anatomy exam 3

Role of calcium in muscle contraction: -t tubules allow conduction of electrical impulses to the itnerior of the myocyte -these electrical impulses signal for the release of Ca2+ from adjacent terminal cisternae into the sarcoplasm -the Ca2+ binds to troponin which moves tropmyosin so the myosin binding sites of Factin are exposed & muscle contraction occurs

In order to contract, a myocyte (muscle fiber) must: 1)be stimulated by a nerve ending (activated) so change in membrane potential occurs 2)propogate an electrical current, or AP, along its sarcolemma 3)have a transient rise in sarcoplasmic Ca2+ concentration, which is the final trigger for contraction -Excitation-contraction coupling is the linkage of the sarcoplasmic electrical signal to the contraction

Membrane potential changes are caused by 3 events: 1)depolarization: inside of membrane becomes less negative (so more positive) 2)repolarization:membrane returns to its resting membrane potential 3)hyperpolarization:inside of membrane becomes more negative than resting potential

Signaling by membrane potential changes: 1)used to integrate, send & receive information 2)membrane potential changes are produced by changes in membrane permeability to ions 3)types of signals-graded potentials & action potentials

Nervous system: PNS 1)sensory(afferent) division: -sensory afferent fibers: carry impulses from sensory receptors in sensory organs,skin,skeletal muscles, & joints to brain -visceral afferent fibers-transmit impulses from visceral organs to brain 2)motor (efferent) division: -transmits impulses from CNS to effector organs: a)somatic nervous system-conscious control of skeletal muscles b)autonomic nervous system (ANS)-regulates smooth & cardiac muscle, & glands -two divisions: sympathetic & parasympathetic

The two principal cell types of nervous system are: 1)Neurons-excitable cells that transmit electrical signals 2)supporting cells (glial cells= neuroglia)-cells that surround & wrap neurons: -provide supportive scaffolding for neurons -segregate & insulate neurons -guide young neurons to proper connections during development -promote growth during development & maintain neuronal health after development

cellular anatomy: (skeletal) -a single muscle cell is a myocyte or muscle fiber -each myocyte is a long, cylindrical cell w/multiple nuclei made of multiple precursor cells= myoblasts -myocyte size:10 to 100 um in diameter, up to many tens of cm long -sarcoplasm has numerous glycosomes and an oxygen binding protein called myoglobin -myocytes contain the usual organelles and special components such as myofibrils, sarcoplasmic reticulum, and T-tubules -glycosomes=granules of stored glycogen that provide glucose during muscle cell activity -myoglobin=red pigment that stores oxygen

(skeletal) myofibrils: densely packed, rodlike contractile elements that make up most of myocyte/cell volume -the arrangement of myofibrils within the fiber results in a perfectly aligned repeated series of dark A bands & light I bands (these bands align perfectly in an intact muscle fiber giving striated appearance) -myofibrils contain sarcomeres, which is the smallest contractile unit of a muscle -sarcomere (muscle segment) is the region of the myofibril between two successive z discs and is composed of thick & thin myofilaments made up of contractile proteins -each dark A band has a lighter region in its midsection called the H zone -Each H zone has a dark vertical line through it=M line (M=middle) formed by myomesin -Each light I band also has a midline, darker area called Z disc/line -contains A band, flanked by half an I band at each end -sarcomeres within each myofibril align end to end like boxcars in a train

-All muscle converts the chemical energy of ATP into mechanical energy (and heat) -3 types of muscle tissue:skeletal, cardiac, & smooth -these types differ in structure, location, function, and means of activation -contraction of all muscle types utilize two kinds of protein myofilaments (actin & myosin) -many of the same terms are used in all muscle: -sarcolemma=muscle cell of plasma membrane -sarcoplasm=cytoplasm of a muscle cell -prefixes (myo, mys, & sarco=muscle)

-Excitatability(excitation-contraction coupling): -muscle cells respond to neuronal input, stretch, or other signals by changing their sarcolemma electrical potential (voltage) -the electrical potential change is coupled to intracellular changes that result in force generation (contraction) -contractility=active shortening of muscle cell & generation of tension (force) -extensibility=passive stretching of muscle cells -elasticity=return of muscle cells to original resting length after being stretched

smooth muscle tissue: -helps maintain blood pressure -found in hollow visceral organs, such as stomach, intestines, urinary bladder and uterus, & in blood vessels & respiratory passages -dilates & constricts eye pupils, forms the arrector pili muscles attached to hair follicles -forces food & other substances through internal body cavities/channels -not striated & contractions are slow & sustained= involuntary control -elongated cells, no striations

