Acetylcholinesterase in the fast extraocular muscle of the mouse by light and electron microscope autoradiography.

Salpeter, Miriam M.; Rogers, Alisdair; Kasprzak, H.; McHenry, Frances A.

doi:10.1083/jcb.78.1.274

Cited by 31 publications

(14 citation statements)

References 39 publications

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“…Additional features in EOMs that are believed to contribute to fast contraction speed are the extensive T-tubules and hypertrophy of the sarcoplasmic reticulum (calcium storage) as well as high mitochondrial content [5]. Furthermore, compared with limb skeletal muscle, expression of acetylcholine receptor subunits and acetylcholinesterase are elevated, possibly due to the high innervation density of EOMs and distinct distribution of acetylcholinesterase in synapses [49, 54]. Furthermore, parvalbumin, one type of calcium-binding protein, appears to be inversely regulated by IGF1 [33].…”

Section: Discussionmentioning

confidence: 99%

“…It is not known how muscles switch from slow to fast kinetics. This likely involves changes of myosin heavy chain isoform expression, calcium handling in E–C coupling, and/or changes in levels of acetylcholine receptor and acetylcholinesterase [54]. Growth factors play an important role in muscle development and plasticity, and they may also control the transition of EOM fiber type composition, and the development of contraction speed and contractile force.…”

Section: Introductionmentioning

confidence: 99%

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How to make rapid eye movements “rapid”: the role of growth factors for muscle contractile properties

Feng

Bartheld

2011

Pflugers Arch - Eur J Physiol

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Different muscle functions require different muscle contraction properties. Saccade-generating extraocular muscles (EOMs) are the fastest muscles in the human body, significantly faster than limb skeletal muscles. Muscle contraction speed is subjected to plasticity, i.e., contraction speed can be adjusted to serve different demands, but little is known about the molecular mechanisms that control contraction speed. Therefore, we examined whether myogenic growth factors modulate contractile properties, including twitch contraction time (onset of force to peak force) and half relaxation time (peak force to half relaxation). We examined effects of three musclederived growth factors: insulin-like growth factor 1 (IGF1), cardiotrophin-1 (CT1), and glial cell line-derived neurotrophic factor (GDNF). In gain-of-function experiments, CT1 or GDNF injected into the orbit shortened contraction time, and IGF1 or CT1 shortened half relaxation time. In lossof-function experiments with binding proteins or neutralizing antibodies, elimination of endogenous IGFs prolonged both contraction time and half relaxation time, while eliminating endogenous GDNF prolonged contraction time, with no effect on half relaxation time. Elimination of endogenous IGFs or CT1, but not GDNF, significantly reduced contractile force. Thus, IGF1, CT1, and GDNF have partially overlapping but not identical effects on muscle contractile properties. Expression of these three growth factors was measured in chicken and/or rat EOMs by real-time PCR. The "fast" EOMs express significantly more message encoding these growth factors and their receptors than skeletal muscles with slower contractile properties. Taken together, these findings indicate that EOM contractile kinetics is regulated by the amount of myogenic growth factors available to the muscle.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

How to make rapid eye movements “rapid”: the role of growth factors for muscle contractile properties

Feng

Bartheld

2011

Pflugers Arch - Eur J Physiol

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“…As for the density of receptor in the subsynaptic membrane, like in the muscle, values of 10000 receptors or 20000 binding sites per ,um2 were reported in the Torpedo electric organ (Heuser & Salpeter, 1979 (Rosenberry, 1975). Since we were not aware of any direct measurement of the density of AChE sites in the Torpedo electric organ, we adopted the endplate value of 2600 (Salpeter, Rogers, Kasprzak & McHenry, 1978).…”

Section: Fish and Chemicalsmentioning

confidence: 99%

Space and time characteristics of transmitter release at the nerve‐electroplaque junction of Torpedo.

