Golgi Tendon Organs

The Golgi tendon organs continuously monitor tension in the tendons produced by muscle contraction or passive stretching of a muscle. Sensory neurons from these receptors synapse with in-terneurons in the spinal cord; these interneurons, in turn, have

Table 12.7 Summary of Events in a Monosynaptic Stretch Reflex

1. Passive stretch of a muscle (produced by tapping its tendon) stretches the spindle (intrafusal) fibers.

2. Stretching of a spindle distorts its central (bag or chain) region, which stimulates dendritic endings of sensory nerves.

3. Action potentials are conducted by afferent (sensory) nerve fibers into the spinal cord on the dorsal roots of spinal nerves.

4. Axons of sensory neurons synapse with dendrites and cell bodies of somatic motor neurons located in the ventral horn gray matter of the spinal cord.

5. Efferent nerve impulses in the axons of somatic motor neurons (which form the ventral roots of spinal nerves) are conducted to the ordinary (extrafusal) muscle fibers. These neurons are alpha motoneurons.

6. Release of acetylcholine from the endings of alpha motoneurons stimulates the contraction of the extrafusal fibers, and thus of the whole muscle.

7. Contraction of the muscle relieves the stretch of its spindles, thus decreasing electrical activity in the spindle afferent nerve fibers.

Muscle 351

inhibitory synapses (via IPSPs and postsynaptic inhibition— chapter 7) with motor neurons that innervate the muscle (fig. 12.28). This inhibitory Golgi tendon organ reflex is called a disynaptic reflex (because two synapses are crossed in the CNS), and it helps to prevent excessive muscle contractions or excessive passive muscle stretching. Indeed, if a muscle is stretched extensively, it will actually relax as a result of the inhibitory effects produced by the Golgi tendon organs.

Golgi Tendon Organ

Tendon Patella

Patellar ligament

■ Figure 12.27 The knee-jerk reflex. This is an example of a monosynaptic stretch reflex.

Damage to spinal nerves, or to the cell bodies of lower motor neurons (by poliovirus, for example), produces a flaccid paralysis, characterized by reduced muscle tone, depressed stretch reflexes, and atrophy. Damage to upper motor neurons or descending motor tracts at first produces spinal shock in which there is a flaccid paralysis. This is followed in a few weeks by spastic paralysis, characterized by increased muscle tone, exaggerated stretch reflexes, and other signs of hyperactive lower motor neurons.

The appearance of spastic paralysis suggests that upper motor neurons normally exert an inhibitory effect on lower alpha and gamma motor neurons. When this inhibition is removed, the gamma motoneurons become hyperactive and the spindles thus become overly sensitive to stretch. This can be demonstrated dramatically by forcefully dorsiflecting the patient's foot (pushing it up) and then releasing it. Forced extension stretches the antagonistic flexor muscles, which contract and produce the opposite movement (plantar flexion). Alternative activation of antagonistic stretch reflexes produces a flapping motion known as clonus.

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