-each skeletal muscle is a discrete organ composed of muscle cells, blood vessels, nerve fibers, & connective tissue -the 3 connective tissue sheaths are: 1)endomysium=(within the muscle)fine sheath of connective tissue composed of reticular fibers surrounding each muscle fiber (surrounds each individual muscle fiber) 2)perimysium=(around the muscle) fibrous connective tissue that surrounds groups of muscle fibers called fascicles (muscle fibers grouped into fascicles, that resemble bundles of sticks, perimysium surrounds each fascicle) 3)epimysium=(outside the muscle) outer layer of dense regular connective tissue surrounding entire muscle

-muscle (organ)=surrounded by epimysium -fascicle(portion of the muscle)=surrounded by perimysium -muscle fiber (cell)=surrounded by endomysium -each muscle is served by one nerve, one artery, and 1 or more veins -each skeletal muscle fiber(cell) is supplied with a nerve ending that controls contraction/its activity -contracting fibers require continuous delivery of oxygen & nutrients from the blood via arteries -wastes must be removed by the blood via veins

-most skeletal muscles span joints and are attached to 2 or more bones -when muscles contract, the moveable bone (insertion) moves toward the immovable bone (origin) -muscles attach: 1)directly=(fleshy attachments)(& are less common) epimysium of the muscle is fused to the periosteum of a bone 2)indirectly=(more common) connective tissue wrappings extend beyond the muscle as a tendon or aponeurosis (-tendons & aponeurosis) -indirect more common bc their durability & small size

upper/forearm: 1)forearm extension: -triceps brachii is prime mover of forearm extension 2)forearm flexion: -brachialis & biceps brachii are chief forearm flexors -the brachioradialis of forearm acts as synergist & helps stabalize elbow

1)Anterior forearm: the muscles are primarily flexors of wrist & fingers (flexor digitorum superficialis, flexor carpi ulnaris, palmaris longus, flexor carpi radialis, pronator quadratus, flexor pollicilis longus, brachioradialis, pronator teres) 2)posterior forearm: muscles primarily extensors of wrist/fingers (ext.pollicilis longus & brevis, abductor pollicis longus, extensor digitorum, ex.carpi radialis brevis, extensor carpi radialis longus, ex.indicis, ext.carpi ulnaris)

Lever systems: 1)lever:rigid bar that moves on a fulcrum, or fixed point 2)effort: force applied to lever 3)load:resistance moved by the effort effort x length of effort arm= load x length of load arm (force x distance) = (resistance x distance)

1)power lever=lever operates at a mechanical advantage 2)speed lever=lever operates at a mechanical disadvantage (take more effort than what the load is to move the load)

-force of muscle contraction depends on number of myosin cross bridges attached. factors that increase force of skeletal muscle contraction: 1)more motor units recruited, greater the muscle force 2)bulkier muscle,more tension it can develop & greater its strength 3)high freq. of stimulation (wave summation & tetanus) 4)muscle & sarcomere stretched slightly over100% of resting length (so degree of muscle stretch) 5)more rapidly a muscle is stimulated, the greater the force it exerts (ex.tetanus)

2 classes of skeletal muscle fibers: 1)slow 2)fast -speed of contraction(speed/ velocity of fiber shortening) determined by speed with with myosin ATPase split ATP -ATP forming pathways: 1)oxidative fibers=use aerobic pathways (oxygen using) 2)glycolytic fibers=use anaerobic glycolysis -these 2 criteria define 3 categories 1)slow oxidative fibers 2)fast oxidative fibers 3)fast glycolytic fibers

AP:2)depolarization phase: -graded potential depolarizes membrane to threshold voltage -critical level of dep.(to-55to-50mV) for opening of VG Na+ channels -VG Na+ gates are opened; VG K+ gates stay closed -Na+permeability increases; reverses (depolarizes) -weak (subthreshold) stimuli dont generate action potential

AP:3)repolarization phase: -VG Na+ channel inactivation gates close -membrane permeability to Na+ declines rapidly to resting levels -as Na+gates close, VG K+ channels open -K+ exits cell * internal negativity of resting neuron is restored (repolarization)

