ps5s05 - MIT Department of Biology 7.013: Introductory...

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MIT Department of Biology 7.013: Introductory Biology - Spring 2005 Instructors: Professor Hazel Sive, Professor Tyler Jacks, Dr. Claudette Gardel NAME_______________________________________________________________TA________ 7.013 Spring 2005 Problem Set 5 FRIDAY April 15th, 2005 Problem sets will NOT be accepted late. Question 1 In the autoimmune disease, myasthenia gravis, antibodies are produced against one’s own acetylcholine (Ach) receptors in muscle. The result of this antibody production can either lead to the degradation of the Ach receptors, or to impaired binding of acetylcholine. a) A post-synaptic muscle cell experiences action potentials similar to a neuron. See the wildtype (WT) diagram below. Compared with the WT muscle action potential, which of the following muscle action potentials (#1-5) would you expect to see from a person with advanced myasthenia gravis. 1 WT # 1 # 2 # 3 # 4 # 5
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b) Acetylcholinesterase is an enzyme that degrades acetylcholine in normal individuals. Which of the following is true? i) Drugs that stimulate acetylcholinesterase would improve myasthenia gravis. ii) Drugs that inhibit acetylcholinesterase would improve myasthenia gravis. iii) Drugs modulating acetylcholinesterase would have no effect on myasthenia gravis. Two other diseases affecting the neuromuscular junction are Lambert-Eaton syndrome and human botulism. In Lambert-Eaton syndrome, an autoimmune disease, antibodies are produced against the presynaptic Ca2+ channels at the neuromuscular junction. In botulism, a bacterial toxin prevents fusion of neurotransmitter-containing vesicles with the presynaptic plasma membrane.
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This note was uploaded on 11/11/2011 for the course BIO 7.012 taught by Professor Lander during the Fall '10 term at MIT.

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ps5s05 - MIT Department of Biology 7.013: Introductory...

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