Muslce - Muscle Relaxants The Neuromuscular Junction Lecture Overview I Review somatic nervous system II Physiology of the neuromuscular junction

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Muscle Relaxants The Neuromuscular Junction
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Lecture Overview I. Review somatic nervous system II. Physiology of the neuromuscular junction The role of Ach and nACh R III. Neuromuscular Blocking Agents 1. Toxins 2. Non-depolarizing Blockers 3. Depolarizing Blockers 4. Others IV. Therapeutics Clinical use of muscle relaxation Myasthenia Gravis and Lambert Eaton
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I. SOMATIC vs. AUTONOMIC Structures innervated Mode of action Effect of de-nervation SOMATIC NERVOUS SYSTEM CNS PNS SKELETAL MUSCLE MYELINATED CHOLINERGIC ACh NICOTINIC RECPTOR
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Somatic Neuron Pathway Fig. 12.13 Germann and Stanfield
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Figure 12.15 Communication at the Neuromuscular Junction (Sarcolemma)
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Acetylcholine at the NMJ potential sites of drug action 1. Synthesis of acetylcholine –uptake of choline inhibited by hemicholinium 2. Uptake into storage vesicles (~10 4 Ach molecules/vesicle) -protects acetylcholine from degradation and inhibited by vesamicol 3. Release of Neurotransmitter-quantal release -blocked by botulinum toxin -spider venom causes release of acetylcholine 4. Binding to Receptor -postsynaptic Nicotinic receptor activated by acetylcholine 5. Degradation of Acetylcholine-only 10% of released Ach gets to receptor -hydrolyzed by cholinesterase in synaptic cleft 6. Recycling of Choline -choline taken up by neuron CH 3 CH 3 -N- CH 3 CH 2 CH 2 OCCH 3 O + Acetylcholine
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Nicotinic Cholinergic Receptor In muscle there are four types of subunit: 2 X α-subunit , b-, g/e- and d -subunits. Ach bind to each of the α-subunits with g/e and d playing role a1b2eg
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Generation of Muscle Current Miniature Endplate Potential: MEPP -created continuously (2/s) at endplate with release of 1-3 vesicles (quanta) Ach –maintains muscle tone When nerve impulse invades: ~200 vesicles released simultaneously … Local Depolarization caused by nACh R activation causes voltage-operated channels to open, triggering widespread depolarization
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From muscle twitch to tetany muscle contraction will increase smoothly up to a point of maximum strength where individual twitches are not observed. tetany : way by which normal muscle contractions occur.
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Block cholinergic transmission between motor nerve endings & nAchR on the neuromuscular end-plate of skeletal muscle: Neurotoxins such as botulinum toxin, bungarotoxins, conium alkaloids, curare Classes of Drugs which Block NMJ: Nondepolarizing- competitive blockade of transmission without activation of the nicotinic receptor Depolarizing -produce an initial activation of the nicotinic receptor, followed by a blockade due to sensitization Drugs acting as acetylcholinesterase Inhibitors
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1. Toxins A. Botulinum toxin •an extremely poisonous protein substance released by the bacterium Clostridium botulinum •type A toxin is the most toxic substance known •1 mg is capable of killing 20 million mice Botulism has mortality rate of 65% in humans:
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This note was uploaded on 12/03/2010 for the course PHAMACOLOG pcl470 taught by Professor Arnot during the Fall '10 term at University of Toronto- Toronto.

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Muslce - Muscle Relaxants The Neuromuscular Junction Lecture Overview I Review somatic nervous system II Physiology of the neuromuscular junction

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