Spindles consist of encapsulated intrafusal muscle fibers that are innervated by specialized group Ia-afferents that relay muscle stretch sensation to the CNS and fusimotor efferents that maintain spindle stretch sensitivity as muscles stretch and contract. Muscle spindles are stretch-sensitive mechanoreceptors embedded within skeletal muscles that mediate limb and axial body position sensation (proprioception), the myotatic stretch reflex and locomotor patterning ( Poppele and Terzuolo, 1968 Goodwin et al., 1972 Akay et al., 2014). These results demonstrate that Egr3 has an essential role in regulating gene expression that promotes normal intrafusal muscle fiber differentiation and fusimotor innervation homeostasis. However, they were not innervated by fusimotor axons and they did not express glial derived neurotrophic factor (GDNF), which is essential for fusimotor neuron survival. These “spindle remnants” persisted into adulthood, remained innervated by Ia-afferents, and expressed neurotrophin3 (NT3), which is required for Ia-afferent neuron survival. Moreover, using genetic tracing, we found that Ia-afferent contacted Egr3-deficient myotubes were induced in normal numbers, but their development was blocked to generate one to two shortened fibers that failed to express some characteristic myosin heavy chain (MyHC) proteins. In the present studies, cell-specific ablation of Egr3 in mice showed that it has a skeletal muscle autonomous function in stretch receptor development. Because Egr3 is widely expressed during development and has a pleiotropic function, whether Egr3 functions primarily in skeletal muscle, Ia-afferent neurons, or in Schwann cells that myelinate Ia-afferent axons remains unresolved. The transcriptional regulator Egr3 is induced in Ia-afferent contacted myotubes by Neuregulin1 (Nrg1)/ErbB receptor signaling and it has an essential role in spindle morphogenesis and function. During skeletal muscle development, sensory (Ia-afferent) innervation induces contacted myotubes to transform into intrafusal muscle fibers that form the stretch receptor core. Proprioception abnormalities are observed in many human neuropathies, but the mechanisms involved in establishing and maintaining muscle spindle innervation and function are still poorly understood. co-activation of both the alpha and gamma motor neurons (step 3) prevents the spindle afferents from becoming completely silent during step 5 (i.e.Muscle stretch proprioceptors (muscle spindles) are required for stretch reflexes and locomotor control.decreased firing of spindle afferent ( negative feedback).muscle contraction (both extra- and intra-fusal fibres).activation of alpha and gamma motor neurons.depolarization and generation of action potentials in the spindle afferent.the sequence is ( click here for an animation):.the patellar reflex is an example of a stretch reflex (muscle spindles in the quadriceps muscle are activated).STRETCH REFLEX: increased activity in the spindle afferents causes depolarization of alpha motor neurons ( monosynaptic reflex), contracting the extrafusal muscle fibres secondary endings are static (they signal the amplitude of the change).primary endings are dynamic (they respond to the velocity of the change).muscle stretch deforms the nerve endings, causing depolarization ( mechanoreception).this tonic activity maintains a basal level of tension in the muscle, due to the same mechanism described below for the stretch reflex.when the muscle is at rest, the spindle has a low level of tonic activity.muscle spindles are mechanoreceptors that signal MUSCLE STRETCH.
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