Girod¹,

Corrèges²,

Jacquet³

et al. 1993

The Journal of Physiology

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MEPPs. 6. Composite MEPPs with multiple peaks as well as bursts of small MEPPs were often encountered, even during periods of low frequency. They were suggestive of a complete disorganization of quantal events.7. Fast, slow and composite MEPPs were analysed using the computer model. To simulate the entire variety of signals we had to assume that the MEPPs were generated by either synchronized or desynchronized emission of small quantities of transmitter. The typical relationship observed between amplitude and time course in the population of fast MEPPs suggested that the different amounts of transmitter composing a quantum were delivered synchronously close to each other (either at the same spot or at less than 200 nm apart); it is proposed that they acted on overlapping fields of receptors and that their responses summed up in a superadditive manner.8. Computer analysis of the slow-rising MEPPs was of particular interest since their rapid decay phase indicated that the postsynaptic links (cholinesterase and receptors kinetics) were apparently not altered in this subpopulation. More probably their slow and often irregular rate of rise arose from some desynchronization of the release process.9. It is concluded that at the nerve-electroplaque junction evoked transmitter release operates in the form of quanta containing ca 10000 acetylcholine molecules; the quanta activate independent but closely adjacent postsynaptic fields. Each quantum is apparently composed of a preferential number of subunits emitted at the same point, or very close to each other. The subunits are delivered synchronously in the majority of events (fast MEPPs) but subunit desynchronization occasionally occurs (slow-rising and composite MEPPs).

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“…This organization consists of a high and stable AcChoR site density a of ;20,000 sites/,gm2 of surface area at the top of the postounctional membrane (1-4) and a uniform distribution of acetylcholinesterase of !2500 sites per gm2 of surface area along the entire postjunctional folded membrane (5)(6)(7)(8). In the present paper we attempt to determine some physiological consequences of this organization by studying the effect of decreasing a on the rise time and amplitude of miniature endplate currents (mepcs) in esterase-inactivated nmjs.…”

mentioning

confidence: 99%

Acetylcholine receptor site density affects the rising phase of miniature endplate currents.

Land¹,

Salpeter²,

Salpeter³

1980

Proc. Natl. Acad. Sci. U.S.A.

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The relationship between acetylcholine receptor (AcChoR) site density (o) and the rising phase of the miniature endplate current was determined in esterase-inactivated lizard intercostal neuromuscular junctions. The currents were recorded by using a voltage clamp. The receptor site density was determined by electron microscope autoradiography ater labeling with 'I-labeled a-bungarotoxin in normal endplates and in those partially inactivated with nonradioactive a-bungarotoxin. We found that as u is decreased the rise time is increased and the amplitude is decreased. These results are compatible with a previously stated "saturating disk" model, which suggests that a quantum of acetylcholine (AcCho) acts on a small postsynaptic area at saturating concentration. We conclude that in the normal neuromuscular 'unction the most likely number of AcCho molecules needed to open an ion channel is 2, and that the 2040% rise time of <100 psec is influenced both by the a-dependent factors such as diffion and binding of AcCho to AcChoR and by the or-independent time delays such as the conformation change time to open the ion channels. From our data we calculate the lower limits to the forward rate constant of AcCho binding to AcChoR 2 3 X 107 M-l sec-1, and the diffusion constant for AcCho in the cleft 2 4 X 10-6 cm2 sec-t.A unique molecular organization of acetylcholine receptors (AcChoRs) and acetyicholinesterase has been found in all neuromuscular junctions (nmjs) of vertebrate twitch muscles examined. This organization consists of a high and stable AcChoR site density a of ;20,000 sites/,gm2 of surface area at the top of the postounctional membrane (1-4) and a uniform distribution of acetylcholinesterase of !2500 sites per gm2 of surface area along the entire postjunctional folded membrane (5-8). In the present paper we attempt to determine some physiological consequences of this organization by studying the effect of decreasing a on the rise time and amplitude of miniature endplate currents (mepcs) in esterase-inactivated nmjs. We found that, as a' is decreased, the rise time increases and the amplitude decreases. From these data we suggest some physiological parameters which control the action of acetylcholine (AcCho) in the cleft. METHODSMuscle Preparation. We used lizard (Anolis carolinensis) intercostal muscle. This muscle has compact endplates that are much smaller than the electrical length constant, and thus may be uniformly clamped. The muscle is thin (one to two fiber layers thick), allowing easy visualization of the endplates with Hoffman modulation optics. The physiological studies were performed on endplates pretreated with diisopropylfluorophosphate (iPr2P-F) (1 mM for 20 min), which effectively inactivates esterases. The AcChoRs were either left intact or were partially inactivated with a-bungarotoxin (BTX) (9) (40 nM) for 20 or 40 min. The muscle was thoroughly washed (30 min) to remove excess iPr2P-F and BTX. The mepcs were measured in fibers that had been voltage clamped at -100 mV (230C), using ...

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Acetylcholinesterase in the fast extraocular muscle of the mouse by light and electron microscope autoradiography.

Cited by 31 publications

References 39 publications

How to make rapid eye movements “rapid”: the role of growth factors for muscle contractile properties

How to make rapid eye movements “rapid”: the role of growth factors for muscle contractile properties

Space and time characteristics of transmitter release at the nerve‐electroplaque junction of Torpedo.

Acetylcholine receptor site density affects the rising phase of miniature endplate currents.

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