LEC 3 (13) - MCB 136 Professor Terry Machen 3/03/09 Lecture...

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MCB 136 Professor Terry Machen 3/03/09 Lecture 13 ASUC Lecture Notes Online is the only authorized note-taking service at UC Berkeley. Do not share, copy or illegally distribute (electronically or otherwise) these notes. Our student-run program depends on your individual subscription for its continued existence. These notes are copyrighted by the University of California and are for your personal use only. D O N O T C O P Y Sharing or copying these notes is illegal and could end note taking for this course. ANNOUNCEMENTS From the midterm, we will hand back all the scantrons this week. If there are any problems with your graded written portion of the test that you received back, re-grades will be due a week from today. In the reader it says there are topics in chapter 13 to go over and questions to answer, but I’m not going to cover that so you don’t have to go over those sections. REVIEW If you excite the skeletal muscle in the absence of Ca 2+ , will it contract or not? The answer is: it will contract for a long time. The DHPR receptor doesn’t let any Ca 2+ go through and so the Ca 2+ inside the skeletal muscle basically recycles all the time. If you excite a nerve under the same conditions will the muscle contract? No, because the release of a neurotransmitter requires Ca 2+ . Will a smooth muscle contract under the same conditions? This one will not. If it does, it will be very small. LECTURE Today I’m going to finish talking about cardiac muscle. There are a couple of small but important things that I emphasized incorrectly last time. The sarcomeres are basically the same as skeletal muscle. There is a branch interconnected with gap junctions. You need an action potential in the membrane to make the heart contract. There are two kinds of K + channels. One of them turns off your extended duration of action potential, and the other one turns on quite late. So the main one is what causes repolarization. So it’s the same as in skeletal muscle, but much slower. Ca 2+ channels are identical and are in transverse tubules and membranes. The difference between Ca 2+ channels in the heart and skeletal muscles, when action potentials come over DHPR opens (it is a Ca 2+ channel). DHPRs are a Ca 2+ blocker and can fuse and alter the contractual strength of the heart. The Ca 2+ that enters is a regulator of contraction and ryanodine receptors. Ryanodine receptor is opened by Ca 2+ entering. The channel is opened by voltage and regulated by cAMP, which is produced by epinephrine. I mentioned that beta receptors generate cyclic AMP, which alters the activity of voltage-gated Ca 2+ channels. They also can open more with cAMP protein kinase, increasing open probability and contractual strength. ACh affects/inhibits this system. That is under some debate. It’s clear that the figure in the reader is exaggerated. Remember that cAMP increases contractility and the rate of contraction. Parasympathetic stimulation stimulates ACh, which slows down the heart but doesn’t affect
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This note was uploaded on 05/07/2009 for the course MCB 58168 taught by Professor Thorner during the Spring '09 term at University of California, Berkeley.

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LEC 3 (13) - MCB 136 Professor Terry Machen 3/03/09 Lecture...

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