Neurotransmitters: -chemicals used for neuronal communication w/body&brain -over 100 different neurotransmitters have been identified -can be classified chemically or functionally -chemical classification main classes: 1)Acetylcholine (ACh) 2)biogenic amines 3)amino acids 4)peptides 5)novel messengers: ATP & dissolved gases(NO & CO)

Acetylcholine (ACh): -first neurotransmitter identified, & most studied -released @neuromuscular junction -synthesized & enclosed in synaptic vesicles -degraded by enzyme acetylcholinerase (AChE) -released by: 1)all neurons that stimulate skeletal muscle 2)some neurons in autonomic nervous system (ANS)

Shape & phases of an AP: 1)resting state at -70mV 2)depolarization(rising) 3)repolarization(begins falling 4)hyperpolarization (below threshold) 1)threshold at -70mV

Action potential:1)Resting state -voltage gates (VG) Na+ & K+ channels closed (bc nothing there to stimulate them) -K+ leak channels cause slight permeability to K+(so membrane potential=-70mV) -Each VG Na+ channel has 2 voltage regulated gates: 1)activation gates:closes in resting state 2)inactivation gates:open in resting state

Graded potentials: -short lives, local changes in membrane potential -decrease in intensity with distance (decremental in nature) -their magnitude varies directly with strength of stimulus -suffiently strong graded potentials can initiate action potentials -this is type of membrane potential change in dendrites

Action potentials: -fast reversal of membrane potential with total amplitude of ~100mV -only generated in muscle cells & neurons &dont decrease in strength over distance (all APs same regardless of stimulus stength) -are the principal means of inter-neural communication, & neural communication to effectors -an AP in axon of a neuron is also called a nerve impulse -All-or-none phenomenon: action potentials either happen completely , or not at all

a)direct phosphorylation -CP-ADP reaction catalyzed by enzyme creatine kinase -1 ATP per CP -no Oxygen used -energy for 15 secs -ex. for 100 m dash b)anaerobic pathway -glycolysis & lactic acid form -glucose energy source -no oxygen used -2 ATP per glucose, lactic acid -energy for 30-40+secs c)aerobic pathway: -uses glucose, pyruvic acid;free fatty acids from adipose tissue, amino acids from protein catabolism -requires oxygen -products=32 ATP per glucose, CO2, H2O, -gives energy for hours= marathon

Anaerobic pathway: glycolysis & lactic acid formation -when muscle contractile activity reaches 70% of maximum: -bulging muscles compress blood vessels -oxygen delivery & blood flow impaired -pyruvic acid is converted into lactic acid which: 1)diffuses into bloodstream 2)picked up & used as fuel by liver, kidney, & heart(as energy source) 3)can be converted back into pyruvic acid(& eventually into glucose) by the liver (& release it back into the bloodstream for muscle use, or convert it to glycogen for storage)

AP:4)hyperpolarization phase: -VG K+gates remain open, causing excessive efflux of K+ -this effluc causes hyperpolarization of membrane (undeshoot) -neuron is less sensitive to stimulus & depolarization during this time (refractory period)

Coding for stimulus intensity: -all action potentials are alike/same regardless of stimulus strength -however, strong stimuli can generate an action potential more often than weaker stimuli

action potential: a transient change in plasma membrane (voltage)/electrical depolarization event that includes polarity reversal of a sarcolemma(or nerve cell membrane) & the propagation of the wave of depolarization along the membrane -AP is the result of a predictable sequence of electrical changes. Once initiated, occur along entire surface of sarcolemma (once threshold reached, AP is generated/initiated)

Effect of ACh on sarcolemmal electrical potential: -ACh binds to its receptors at the motor end plate -binding opens ligand-gated channel function of ACh receptor -small amount of Na+ diffuses into myocyte & inside of the surface of sarcolemma becomes less negative -this is called the depolarization end plate potential of myocyte -this depolarization then spreads out on rest of sarcolemma in both directions by opening of voltage-gated Na+ channels (depolarizing phase of action potential) (ACh binding opens channels=more Na+ in than K+ out=depolarization =becomes less negative

