Comparison of skeleto‐fusimotor innervation in cat peroneus brevis and peroneus tertius muscles.

Emonet-Dénand, F; Petit, J.; Laporte, Y

doi:10.1113/jphysiol.1992.sp019431

Cited by 23 publications

(13 citation statements)

References 14 publications

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“…The phenotype of these excess labeled MN axons may be either ␥-MNs or the often overlooked ␤-MN population (Burke, 1981;Matthews, 1981;Vult von Steyem et al, 1999) in which individual MN axons branch and innervate both extrafusal and intrafusal (muscle spindles) muscles. It has been estimated that one-third of mammalian muscle spindles are innervated by ␤-MNs (Emonet-Denand et al, 1992;Floeter, 1999). The increase in smaller-sized MNs having the anatomical characteristics of fast twitch, fatigue-resistant MNs (Burke, 1981), together with the altered MyoGDNF muscle phenotype that resembles type IIA/fast twitch, fatigue-resistant, oxidative, glycolytic muscle, is what might be expected if these represent a population of ␤-like MNs.…”

Section: The Fate Of Supernumerary Motoneurons In Myogdnf Micementioning

confidence: 99%

Neuromuscular Development in the Absence of Programmed Cell Death: Phenotypic Alteration of Motoneurons and Muscle

Buss

Gould²,

Ma³

et al. 2006

J. Neurosci.

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The widespread, massive loss of developing neurons in the central and peripheral nervous system of birds and mammals is generally considered to be an evolutionary adaptation. However, until recently, models for testing both the immediate and long-term consequences of preventing this normal cell loss have not been available. We have taken advantage of several methods for preventing neuronal death in vivo to ask whether rescued neurons [e.g., motoneurons (MNs)] differentiate normally and become functionally incorporated into the nervous system. Although many aspects of MN differentiation occurred normally after the prevention of cell death (including the expression of several motoneuron-specific markers, axon projections into the ventral root and peripheral nerves, ultrastructure, dendritic arborization, and afferent axosomatic synapses), other features of the neuromuscular system (MNs and muscle) were abnormal. The cell bodies and axons of MNs were smaller than normal, many MN axons failed to become myelinated or to form functional synaptic contacts with target muscles, and a subpopulation of rescued cells were transformed from ␣-to ␥-like MNs. Additionally, after the rescue of MNs in myogenin glial cell line-derived neurotrophic factor (MyoGDNF) transgenic mice, myofiber differentiation of extrafusal skeletal muscle was transformed and muscle physiology and motor behaviors were abnormal. In contrast, extrafusal myofiber phenotype, muscle physiology, and (except for muscle strength tests) motor behaviors were all normal after the rescue of MNs by genetic deletion of the proapoptotic gene Bax. However, there was an increase in intrafusal muscle fibers (spindles) in Bax knock-out versus both wild-type and MyoGDNF mice. Together, these data indicate that after the prevention of MN death, the neuromuscular system becomes transformed in novel ways to compensate for the presence of the thousands of excess cells.

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Section: The Fate Of Supernumerary Motoneurons In Myogdnf Micementioning

confidence: 99%

Neuromuscular Development in the Absence of Programmed Cell Death: Phenotypic Alteration of Motoneurons and Muscle

Buss

Gould²,

Ma³

et al. 2006

J. Neurosci.

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“…In the present simulations, the term "␤" implies a source of fusimotor drive that receives a fraction of Ia afferent output, whereas "␥" indicates a fusimotor drive source with no such feedback. Each fusimotor input (␥ or ␤) is assumed to be either static or dynamic because convergence of static and dynamic ␤ innervation onto the same spindle is relatively uncommon in tenuissmus (Jami et al 1978) and triceps surae (Grill and Rymer 1987), although it is more frequent in peroneus brevis and peroneus tertius (Emonet-Dènand et al 1992). Our model assumes that the effect on spindle afferent firing of ␤ motoneuron activity has the same strength and time course as the TABLE 1.…”

