BIOL 252 1st Edition Lecture 11 Outline of Last Lecture I. Poll EverywhereII. Bone Growth and RemodelingIII. Calcium HomeostasisIV. HypercalcemiaV. OsteoporosisVI. Muscles – basic structure of skeletal muscle Outline of Current LectureI. SarcomereII. Transferring contractile forces to whole musclesIII. Nerve-Muscle RelationshipIV. Muscle Contraction and RelaxationCurrent LectureI. Sarcomerea. Unit of contractionb. A Band: dark bandc. In between dark bands are I bands (light)d. M line: holds bands of myosin together (midline)i. Myosin molecules pull actin toward M line and opposite side pulls the other way – also toward M linee. Z disc: plate that holds thin filaments on one side and thin filaments on reverse side for neighboring sarcomere i. Anchor between two adjacent sarcomeres, holds thin filaments togetherf. When muscle contracts and sarcomere shortens, which of the following also shortens?i. Thin filament – do not contract, do not shrink in size, thin slide past thick, by sliding past each other, make overall sarcomere shorterii. Thick filament – same reasoning as thin filamentiii. I-band – DO SHORTEN, space between myosin and myosin (where there isno myosin)iv. A-band – does not shrinkv. M-line – lines that mark center of A bandvi. Z-disc – by itself, anchoring point for thin filamentsThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.II. Transferring contractile forces to whole musclesa. Accessory proteinsb. Endomysium – dense, connective tissuei. Connected to tendons -> connected to bonesii. Separates individual muscle fibersc. Fascicle – wrapped by perimysiumd. Epimysium – around perimysiume. Connective tissue makes up tendon (attaches to bone) f. Linking proteinsi. Bridge from inside to outside of cellg. To connect cell membrane proteins: dystrophini. Muscular dystrophy1. Involves faulty dystrophin molecule2. Weak muscles cannot transfer forces properlyIII. Nerve-Muscle Relationshipa. Somatic motor innervationb. Motor unit: each neuron branches out to a number of muscle fibersc. Each neuron controls >1 muscle celld. Smallest ratio is 1:6 e. All muscle fibers the neuron is attached to are stimulated/contract at the same timef. Neuromuscular Junctioni. Where neuron meets muscle = special synapseii. Motor neuron axon terminals make connection w/ muscle fiberiii. Synaptic vesicles contain Ach iv. Motor end plate – acts like dendrite, depolarizations are produced that generate action potentialsv. Everywhere except motor end plate functions like an axonvi. A 20-year-old woman exhibits bilateral flaccid paralysis in her facial muscles. She is unable to smile, frown, or squint. Which is NOT a viable explanation?1. Myasthenia gravis – autoimmune attack on ACh receptorsa. Cannot get signal across from one cell to the nextb. Have fewer and fewer ACh receptors2. ANSWER: Organophosphate exposure (inhibition of AChE) – breaks down ACh so muscles aren’t constantly contractinga. If you inhibit AChE => elevated ACh 3. Somatic nerve damage4. Overexposure to Botox (prevents ACh release)IV. Muscle Contraction and Relaxationa. Excitation: muscle receiving electrical stimulusb. => Contraction results c. What connects these two?i. Excitation-contraction couplingii. When you are done contracting, want to relax muscles (active process)d. Steps:i. Excitation of Muscle Fiber1. Action Potential2. ACh release3. Binding of ACh to receptor4. Opening of ligand-regulated ion gate; creation of end-plate potential (type of local potential in muscle cells) (in neurons it wascalled EPSP)5. Opening of voltage-regulated ion gates; creation of action potentialsii. Excitation-contraction coupling1. Action potentials stimulate release of calcium from SR2. Terminal cisternae: SR / t-tubule / SR (triad)3. What happens to calcium?a. Calcium binds to troponin and free myosin-binding sitesiii. Contraction1. Cross bridge formationa. Binding causes minor changes in myosin molecule2. Power strokea. Transfer of force3. Cross bridge detachmenta. Requires new molecule of ATPb. Rigor mortis – no more ATP to detach cross bridges, muscles lock up after death4. Hydrolysis of ATP: activation of myosin heada. ATP => ADP and Pb. Reactivation of myosin head (repeat process again)c. Process continues so long as calcium presentd. Take away calcium – binding sites no longer availableiv. Relaxation1. Absence of excitation leads to diminished calcium and myosin-binding sites become covered w/ tropomyosine. Will you get contraction?CalciumTroponin Tropomyosin ATP Contraction? Why?1 + - - - NO Never contraction w/out ATP2 + - - + YES Because we have actin andno troponin andtropomyosin (regulatory),binding sites are open3 + + - + YES Tropomyosin is the oneactually covering bindingsites4 - - + + NO (butquestionable)W/out calcium, don’t needtroponin but tropomyosinstill blocks binding sites5 - - - + YES Troponin and tropomyosinabsent so it doesn’t matter ifcalcium is there (noblockage of