Muscle tone:low levels of contractile activity in relaxed muscle=constant, low level stimulation of muscles (doesnt produce active movement) -keeps muscles firm, healthy &ready to respond to stimulus -spinal reflexes account for muscle tone by: activating motor unit & then another, and by responding to activation of stretch receptors in muscles & tendons

Energy for contraction: ATP is only source used directly for contractile activity(so must be generated as quickly as its broken down to use) -as soon as available stores of ATP hydrolyzed, they're regenerated by: 1)direct phosphorylation of ADP by creatine phosphate(CP to ADP) 2)anaerobic,glycolysis,which converts glucose to lactic acid 3)aerobic respiration(glucose, fatty or amino acids plus O2 are fuel) -ATP also required for muscle relaxation: Ca2+ ATPase in SR takes Ca2+ ions out of sarcoplasm back to SR &requires ATP

1)resting membrane potential set by Na+ & K+, higher permeability to K+ 2)initial depolarizing membrane potential change by binding ACh to its receptor & opening its ligand-gated Na+ channel function(end plate potential) 3)Voltage gated Na+ channels next to neuromuscular junction sense depolarization & open transiently to allow Na+ to enter cell(normally Na+ restricted from entering), starting a wave of depolarization along the sarcolemma(AP propogation) 4)repolarization(restoring the sarcolemma to its initial polarized state)occurs as the voltage gated Na+channels close & voltage gated K+ channels open to allow K+ to flow out of the cell down its concentration gradient -since the K+ conc. is way higher inside cell than outside, K+ diffuses rapidly out of muscle fiber & into cell, restoring negatively charged conditions inside -repolarization occurs in same direction as depolarization & must occur b4 muscle can be stimulated again(refractory period) -ionic concentration of resting state is restored by Na+-K ATPase Pump -Depolarization bc Na+ entry -top of peak, Na+ closes,K+ opens -repolarization due to K+ exit

Excitation-contraction coupling: when voltage sensitive tubule proteins change shape, cuases Ca2+ release channels in terminal cisterns of SR to open, so Ca2+ flows out into cytosol -once generated, the AP: +is propogated along sarcolemma away from NM junctions +travels down T tubules +triggers Ca2+ release from terminal cisternae of SR -Ca2+ binds to troponin & causes: +blocking action of tropomyosin to cease, myosin binding sites on actin to be exposed, and myosin cross bridges alternately attach & detach (cross bridge formation=attachment of myosin heads to actin, requires Ca2+) -thin filaments move toward center of sarcomere (as long as calcium signal & adequate ATP present) -energy from ATP hydrolysis powers this cycling process -Ca2+ is taken back up into sarcomere into SR, tropomyosin blockage is restored, & muscle fiber relaxes -low calcium levels=relaxed muscle cell & tropomyosin blocks active (myosin-binding) sites on actin -tropomyosin blockade removed when sufficient Ca2+ present -once binding sites on actin exposed=events at cross bridge cycle occur rapidly -each time an AP arrives at NM junction, sequence of EC coupling is repeated -once EC coupling over, cross bridge cycling begins

channel-linked receptors (direct mechanism): -composed of integral membrane protein -action is immediate, brief, simple & highly localized -neurotransmitter binds receptor & specific ions enter cells -excitatory receptors depolarize membranes -inhibitory receptors hyperpolarize membranes

Gprotein coupled receptors(GPCRs): -reponses are indirect, slow, complex, prolonged, &often diffuse -GPCRs are integral membrane protein complexes -ex. muscarinic ACh, neuropeptide, &biogenic amine receptors -representative mechanism ex. 1)neurotransmitter binds to GPCR 2)G-protein is activated & GTP is hydrolyzed to GDP 3)activated Gprotein complex activates adenylate cyclase 4)Adenylase cyclase converts ATP to cAMP (a second messenger) 5)cAMP brings about various cellular responses (cAMP changes membrane permeability by opening or closing ion channels)

Muscle twitch: response of muscle to a single AP stimulus of its motor neuron -muscle fibers contract quickly & then relax -external tension always less than internal tension, but when muscle stimulated rapidly, contractions are summed, becoming stronger & more vigorous & ultimately producing tetanus) -3phases of twitch monogram 1)latent period:first few milli-seconds after stimulation, hen EC coupling taking place (cross bridges begin to cycle but muscle tension not yet measureable & myogram shows no response) 2)period of contraction (upslope):cross bridges are active/cycle& muscle shortens /develops tension 3)period of relaxation:Ca2+ is sequestered into SR & muscle tension goes to zero -if muscle shortened during contraction, now returns to its initial length -calcium gets low enough that all myelin binding sites are covered/dont generate force

