T. G. Mattio ◽  
E. Giacobini
Keyword(s):  
Nerve Terminals ◽  
Dependent Manner ◽  
Parasympathetic Nerve ◽  
Drug Concentrations ◽  
Release Of Acetylcholine ◽  
Rat Iris ◽  
Anticholinergic Side Effects ◽  
Dose Dependent ◽  
Drug Free

The electrically stimulated release of [3H]acetylcholine from the parasympathetic nerve terminals of the rat iris in vitro is increased in a dose-dependent manner by scopolamine but is decreased by the tricyclic antidepressants amitriptyline and imipramine. The increased release in the presence of scopolamine seems to be due to the blockade of a presynaptic muscarinic autoreceptor that, in the drug-free state, inhibits the release of acetylcholine. However, at drug concentrations that should have comparable antimuscarinic potency, the antidepressants inhibit the release of acetylcholine. This suggests that the anticholinergic side effects of the antidepressants may be due to the reduced release of acetylcholine from parasympathetic nerve terminals as well as a possible direct postsynaptic muscarinic receptor blocking action. Whatever the mechanism of this action, the antidepressants do not have the same effect as scopolamine at the presynaptic muscarinic autoreceptor in the rat iris.

The K+-evoked release of [3H]acetylcholine from slices of rat globus pallidus: modulation by δ-opioid receptors

1991 ◽  
Vol 69 (3) ◽  
pp. 414-418 ◽  
Author(s):  
Bianca B. Ruzicka ◽  
Khem Jhamandas
Keyword(s):  
Globus Pallidus ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Cholinergic Neurons ◽  
Receptor Activation ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Release Of Acetylcholine ◽  
Δ Opioid Receptor ◽  
Tritium Release

Previous investigations have shown that the activation of δ-opioid receptors depresses the release of acetylcholine (ACh) in the rat caudate putamen. This finding raised the possibility that the release of ACh is similarly modulated in the globus pallidus, a region containing a distinct population of cholinergic neurons and enriched in enkephalinergic nerve terminals. In the present study the pallidal release of ACh was characterized and the effects of δ-opioid receptor activation on this release were examined. The results show that this release is stimulated by high K+ in a concentration- and Ca2+-dependent manner. D-Pen2,L-Pen5-enkephalin (0.1 – 10 μM), a selective δ-opioid receptor agonist, produced a dose-related inhibition of the 25 mM K+-evoked tritium release. The maximal inhibitory effect, representing a 34% decrease in the K+-induced tritium release, was observed at a concentration of 1 μM. This opioid effect was attenuated by the selective δ-opioid receptor antagonist, ICI 174864 (1 μM). These findings support the role of a δ-opioid receptor in the modulation of ACh release in the rat globus pallidus.Key words: globus pallidus, acetylcholine, enkephalin, release.

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