1101 1102 ## Types of Synaptic Arrangements 1103 1104 There are several types of relationships between the input to a synapse (the presynaptic element) and the output (the postsynaptic element): one-to-one, one-to-many, or many-to-one. 1105 1106 One-to-one synapses. The one-to-one synapse is illustrated by the neuromuscular junction (see Fig. 1.16). A single action potential in the presynaptic cell, the motoneuron, causes a single action potential in the postsynaptic cell, the muscle fiber. 1107 1108 One-to-many synapses. The one-to-many synapse is uncommon, but it is found, for example, at the 1109 1110 *TABLE 1.3 Agents Affecting Neuromuscular Transmission* 1111 1112 1113

Example	Action	Effect on Neuromuscular Transmission
Botulinus toxin	Blocks ACh release from presynaptic terminals	Total blockade, paralysis of respiratory muscles, and death
Curare	Competes with ACh for receptors on motor end plate	Decreases size of EPP; in maximal doses produces paralysis of respiratory muscles and death
Neostigmine	AChE inhibitor (anticholinesterase)	Prolongs and enhances action of ACh at motor end plate
Hemicholinium	Blocks reuptake of choline into presynaptic terminal	Depletes ACh stores from presynaptic terminal

1114 1115 *ACh, Acetylcholine; AChE, acetylcholinesterase; EPP, end plate potential.* 1116 1117 1118 1119 1120 ## BOX 1.5 Clinical Physiology: Myasthenia Gravis 1121 1122 DESCRIPTION OF CASE. An 18-year-old college woman comes to the student health service complaining of progressive weakness. She reports that occasionally her eyelids “droop” and that she tires easily, even when completing ordinary daily tasks such as brushing her hair. She has fallen several times while climbing a flight of stairs. These symptoms improve with rest. The physician orders blood studies, which reveal elevated levels of antibodies to ACh receptors. Nerve stimulation studies show decreased responsiveness of skeletal muscle on repeated stimulation of motoneurons. The woman is diagnosed with myasthenia gravis and is treated with the drug pyridostigmine. After treatment, she reports a return of muscle strength. 1123 1124 EXPLANATION OF CASE. This young woman has classic myasthenia gravis. In the autoimmune form of the disease, antibodies are produced to ACh receptors on the motor end plates of skeletal muscle. Her symptoms of severe muscle weakness (eye muscles; arms and legs) are explainable by the presence of antibodies that block ACh receptors. Although ACh is released in normal amounts from the terminals of motoneurons, binding of ACh to its receptors on the motor end plates is impaired. Because ACh cannot bind, depolarization of the motor end plate (EPP) will not occur and normal action potentials cannot be generated in the skeletal muscle. Muscle weakness and fatigability ensue. 1125 1126 TREATMENT. Treatment of the patient with myasthenia gravis depends on a clear understanding of the physiology of the neuromuscular junction. Because this patient's condition improved with the administration of pyridostigmine (a long-acting AChE inhibitor), the success of the treatment confirmed the diagnosis of myasthenia gravis. AChE on the motor end plate normally degrades ACh (i.e., AChE terminates the action of ACh). By inhibiting the ACh-degradative enzyme with pyridostigmine, ACh levels in the neuromuscular junction are maintained at a high level, prolonging the time available for ACh to activate its receptors on the motor end plate. Thus a more normal EPP in the muscle fiber can be produced even though many of the ACh receptors are blocked by antibodies [... Output truncated due to length. 1816 tokens/6957 characters removed ...]