Graded muscle responses:variations in amount/degree of force generation during muscle contraction by changing either frequency or strength of stimulus) -required for proper control of skeletal movement -responses are graded by changing the frequency (AP) or strength of stimulation_____________ -a single stimulus results in single contractile response=a muscle twitch -low stimulus frequency increases contractile force bc muscle doesnt have time to completely relax=wave summation -higher stimulus frequency result in incomplete tetanus -if stimulus frequency is high enough, complete tetanus results (all evidence of muscle relaxation disappears=smooth picture) -if 2 identical stimuli delivered to muscle rapidly,2nd twitch will be stronger than 1st=wave/temporal summation, bc 2nd contraction b4 muscle has completely relaxed -2nd contraction also causes more shortening than 1st -basically, contractions added together/summed -refractory period=if 2nd stimulus arrives b4 repolarization complete, no wave summation occurs

Role of Ca2+ in contraction (smooth muscle): -Ca2+ binds to calmodulin & activates it -activated calmodulin activates the MLCK (myosin light chain kinase) enzyme -activated MLCK transfers phosphate from ATP to myosin head group -phosphorylated myosin head groups can hydrolyse ATP & interact w/actin -as long as enough ATP present, power stroke occur to produce shortening -smooth muscle relaxes when intracellular Ca2+ conc. drops & the above steps reversed -smooth muscle takes 30xs longer to contract & relax than skeletal, but can maintain same contractile tension for longer & use less energy to do it

Growth of smooth muscle: (makes ATP via aerobic pathway) -some smooth muscle cells can undergo mitosis & increase their numbers by undergoing hyperplasia (different than skeletal) -this is seen in estrogen's effect on the uterus: 1)at puberty, estrogen stimulates synthesis of more smooth muscle, causing uterus to grow to adult size 2)during pregnancy, estrogen stimulates uterine growth to accomodate increasing size of growing fetus -hypertrophy=increase in cell size (all muscle cells can) -hyperplasia=divide to increase their number (certain smooth muscle fibers can do this) -atrophy=wasting away of muscles, decrease in muscle size

Hand (intrinsic): -small muscles lie in palm of hand (none on dorsal side) -control precise movements (ex.threading a needle) -main abductors & adductors of fingers -produce opposition, move the thumb toward little finger

Hip/thigh: -ball and socket hip joint permits flexion, extension, abduction, adduction,circumduction,& rotation -most important thigh flexors are iliopsoas(prime mover), tensor fasciae latae, &rectus femoris -medially located adductor muscles & sartorius assist in thigh flexion -thigh extension primarily affected by hamstring muscles (biceps femoris, semitendinosus, semimembranosus) -forceful extension aided by gluteus maximus

Phases leading to muscle fiber contraction: Phase 1( motor neuron stimulates muscle fiber) 1)AP arrives at axon terminal at NM junction 2)ACh released;binds receptors on sarcolemma 3)ion permeability of sarcolemma changes 4)local change in membrane voltage (depolarization)occurs 5)local depolarization(end plate potential)ignites AP in sarcolemma Phase 2(EC coupling occurs): 6)AP travels across the entire sarcolemma 7)AP travels along T tubules 8)SR releases Ca2+;Ca2+ binds to troponin; myosin- binding sites (active sites)on actin exposed 9)myosin heads bind to actin;contraction begins

Innervation of skeletal muscles: -skeletal muscles are stimulated by motor neurons (nerve cells that activate skeletal muscle fiber) of somatic nervous system(voluntary) -skeletal muscle must be stimulated by a motor neuron or it will not contract (paralysis) -axons of these neurons travel in nerves to the muscle cells that they serve, but their cell bodies are in the brainstem & spinal cord -axons of motor neurons branch profusely as they enter muscles -each axonal branch forms a neuromuscular junction(end plate) with a single myocyte(muscle fiber) -each motor neuron & all the myocytes it innervates is called a motor unit -each muscle fiber has only 1 NM junction, which is located ~midway along its length

unique smooth muscle characteristics: -smooth muscle tone (state of partial contraction) -slow, prolonged contractile activity -low energy requirements -some smooth muscle exhibits a phenomenon called Stress-Relaxation Response: -smooth muscle responds to stretch only briefly, & then adapts to its new length -the new length however, retains its ability to contract -this enables organs such as the stomach, urinary bladder, & uterus to temporarily expand to store contents (good bc if didnt have this, we'd spend 24/7 in bathroom)

