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| Muscle spindle | |
|---|---|
 Mammalian muscle spindle showing typical position in a muscle (left), neuronal connections in spinal cord (middle) and expanded schematic (right). The spindle is a stretch receptor with its own motor supply consisting of several intrafusal muscle fibres. The sensory endings of a primary (group Ia) afferent and a secondary (group II) afferent coil around the non-contractile central portions of the intrafusal fibres. Gamma motor neurons activate the intrafusal muscle fibres, changing the resting firing rate and stretch-sensitivity of the afferents.[a] | |
| Details | |
| Part of | Muscle |
| System | Musculoskeletal |
| Identifiers | |
| Latin | fusus neuromuscularis |
| MeSH | D009470 |
| TH | H3.11.06.0.00018 |
| FMA | 83607 |
| Anatomical terminology | |
Muscle spindles arestretch receptors within the body of askeletal muscle that primarily detect changes in the length of the muscle. They convey length information to thecentral nervous system viaafferent nerve fibers. This information can be processed by the brain asproprioception. The responses of muscle spindles to changes in length also play an important role in regulating thecontraction of muscles, for example, by activatingmotor neurons via thestretch reflex to resist muscle stretch.
The muscle spindle has both sensory and motor components.
Muscle spindles are found within thebelly of askeletal muscle. Muscle spindles arefusiform (spindle-shaped), and the specialized fibers that make up the muscle spindle are calledintrafusal muscle fibers. The regular muscle fibers outside of the spindle are calledextrafusal muscle fibers. Muscle spindles have a capsule ofconnective tissue, and run parallel to the extrafusal muscle fibers unlikeGolgi tendon organs which are oriented in series.[citation needed]
Muscle spindles are composed of 5–14muscle fibers, of which there are three types: dynamicnuclear bag fibers (bag1 fibers), static nuclear bag fibers (bag2 fibers), andnuclear chain fibers.[2][3]
Primarytype Ia sensory fibers (large diameter) spiral around all intrafusal muscle fibres, ending near the middle of each fibre.Secondarytype II sensory fibers (medium diameter) end adjacent to the central regions of the static bag and chain fibres.[3]These fibres send information by stretch-sensitive mechanically gatedion-channels of theaxons.[4]
The motor part of the spindle is provided by motor neurons: up to a dozengamma motor neurons also known asfusimotor neurons.[5] These activate the muscle fibres within the spindle. Gamma motor neurons supply only muscle fibres within the spindle, whereas beta motor neurons supply muscle fibres both within and outside of the spindle. Activation of the neurons causes a contraction and stiffening of the end parts of the muscle spindle muscle fibers.[citation needed]
Fusimotor neurons are classified as static or dynamic according to the type of muscle fibers they innervate and their effects on the responses of the Ia and II sensory neurons innervating the central, non-contractile part of the muscle spindle.
Efferent nerve fibers ofgamma motor neurons also terminate in muscle spindles; they makesynapses at either or both of the ends of the intrafusal muscle fibers and regulate the sensitivity of the sensory afferents, which are located in the non-contractile central (equatorial) region.[6]
When a muscle is stretched, primary type Ia sensory fibers of the muscle spindle respond to both changes in muscle length and velocity and transmit this activity to thespinal cord in the form of changes in the rate ofaction potentials. Likewise, secondary type II sensory fibers respond to muscle length changes (but with a smaller velocity-sensitive component) and transmit this signal to the spinal cord. The Ia afferent signals are transmittedmonosynaptically to manyalpha motor neurons of the receptor-bearing muscle. The reflexly evoked activity in the alpha motor neurons is then transmitted via their efferent axons to the extrafusal fibers of the muscle, which generate force and thereby resist the stretch. The Ia afferent signal is also transmitted polysynaptically throughinterneurons (Ia inhibitory interneurons), which inhibit alpha motorneurons of antagonist muscles, causing them to relax.[7]
The function of the gamma motor neurons is not to supplement the force of muscle contraction provided by the extrafusal fibers, but to modify the sensitivity of the muscle spindle sensory afferents to stretch. Upon release ofacetylcholine by the active gamma motor neuron, the end portions of the intrafusal muscle fibers contract, thus elongating the non-contractile central portions (see "fusimotor action" schematic below). This opens stretch-sensitiveion channels of the sensory endings, leading to an influx ofsodiumions. This raises theresting potential of the endings, thereby increasing the probability ofaction potential firing, thus increasing the stretch-sensitivity of the muscle spindle afferents.
Recent transcriptomic and proteomic studies have identified unique gene expression profiles specific to muscle spindle regions. Distinct macrophage populations, known as muscle spindle macrophages (MSMPs), have been observed, suggesting an immunological component in muscle spindle maintenance and function.[8] Immunostaining and sequencing have enabled tissue-level identification of novel markers, contributing to an advanced cellular atlas of the muscle spindle. Regarding the structural-functional correlation; muscle spindle density is not uniform across the musculoskeletal system. Recent biomechanical modeling suggests that spindle abundance correlates with muscle fascicle length and fiber velocity during dynamic movement, emphasizing the relationship between muscle structure and proprioceptive requirements.[9]
How does the central nervous system control gamma fusimotor neurons? It has been difficult to record from gamma motor neurons during normal movement because they have very small axons. Several theories have been proposed, based on recordings from spindle afferents.
Genetic pathways critical for spindle formation include neuregulin-1 signaling via ErbB receptors, which induce intrafusal fiber differentiation upon sensory innervation. Disruption of these pathways impairs proprioception, as seen in gene knockout models.[14]
It is also believed that muscle spindles play a critical role insensorimotordevelopment. Additionally, gain-of-function mutations in HRAS (e.g.: G12S) observed in Costello syndrome are associated with increased spindle number, providing insight into genetic regulation of spindle density.[15]
Dysfunction in muscle spindle signaling has been implicated in sensory neuropathies and coordination disorders such as ataxia. Enhanced understanding of genetic mutations affecting spindle development (e.g. HRAS and Egr3-linked pathways) opens avenues for targeted therapies in proprioceptive deficits and neuromuscular diseases.
Afterstroke or spinal cord injury in humans, spastichypertonia (spastic paralysis) often develops, whereby the stretch reflex in flexor muscles of the arms and extensor muscles of the legs is overly sensitive. This results in abnormal postures, stiffness and contractures. Hypertonia may be the result of over-sensitivity of alpha motor neurons and interneurons to the Ia and II afferent signals.[16]
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