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Introduction (muscle cell = muscle fibers) o Myoblasts – stem cells that produce different lines of muscle tissue (embryonic = mesoderm) Lack myofilaments, but contain polysomes used to synthesize them ALL muscle cells surrounded by an external (basal) lamina Fates: Skeletal muscle cells o Fusion of 2 or more myoblastslg multinucleated, cylindrical o Striated; Somatic (voluntary) division of nervous system o Satellite cells – undifferentiated cells b/w PM & external lamina limited skeletal muscle regeneration Cardiac muscle cells o Mesenchyme – mesodermal cells forming embryonic CT; give rise to cardiac muscle cells o Mono- or binucleate, striated & branched muscle cells o Autorhythmic modulated by sympathetic & parasympathetic o Very limited regeneration o Intercalated disks Smooth muscle cells o Centrally-placed nucleus o Mesenchymal myoblasts also form mononucleate smooth mm o Nonstriated, mononucleate, spindle-shaped (fusiform) cells o Usually in sheets around tubular organs o Capable of moderate regeneration Skeletal Muscle o Organization: // arrays of actin + myosin repeating subunits, sarcomeres long tubular, striated elements, myofibrils long, striated, cylindrical, multinucleated muscle fibers/muscle cells (endomysium & ext. lamina) fascicles (perimysium) gross muscle (epimysium) Epimysium: thick, irregular DCT covering the gross muscle Perimysium: septae of collagenous CT that wall off bundles (fascicles) of muscle cells Endomysium: highly vascularized, LCT matrix of Type I & III (reticular) collagen that surrounds individual muscle cells. Satellite cells – interior to ext. lamina & external to PM (sarcolemma) Can become mitotic Limited mm repair o Structure: Understand figure 11.4 Sarcomere: the morphological & fxn’l unit of contraction in muscle Z-line to Z-line; dark line (end of one actin to end of other actin); length Δ’s o 2 x ½ I-bands: lightly stained (end of one myosin of 1st sarcomere to end of another myosin of next sarcomere); length Δ’s A-bands: dark stained (end of one myosin to end of other myosin); length ≠Δ o H-band: center where actin does not overlap with myosin M-Line: center of sarcomere; myosin anchored to it Desmin & Vimentin: intermediate filaments which link adjacent myofibrils together Actin filaments: Twisted array of globular actin monomers, tropomyosin & troponin Actin to Z-line anchored by α-actin; extend into A-band Nebulin: regulate actin filament length Myosin filament bundles: Thick; across A-band Myosin molecules arranged in bundles o 2 heavy chains consisting of: rod-like backbone of helical chains 2 globular heads w/ ATP binding site & ATPase o 2 light chains o Symmetrical around M-Line w/ backbone twd M-Line o Titin: b/w Z & M-Lines; centers myosin in the sarcromere Myomesin – anchors myosin to center of sarcomere at M-Line Pure actin & myosin molecules will combine spontaneously o Contraction: B/w myofibrils Energy: mitochondria (ATP) & glycogen (Glu storage); backup = hydrolysis of phosphocreatine Regulation of contraction by [Ca2+]: sER (sarcoplasmic reticulum); sequesters Ca2+ via calsequestrin (Ca2+ binding protein) T-tubules: run transversely to myofibrils at A/I band jxns Continuation of PM that conducts axn potential into depths of mm cells Contraction “Uniform” contraction by: o signal conducts quickly along length of muscle o T-tubules conduct through depth of muscle cells (voltagesensitive receptors) Electrical activity opens voltage-gated receptor to open Ca2+ channels in sarcoplasmic reticulum Influx of Ca2+ into cytoplasm Ca2+ binds to troponin & begin the cycle of contraction/”power stroke” Power Stroke o Troponin – Ca2+ and tropomyosin binding domains (TnC/TnT) o Troponin binds Ca2+ causing conformational Δ in actintropomyosin complex revealing the myosin binding site o Myosin globular head binds to actin & rotates (“powerstroke”) to move the actin relative to the myosin o Actin filaments & attached Z-line are effectively moved toward the M-line, thus the I-band & sarcomere shortens o Muscle contracts b/c process is simultaneous in all sarcomeres Ca2+-ATPase membrane proteins – pump Ca2+ back into sarcoplasmic reticulum Clinical Correlation: Dystrophin – spectrin-like actin binding protein; anchors actin to PM Dystrophinlaminincollagenous CT of tendonbone periosteum (sharpey’s fibers) Muscular Dystrophy: defect or absence in dystrophin progressive weakening of skeletal muscles Rigor Mortis: ATP is required to break the interaction b/w the actin & myosin; lack of ATP is t/f the basis for the stiffening of muscles Cardiac Muscle – RAN OUT OF TIME & COULDN’T FINISH Smooth Muscle – RAN OUT OF TIME & COULDN’T FINISH SUMMARY Nuclei Location Striated? Shape Axon contact? Conscious control Autonomic control T-tubule location Myofibrils? External lamina? Anchored by Tissue Coverings SKELETAL Many Peripheral Yes Cylinder All Yes No A/I Yes Yes Endomysium Epimysium Perimysium Endomysium CARDIAC 1–2 Central Yes Branched Purkinje fibers No Yes Z Yes Yes Intercalated disc Epicardium Endocardium SMOOTH 1 Central No Spindle Some No Yes ? No Yes CT CT