Innervation of smooth muscle: -smooth muscle cells do not directly receive neural input (bc no true neuromuscular junctions) -contraction of smooth muscle is involuntary -innervating nerves have bulbous swellings called varicosities -varicosities release neurotransmitters into wide synaptic clefts called diffuse junctions

Shortening of muscle: cross bridge cycling: (series of events where myosin heads pull thin filaments toward center of sarcomere) 1)cross bridge formation-myosin heads attaches to actin filament 2)working power stroke-myosin head pivots & pulls actin filament toward M line (if no ATP present, myosin heads wont detach=rigor mortis) 3)cross bridge detachment-ATP binds to myosin head & cross bridge detaches 4)cocking of myosin head-energy from hydrolysis of ATP cocks myosin head back into high energy state

Length-tension relationship: (of sarcomeres) -amount of tension muscle develops depends on length of muscle before stimulation -if muscle short at beginning of contraction: thin filaments overlap & disrupt sarcomere structure -if muscle long at beginning of contraction:very little overlap of thin & thick filaments so fewer number of cross bridges can form -optimal length4 force generation: all myosin heads can form cross bridges w/thin filaments but there is no thin filament overlap -a muscle generates maximum foce when its between 80&120% of its optimal resting length -increases/decreases beyond this range reduce its force/ability to generate tension

Knee: -sole extensor of knee is quadriceps femoris -hamstring muscles flex knee, & are antagonists to quadriceps femoris Foot: -these muscles help flex,extend, abduct, & adduct toes -in addition, along with some leg tendons, they support arch of foot -there is a single dorsal foot muscle, the extensor digitorum brevis, which extends the toes

Lower leg/foot: 1)these anterior muscles are primary toe extensors & ankle dorsiflexors: -tibialis anterior, extensor digitorum longus, extensor hallucis longus, & fibularis tertius 2)these lateral compartment muscles plantar flex & evert foot -they include fibularis longus & fibularis brevis muscles 3)these posterior compartment muscles primarily flex foot & toes -they include gastrocnemius, soleus, tibialis posterior, flexor digitorum longus, & flexor hallucis longus

Chemical synapses: -specialized for release & reception of neurotransmitters -typically composed of 2 parts 1axonal terminal-of presynaptic neuron (presynaptic knob),which contains synaptic vesicles 2receptor region-on dendrites or soma of postsynaptic neuron (postsyn. membrane) -synaptic cleft: 1)fluid filled space separating pre & postsynaptic neurons 2)prevents nerve impulses from directly passing from one neuron to next 3)transmission across synaptic cleft: -is a chemical event -ensures unidirection communication between neurons

Mechanism of chemical communication: 1)nerve impulses (APs) reach axonal terminal of presynaptic neuron & open Voltage gated Ca2+ channels 2)neurotransmitter released from vesicles into synaptic cleft via exocytosis 3)neurotransmitter diffuses across synaptic cleft & binds to specific receptors on postsynaptic neuron 4)postsynaptic membrane ion permeability changes, causing an excitatory or inhibitory electrical effect

Neurotransmitter functional classification: 1excitatory-neurotransmitters cause depolarizations -EPSPs (glutamate) 2)inhibitory neurotransmitters cause hyperpolarizations -IPSPs (Gaba & glycine) -some neurotransmitters have both excitatory & inhibitory effetcs -determined by receptor subtype of postsynaptic neuron ex. ACh: excitatory at NMjunction w/skeletal muscle ,inhibitory in cardiac muscle

Mechanisms of action of neurotransmitter receptors: 1)direct:neurotransmitters that open ion channels -promote rapid reponses ex. ACh & amino acids 2)indirect:neurotransmitters that act through second messengers -promote slower but more long- lasting effects. ex. biogenic amines, peptides, & dissolved gasses

