Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Anatomy and Physiology 2211K - Lecture 4 Slide 2 – Cytology of a muscle fiber Slide 5 – Protein filaments Slide 4 – Actin molecule Slide 7 – Myosin molecule Slide 8 – Tropomyosin and troponin Slide 9 - Tinin Slide 10 - Nebulin Slide 3 - Myofibrils Slide 4 – Myofibrils II Slide 16 – Sarcomere Slide 12 – Energy molecules II Slide 12 – Nucleosides Nucleoside diphosphokinase NTP + ADP NDP + ATP Nucleoside triphosphate (NTP) is a general name for all energy molecules such as ATP, TTP, CTP, GTP, UTP Since the conformational change of the heavy meromyosin (e.g. as an result muscle contraction) is energized by ATP only, the remaining energy sources (e.g. TTP, CTP, GTP, UTP) could be salvaged in an emergency to recharge ADP As shown above, the nucleoside triphosphate (NTP) which are the remaining energy molecules of TTP, CTP, GTP, UTP could be utilized to recharge ADP by transferring its high energy bond Nucleoside diphosphokinase is the enzyme used to transfer the high energy bone and a phosphate from NTP to ADP thereby forming ATP Slide 13 – Creatine phosphate Creatine Kinase Creatine Phosphate + ADP Creatine + ATP Creatine phosphate is the major reserve energy source in muscles Creatine possesses a a high energy bond (and a phosphate) and it is formed when the muscle is at rest In an emergency, the high energy bond (and a phosphate) is transferred to ADP thereby reforming a charged energy molecule ATP Creatine kinase is responsible for transferring the high energy bond from creatine phosphate to ADP Slide 14 – adenylate kinase Adenylate Kinase ADP + ADP AMP + ATP As an last ditch effort to gain energy, your body will salvage even a spent energy molecule like Adenosine diphosphate (ADP) The enzyme adenylate kinase is used to transfer a phosphate from ADP to another ADP to create a new high energy bond or a recharged ATP Slide 18 – Neuromuscular junction Slide 19 – sodium and potassium concentrations Slide 18: Polarized Slide 18: Ionotropic and metabotropic receptor Slide 20: Reaching threshold Slide 20 – Spread of action potential I Figure 17: Graphic illustration of the formation of an action potential. Please note that the ① pore of the ligand gated Na+ channel (red) will open after the binding of ACh which allows the initial influx of Na+ and the generation of an electric impulse (red arrow). ② Subsequently, the electric impulse will spread down the membrane by causing the first voltage gated Na+ channel to open which in turn will create another electric impulse and ③ opening another voltage gated Na+ channel. ④ Like falling dominos, another electric impulse will be generated whereby causing other voltage gated Na+ channel to open Slide 22: DHP Receptor Figure 18: Graphic illustration of the interactions between DHP receptor, ryanodine receptor and calcium release channel. ① The generated action potential activates the DHP receptor which causes this voltage gated Ca++ channel to open. ② Ca++ cations from the extracellular matrix to flow into the cell. ③ The Ca++ cations bonds to ryanodine receptor causing it to activate. ④The activated ryanodine receptor trigger the opening of the calcium release channel thereby allowing the Ca++ stored within the sarcoplasmic reticulum to be released into the sarcoplasm Slide 21: muscle contraction summary I Slide 24 – Cross bride and power stroke Slide 24: muscle contraction summary II Figure 22: Graphic illustration of excitationcontraction coupling. ① Action potential arrives at the neuromuscular junction which causes AChE to be released via exocytosis. ② AChE diffuses cross the synaptic cleft and binds with nAChR and initiates an action potential. ③ Action potential travels to the t-tubules and activates the DHP receptor which in turn causes the sarcoplasmic reticulum to release Ca++. ④ Ca++ is released into the sarcoplasm and ⑤ binds with troponin which in turn moves tropomyosin away from the active site. Cross bridge is formed between the myosin and actin myofilament and actin-myosin cycling begins. ⑥ actin-myosin cycling results in the shortening of the sarcomere. The shortening of the sarcomere causes the shortening of the myofibril. ⑦ The shortening of the myofibril results in muscle contraction Slide 23: Depolarized Slide 26: Repolarization Slide 27: return to polarization Slide 22 – Return to polarization and muscle relaxation summary Figure 25: Graphic illustration of skeletal muscle relaxation. ① Acetylcholinesterase removed AChE which causes the nAChR to close. ② Lack of action potential causes the voltage gated Na+ channel to close. ③ DHP receptor turns “off” which causes the reabsorption of Ca++ by the terminal cisternae and subsequent storage in the sarcoplasmic reticulum. ④Removal of Ca++ from TnC which causes troponin to return to its original shape. Regaining its shape, troponin moves tropomyosin back to its original conformation. Tropomyosin covers the active site of actin myofilament and severs the cross bridge. ⑤ Sarcomere and myofibril return to its relaxed state. ⑥ muscle relaxation Slide 27 - Myoglobin Slide 31: Cellular respiration overview Slide: Anaerobic respiration Slide 26 – Creatine phosphate Slide 43 – oxygen debt and lactic acid Slide 35: aerobic and anaerobic respiration overview Slide 36 – Types of muscle Slide 47 – Origin, insertion and joint Slide 48 – Flexor and extensors Slide 49 - fasia Slide 40 – Smooth muscle