Section: Simulation Of ␤ Loop Feedbackmentioning

confidence: 99%

Spindle Model Responsive to Mixed Fusimotor Inputs and Testable Predictions of β Feedback Effects

Maltenfort

Burke

2003

Journal of Neurophysiology

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Skeletofusimotor (beta) motoneurons innervate both extrafusal muscle units and muscle fibers within muscle spindle stretch receptors. By receiving excitation from group Ia muscle spindle afferents and driving the muscle spindle afferents that excite them, they form a positive feedback loop of unknown function. To study it, we developed a computationally efficient model of group Ia afferent behavior, capable of responding to multiple fusimotor inputs, that matched experimental data. This spindle model was then incorporated into a simulation of group Ia feedback during ramp/hold and triangular stretches with and without closure of the beta loop, assuming that gamma and beta fusimotor drives of the same type (static or dynamic) have identical effects on spindle afferent firing. The effects of beta feedback were implemented by driving a fusimotor input with a delayed and filtered fraction of the spindle afferent output. During triangular stretches, feedback through static beta motoneurons enhanced Ia afferent firing during shortening of the spindle. In contrast, closure of a dynamic beta loop increased Ia firing during lengthening. The strength of beta feedback, estimated as a "loop gain" was comparable to experimental estimates. The loop gain increased with velocity and amplitude of stretch but decreased with increased superimposed gamma fusimotor rates. The strongest loop gains were seen when the beta loop and the gamma bias were of different types (static vs. dynamic).

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“…; Emonet‐Dénand et al . ; Manuel & Zytnicki, ). However, our current understanding of these neurons is very limited and further research into this matter is required.…”

Section: Discussionmentioning

confidence: 99%

Physiological tremor increases when skeletal muscle is shortened: implications for fusimotor control

Jalaleddini

Nagamori

Laine

et al. 2017

The Journal of Physiology

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The involuntary force fluctuations associated with physiological (as distinct from pathological) tremor are an unavoidable component of human motor control. While the origins of physiological tremor are known to depend on muscle afferentation, it is possible that the mechanical properties of muscle-tendon systems also affect its generation, amplification and maintenance. In this paper, we investigated the dependence of physiological tremor on muscle length in healthy individuals. We measured physiological tremor during tonic, isometric plantarflexion torque at 30% of maximum at three ankle angles. The amplitude of physiological tremor increased as calf muscles shortened in contrast to the stretch reflex whose amplitude decreases as muscle shortens. We used a published closed-loop simulation model of afferented muscle to explore the mechanisms responsible for this behaviour. We demonstrate that changing muscle lengths does not suffice to explain our experimental findings. Rather, the model consistently required the modulation of γ-static fusimotor drive to produce increases in physiological tremor with muscle shortening - while successfully replicating the concomitant reduction in stretch reflex amplitude. This need to control γ-static fusimotor drive explicitly as a function of muscle length has important implications. First, it permits the amplitudes of physiological tremor and stretch reflex to be decoupled. Second, it postulates neuromechanical interactions that require length-dependent γ drive modulation to be independent from α drive to the parent muscle. Lastly, it suggests that physiological tremor can be used as a simple, non-invasive measure of the afferent mechanisms underlying healthy motor function, and their disruption in neurological conditions.

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Comparison of skeleto‐fusimotor innervation in cat peroneus brevis and peroneus tertius muscles.

Cited by 23 publications

References 14 publications

Neuromuscular Development in the Absence of Programmed Cell Death: Phenotypic Alteration of Motoneurons and Muscle

Neuromuscular Development in the Absence of Programmed Cell Death: Phenotypic Alteration of Motoneurons and Muscle

Spindle Model Responsive to Mixed Fusimotor Inputs and Testable Predictions of β Feedback Effects

Physiological tremor increases when skeletal muscle is shortened: implications for fusimotor control

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