CARDIAC MUSCLE: -found only in heart -striated like skeletal -mechanism of contraction same as skeletal -has significant differences from skeletal muscle: -myocytes are branched -myocytes joined to eachother at intercalated discs (mechanical syncytium) -gap junctions in intercalated discs allow electrical signaling between myocytes (electrical syncytium) -requires some Ca2+ from extracellular fluid to enter for contraction to occur -very long action potentials (200-300millisecs) compared to skeletal (2-5millisecs)

Muscle tissue develops from embryonic cells called myoblasts -multinucleated skeletal muscles form by fusion of many myoblasts -as muscles brought under control of somatic( voluntary) nervous system, numbers of fast & slow also determined -cardiac & smooth muscle myoblasts dont fuse= develop gap junctions at early embryonic stage

1)First class lever system: the fulcrum is between the load and effort (LFE) ex.in body=raises your head off chest. neck muscles provide effort, atlanto occipital joint is fulcrum, weight lifted is facial skeleton 2)Second class lever system: load between fulcrum & effort (FLE) ex.when stand on tip-toe -effort:calf muscles pulling up on heel, joints of ball of foot are fulcrum, & weight of body is load

Muscles for moving head: -major head flexor is sternocleidomastoid -synergists to head flexion are suprahyoid & infrahyoid -lateral head movements done by sternocleidomastoid & scalene -head extension accomplished by deep splenius muscles & aided by superficial trapezius

1)Slow oxidative fibers(muscle fiber best for endurance type activities like marathon): contract slowly bc myosin, have slow acting myosin ATPase & are fatigue resistant (thin, little power, 1st in recruitment,has mitochondria) 2)fast oxidative fibers(sprints, walking):contract quickly, have fast myosin ATPase, & moderate resistance to fatigue 3)fast glyoclytic fibers(best for short term,rapid, intense movements like moving furniture across room of hitting baseball): contract quickly, have fast myosine ATPase, are easily fatigued (no oxygen used)

Muscular dystrophies: group of inherited muscle-destroying diseases where muscles enlarge due to fat & connective tissue deposits, but muscle fibers themselves atrophy & degenerate -most are progressive diseases that start w/mild symtomology(muscle weakness) & progress to debilitation & finally death

Smooth muscle cellular characteristics: -SR less developed than in skeletal&lacks specific pattern -T tubules absent, instead plasma membranes have pouchlike infoldings called caveoli(caveolae)=sequestered bits of extracellular fluid containing high conc. of Ca2+ close to membrane( when Ca2+channels in caveolae open, Ca2+ influx occurs fast (different from skeletal muscle, which doesnt depend on extracellular Ca2+ for EC coupling) -no visible striations & no sarcomeres -thin (actin) & thick (myosin) filaments are present -involuntary

Myofilament characteristics: -ratio of thick to thin filaments is much lower than in skeletal muscle -so fewer thick filaments -thick filaments have heads along their entire length (actin-gripping myosin heads) -no troponin complex (instead has protein called CALMODULIN, that acts as the calcium binding site) -thick & thin filaments arranged diagonally causing smooth muscle to contract in a corkscrew manner -noncontractile intermediate filament bundles attach to dense bodies (analogous to Z discs in cardiac muscle) at regular intervals -dense bodies act as anchoring points for thin filaments -dense bodies=cytoplasmic structures

Glial cells: 1)astrocytes: most abundant, versatile, & highly branched glial cells. they cling to neurons & their synaptic endings, & cover capillaries -functionally, they: a)SUPPORT & brace neurons b)ANCHOR neurons to their nutrient supply/blood vessels c)GUIDE MIGRATION of young neurons d)CONTROL the chemical environment 2)microglia: small, ovoid cells with spiny processes -transform into phagocytes that monitor neurons health & gobble up debris & infectious microorganisms 3)Oligodendrocytes (CNS):branched cells that wrap & insulate CNS nerve fibers from other neurons 4)Schwann cells(PNS): cells that wrap around fibers of the PNS neurons -serve to insulate & increase conduction velocity of action potentials down nerve fibers (Satellite & Schwann cells form myelin which surrounds neurons in PNS)

