An 18-year-old man, who was recently started on risperidone therapy for schizophrenia, comes to the office due to involuntary deviation of his head. On examination, the patient's head is tilted toward the right side and the chin is rotated to the left. There is palpable tightening of the right sternocleidomastoid muscle. It is determined that the patient is experiencing a medication-induced dystonic reaction due to motor neuron hyperactivity. The persistent myocyte stimulation causes a substance to be released from the sarcoplasmic reticulum. This substance most likely binds to which of the following proteins to cause this patient's symptoms?

Question

An 18-year-old man, who was recently started on risperidone therapy for schizophrenia, comes to the office due to involuntary deviation of his head.  On examination, the patient's head is tilted toward the right side and the chin is rotated to the left.  There is palpable tightening of the right sternocleidomastoid muscle.  It is determined that the patient is experiencing a medication-induced dystonic reaction due to motor neuron hyperactivity.  The persistent myocyte stimulation causes a substance to be released from the sarcoplasmic reticulum.  This substance most likely binds to which of the following proteins to cause this patient's symptoms?

Quizplus · Accepted Answer

11ec160b_3d01_c4be_9249_2d867bdf6575_MD0001_00 The sarcoplasmic reticulum (SR) is a modified endoplasmic reticulum within skeletal muscle cells. The SR forms a network of tubules with terminal cisterns that are in close contact with the T tubules (cytoplasmic membrane invaginations), allowing the membrane depolarization signal to reach the SR. The Ca²⁺-ATPase pump in the SR membrane actively sequesters calcium to keep intracellular concentrations low. Cell membrane depolarization causes calcium release from the SR into the cytoplasm via the SR ryanodine receptor. Actin filaments, troponin complex (troponins C, T, and I), and tropomyosin form the thin filaments of muscle fibers. In the resting state, tropomyosin covers the myosin binding sites on the actin filaments. On release from the SR, calcium binds to troponin C on the thin filaments (Choices A and C). This induces a conformation change in the troponin complex, causing it to displace tropomyosin and expose the myosin binding sites on the actin filaments. Myosin makes up the thick filaments of skeletal muscle. ATP is bound by the myosin head and cleaved to form ADP and inorganic phosphate ion, which are retained at the myosin head. When the myosin head binds to an actin filament, a conformational change causes the myosin to pull the actin filament, leading to muscle contraction and ADP release. A new ATP molecule then is bound to the myosin head, causing release of the actin filament. The cycle then repeats until calcium is displaced from troponin C and the myosin binding sites are again covered (Choice B). The pulse of elevated intracellular calcium lasts only a fraction of a second before the calcium is resequestered within the SR. (Choice E) Protein kinase A is activated by high intracellular concentrations of cAMP and is involved in the second messenger pathways of numerous hormones, including glucagon, beta adrenergic receptors, parathyroid hormone and others. Educational objective: During skeletal muscle contraction, calcium is released from the sarcoplasmic reticulum and binds troponin C, thereby allowing the binding of actin to myosin. __________ References: Troponin: regulatory function and disorders. (http://www.ncbi.nlm.nih.gov/pubmed/18154728)

An 18-Year-Old Man, Who Was Recently Started on Risperidone Therapy