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Skeletal Muscle
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The intrafusal fibers are connected in parallel with the extrafusal fibers, so when the latter are stretched, the former will also be stretched and will fire accordingly. But when the extrafusal fibers contract, the intrafusal fibers will be relieved of stretch and the muscle spindles may go silent, so they will not signal any information about muscle length or speed of contraction. Activation of the fusimotor fibers will cause contraction of the intrafusal muscle fibers, so they will send the appropriate signals under these conditions. The role that this fusimotor drive plays in the control of movement is discussed in Section 13.5.1.
Muscle Spindles, Golgi Tendon Organs and Spinal Reflexes
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
There are two types of intrafusal muscle fibres: Nuclear bag fibres which are longer and thicker with nuclei aggregated in the central region, andNuclear chain fires which are shorter and thinner with the nuclei arranged in a chain (row) along the centre of the fibre. Typically, a muscle spindle contains one to three nuclear bag fibres and three to nine nuclear chain fibres (Figure 13.2).
Physiology of the nervous system
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2015
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
During a muscle contraction, there tends to be a reduced rate of Ia afferent discharge from the muscle spindles, preventing the CNS from detecting the rate and extent of muscle shortening because of the shortening of intrafusal fibres. However, this is avoided by spontaneous γ motor neuron activity, which causes the intrafusal muscle fibres to shorten along with the extrafusal fibres; as the central region of intrafusal fibres does not contain sarcomeres, it remains stretched, thus maintaining afferent nerve activity. Thus, coactivation of α and γ motor neurons maintains Ia afferent discharge during muscle contraction. Direct stimulation of γ motor neurons can initiate movements, but this does not normally occur.
Regenerative replacement of neural cells for treatment of spinal cord injury
Published in Expert Opinion on Biological Therapy, 2021
William Brett McIntyre, Katarzyna Pieczonka, Mohamad Khazaei, Michael G. Fehlings
Motor neurons (MNs) are detrimentally affected in SCI, where synaptic connections regulating coordinated movement are disrupted. In the healthy cord, functionally and molecularly diverse spinal MN subtypes exhibit distinct profiles of activation and patterns of connectivity. Alpha MNs (α-MNs; Fox3+/Err3-) innervate force-generating extrafusal muscle fibers that control skeletal movement through muscle contractile forces. Gamma MNs (γ-MNs; Fox3-/Err3+) are abundant in the spinal cord, where they connect to intrafusal muscle fibers in muscle spindles. They modulate the sensitivity of muscle spindles to stretch [96], as well as regulate proprioceptive afferent feedback to α-MNs [97]. In several models of degenerative MN diseases, the excitatory afferent feedback present only in α-MNs is implicated in their rapid death following disease onset [97]. Interestingly, this phenomenon is not observed in spinal cord transection, as both α-MNs and γ-MNs exhibit a higher proportion of inhibitory:excitatory inputs, which can be correlated to poor bipedal stepping [98]. This could effectively explain failed attempts to restore α-MN circuitry after spinal transection [99], where it is likely that a diverse group of MN-pools require restoration following spinalization.
Effects of Botulinum Toxin A Injection on Ambulation Capacity in Patients with Cerebral Palsy
Published in Developmental Neurorehabilitation, 2019
Sibel Çağlar Okur, Mahir Uğur, Kazım Şenel
The mode of action of botulinum toxin includes extracellular binding to glycoprotein structures on cholinergic nerve terminals and intracellular blockade of the acetylcholine secretion. Thus, it prevents the release of acetylcholine at the neuromuscular junction, causing presynaptic neuromuscular blockade. BT affects the spinal stretch reflex by blockade of intrafusal muscle fibers with consecutive reduction of Ia/II afferent signals and muscle tone without affecting muscle strength (reflex inhibition).7 Thus, it allows muscles to become paralyzed for 3–6 months. Although its lethal dose is rather low, no significant side effect has been observed in the treated patients. Sometimes, it can cause temporary weakness in adjacent muscle groups, and local pain and tenderness may occur at the injection site. It is a reliable drug except for these side effects.8
No Relationship Between Joint Position Sense and Force Sense at the Shoulder
Published in Journal of Motor Behavior, 2018
David Phillips, Andrew Karduna
The lack of relationship in normalized RMS error between the two protocols may also be due to variations in feedback from the peripheral mechanoreceptors during isometric and concentric contractions. When contracting a muscle both alpha and gamma (fusimotor) motor neurons fire simultaneously, which is referred to as alpha-gamma coactivation (Vallbo, 1970). This prevents a muscle spindle from becoming slack and unable to respond to the muscle lengthening. During isometric contractions, the agonist muscle's muscle spindles firing increases at an inconsistent rate (Vallbo, 1974). In this case the alpha-gamma coactivation may be attempting to shorten intrafusal muscle fibers that are remaining at the same length and applying tension on the muscle spindle increasing its firing rate. This would be the only signal from muscle spindles since during an isometric contraction the antagonist muscle will also remain at a constant length. However, it is argued that these fusimotor induced signals from muscle spindles during an isometric contraction are filtered out because they do not induce an illusion of movement at the joint (McCloskey, Gandevia, Potter, & Colebatch, 1983).