The body of the Golgi tendon organ is made up of braided strands of collagen (intrafusal fasciculi) that are less compact than elsewhere in the tendon and are encapsulated.[2]
The capsule is connected in series (along a single path) with a group of muscle fibers (10-20 fibers[3]) at one end, and merge into the tendon proper at the other.
Each capsule is about 1 mm long, has a diameter of about 0.1 mm, and is perforated by one or more afferent type Ib sensory nerve fibers (Aɑ fiber), which are large (12-20 μm)myelinated axons that can conduct nerve impulses very rapidly.
Inside the capsule, the afferent fibers lose their medullary sheaths, branch, intertwine with the collagen fibers, and terminate as flattened leaf-like endings between the collagen strands (see figure).[4][5]
Function
When the muscle generates force, the sensory terminals are compressed. This stretching deforms the terminals of the Ib afferent axon, opening stretch-sensitive cation channels. As a result, the Ib axon is depolarized and fires nerve impulses that are propagated to the spinal cord. The action potential frequency signals the force being developed by 10-20 extrafusal muscle fibers in the muscle. Average level of activity in a tendon organ population is representative of the whole muscle force.[4][7]
The Ib sensory feedback generates stretch reflexes and supraspinal responses which control muscle contraction. Ib afferents synapse with interneurons in the spinal cord that also project to the brain cerebellum and cerebral cortex. The Golgi tendon reflex assists in regulating muscle contraction force. It is associated with the Ib. Tendon organs signal muscle force through the entire physiological range, not only at high strain.[7][8]
During locomotion, Ib input excites rather than inhibits motoneurons of the receptor-bearing muscles, and it affects the timing of the transitions between the stance and swing phases of locomotion.[9] The switch to autogenic excitation is a form of positive feedback.[10]
Until 1967, it was believed that Golgi tendon organs had a high threshold, only becoming active at high muscle forces. Consequently, it was thought that tendon organ input caused "weightlifting failure" through the clasp-knife reflex, which protected the muscle and tendons from excessive force. [citation needed] However, the underlying premise was shown to be incorrect by James Houk and Elwood Henneman in 1967.[11]
^MacIntosh, Brian R. (2006). Skeletal muscle : form and function (2nd ed.). Champaign, IL: Human Kinetics. pp. 48–49. ISBN0736045171.
^Mancall, Elliott L; Brock, David G, eds. (2011). "Chapter 2 - Overview of the Microstructure of the Nervous System". Gray's Clinical Neuroanatomy: The Anatomic Basis for Clinical Neuroscience. Elsevier Saunders. p. 29. ISBN978-1-4160-4705-6.
^ abPurves et al (2018), Mechanoreceptors Specialized for Proprioception, pp. 201-202
^Barrett, Kim E; Boitano, Scott; Barman, Susan M; Brooks, Heddwen L (2010). "Chapter 9 - Reflexes". Ganong's Review of Medical Physiology (23rd ed.). McGraw-Hill. INVERSE STRETCH REFLEX, pp. 162-163. ISBN978-0-07-160567-0.
Saladin, KS (2018). "Chapter 13 - The Spinal Cord, Spinal Nerves, and Somatic Reflexes". Anatomy and Physiology: The Unity of Form and Function (8th ed.). New York: McGraw-Hill. ISBN978-1-259-27772-6.
Purves, Dale; Augustine, George J; Fitzpatrick, David; Hall, William C; Lamantia, Anthony Samuel; Mooney, Richard D; Platt, Michael L; White, Leonard E, eds. (2018). "Chapter 9 - The Somatosensory System: Touch and Proprioception". Neuroscience (6th ed.). Sinauer Associates. ISBN9781605353807.
Pearson, Keir G; Gordon, James E (2013). "35 - Spinal Reflexes". In Kandel, Eric R; Schwartz, James H; Jessell, Thomas M; Siegelbaum, Steven A; Hudspeth, AJ (eds.). Principles of Neural Science (5th ed.). United States: McGraw-Hill. ISBN978-0-07-139011-8.