The Neuromuscular Junction

The functional connection between a nerve fiber and its target cell is called a synapse (SIN-aps). When the second cell is a muscle fiber, the synapse is called a neuromuscular

Saladin: Anatomy & I 11. Muscular Tissue I Text I © The McGraw-Hill

Physiology: The Unity of Companies, 2003 Form and Function, Third Edition

414 Part Two Support and Movement

414 Part Two Support and Movement

Neuromuscular Junction Mcgraw
Figure 11.5 Innervation of Skeletal Muscle.

Motor unit

Skeletal muscle fibers

Muscle fiber nucleus

Neuromuscular junctions

Motor nerve fiber

Figure 11.6 A Motor Unit. The motor nerve fiber shown here branches to supply those muscle fibers shown in color. The other muscle fibers (gray) belong to other motor units.

Motor unit

Skeletal muscle fibers

Muscle fiber nucleus

Neuromuscular junctions

Motor nerve fiber

Figure 11.6 A Motor Unit. The motor nerve fiber shown here branches to supply those muscle fibers shown in color. The other muscle fibers (gray) belong to other motor units.

junction (fig. 11.7). Each branch of a motor nerve fiber ends in a bulbous swelling called a synaptic (sih-NAP-tic) knob, which is nestled in a depression on the sarcolemma called the motor end plate. The two cells do not actually touch each other but are separated by a tiny gap, the synaptic cleft, about 60 to 100 nm wide. A third cell, called a Schwann cell, envelops the entire neuromuscular junction and isolates it from the surrounding tissue fluid.

The electrical signal (nerve impulse) traveling down a nerve fiber cannot cross the synaptic cleft like a spark jumping between two electrodes—rather, it causes the nerve fiber to release a neurotransmitter that stimulates the next cell. Although many chemicals function as neuro-transmitters, the one released at the neuromuscular junction is acetylcholine (ASS-eh-till-CO-leen) (ACh). ACh is stored in spherical organelles called synaptic vesicles.

Directly across from the synaptic vesicles, the sar-colemma of the muscle cell exhibits infoldings called junctional folds, about 1 ^m deep. The muscle fiber has about 50 million membrane proteins called ACh receptors, which bind the acetylcholine release by the nerve fiber. Most ACh receptors are concentrated in and near these junctional folds. Very few ACh receptors are found anywhere else on a muscle fiber. Junctional folds increase the surface area for receptor sites and ensure a more effective response to ACh. The muscle nuclei beneath the junc-tional folds are specifically dedicated to the synthesis of ACh receptors and other proteins of the motor end plate. A deficiency of ACh receptors leads to muscle paralysis in the disease myasthenia gravis (see insight 11.4, p. 437).

The entire muscle fiber is surrounded by a basal lamina that passes through the synaptic cleft and virtually fills it. Both the sarcolemma and that part of the basal lamina in the cleft contain an enzyme called acetylcholinesterase (ASS-eh-till-CO-lin-ESS-ter-ase) (AChE), which breaks down ACh, shuts down the stimulation of muscle fibers, and allows a muscle to relax (see insight 11.1).

Insight 11.1 Clinical Application

Neuromuscular Toxins and Paralysis

Toxins that interfere with synaptic function can paralyze the muscles. Some pesticides, for example, contain cholinesterase inhibitors that bind to acetylcholinesterase and prevent it from degrading ACh. This causes spastic paralysis, a state of continual contraction of the muscle that poses the danger of suffocation if the laryngeal and respiratory muscles are affected. A person poisoned by a cholinesterase inhibitor must be kept lying down and calm, and sudden noises or other disturbances must be avoided. A minor startle response can escalate to dangerous muscle spasms in a poisoned individual.

Tetanus ("lockjaw") is a form of spastic paralysis caused by a toxin from the bacterium Clostridium tetani. In the spinal cord, an inhibitory neurotransmitter called glycine stops motor neurons from producing unwanted muscle contractions. The tetanus toxin blocks glycine release and thus allows overstimulation of the muscles. (At the cost of

Saladin: Anatomy & I 11. Muscular Tissue I Text I © The McGraw-Hill

Physiology: The Unity of Companies, 2003 Form and Function, Third Edition

Chapter 11 Muscular Tissue 415

Motor nerve fiber Myelin

Axon terminal Schwann cell

Sarcolemma Region of

Motor nerve fiber Myelin

Axon terminal Schwann cell

Sarcolemma Region of

Junctional Folds And Synaptic Cleft

Synaptic vesicles (containing ACh)

Basal lamina (containing AChE)

Synaptic cleft

Junctional folds

Synaptic vesicles (containing ACh)

Basal lamina (containing AChE)

sarcolemma with ACh receptors

Nucleus of muscle fiber ■

Synaptic cleft

Junctional folds

Nucleus of muscle fiber ■

Figure 11.7 A Neuromuscular Junction.

some confusion, the word tetanus also refers to a completely different and normal muscle phenomenon discussed later in this chapter.)

Flaccid paralysis is a state in which the muscles are limp and cannot contract. It can cause respiratory arrest when it affects the thoracic muscles. Flaccid paralysis can be caused by poisons such as curare (cue-RAH-ree) that compete with ACh for receptor sites but do not stimulate the muscle. Curare is extracted from certain plants and used by some South American natives to poison blowgun darts. It has been used to treat muscle spasms in some neurological disorders and to relax abdominal muscles for surgery, but other muscle relaxants have now replaced curare for most purposes.

You must be very familiar with the foregoing terms to understand how a nerve stimulates a muscle fiber and how the fiber contracts. They are summarized in table 11.2 for your later reference.

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Responses

  • livia
    What is the intended region of the sarcolemma that participates in the neuromuscular called?
    2 years ago

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