Nerve cells (Neurons): -basic structural & functional units of nervous system -composed of a cell body (some), one axon, & many dendrites -bc are amitotic,must be long-lived (last throughout lifetime) -have high metabolic rate (so require constant source of oxygen & glucose) -Their plasma membrane functions in: 1)electrical signaling 2)cell-to-cell signaling during development -dendrites-receive information from other neurons -soma-processing center & biosynthetic center of neuron -axon-output information to effectors via action potentials structural neuron classes: 1)multipolar: most abundant in body, major neuron of CNS 2)bipolar:rare, some sensory organs like eye or ear 3)unipolar:mainly in PNS, common in dorsal root ganglia of spinal cord & sensory ganglia of cranial nerves

Chapter 11:NERVOUS SYSTEM: the body's master control & communication system -Functional organization: 1)sensory(afferent)input- monitoring stimuli occurring inside & outside body 2)integration-interpretation of sensory input by CNS 3)motor(efferent) output- response to stimuli by activating effector organs

Nervous system-anatomical organization: 1)Central nervous system -consists of brain & spinal cord -integration & command center 2)peripheral nervous system(PNS): -paired spinal & cranial nerves -carries messages to & from CNS (all of the nervous system outside the CNS) (sensory input & motor output)

-The neuromuscular junction consists of: axon terminals, synaptic cleft, junctional folds of the sarcolemma -axon terminal, has small membranous sacs(synaptic vesicles) that contain the neurotransmitter acetylcholine(ACh) -the motor endplate of a myocyte, is a specific of the sarcolemma that contains ACh receptors -though very close, axon terminals & motor endplates are always separated by a space called synaptic vesicles(synaptic cleft)

Neuromuscular toxins & paralysis: -many pesticides contain inhibitors of acetylcholinesterase that to its active site & prevent it from degrading ACh: this can cause rigid paralysis & suffocation 1)Tetanus(lockjaw) is a spastic rigid paralysis caused by a toxin produced by Clostridium bacteria[basically a bacterial disease that causes severe unvoluntary contractions) (toxin blocks release of inhibitory neurotransmitter in spinal cord & causes overstimulation of muscles) 2)Curare-from skin of poisonous frogs in central & south america blocks the action of Ach by preventing it from binding to its sarcolemma receptor -causes flaccid paralysis w/no loss of consciousness

second messengers activated by GPCRs: -GPCRs activate intracellular second messengers including Ca2+, cGMP,diacylglycerol, & cAMP -second messengers: 1)open or close ion channels 2)activate kinase enzymes which can phosphorylate channel proteins 3)activate/inactivate genes & change protein synthesis

Neuronal pools(circuits): -functional groups of neurons that integrate incoming information & forward processed info to its appropriate destination -simple neuronal pool: 1)input fiber=presynaptic fiber 2)discharge zone=neurons most closely associated w/incoming fiber 3)facilitated zone=neurons farther away from incoming fiber

Neuronal Pools: 1)divergent: one incoming fiber stimulates ever increasing number of fibers, often amplifying circuits (would process sensory info) 2)convergent: opposite of divergent circuits, resulting in either strong stimulation or inhibition

Neuronal pools:reverberating: chain of neurons containing collateral synapses w/previous neurons in each chain -signals travel through a chain of neurons, each feeding back to previous neurons -an oscillating circuit -controls rhythmic activity -ex.involved in breathing, sleep-wake cycle, & repetitive motor activities such as walking

Two patterns of neural processing: 1)serial processing -input travels alone 1 pathway to a specific destination -works in an all-or-none manner (ex.spinal reflexes) 2)parallel processing -input travels along several pathways -pathways integrates in different CNS systems -one stimulus promotes numerous responses ex.a smell may remind you of odor & associated experiences

Pathophysiology: Multiple sclerosis (MS): an autoimmune disease that mainly affects young adults -symptoms include visual disturbances, weakness, loss of muscular control, & urinary incontinence -myelin sheaths in CNS degenerate & become nonfunctional scleroses (scars) -shunting & short-circuiting of nerve impulses occurs

Biogenic amines: include: 1)GABA (Gamma aminobutyric acid) 2)Glycine 3)aspartate 4)glutamate -Found only in CNS -can be excitatory (generate EPSPs) or inhibitory (generate IPSPs)

Peptides:(P stands for pain)include: 1)Substance P-mediator of pain signals 2)beta endorphin, dynorphin, & enkephalins -act as natural opiates, reducing out perception of pain -bind to the same receptors as opiates & morphone -gut-brain peptides=somatostatin, & cholecystokinin

Action potentials: or nerve impulses, are: -electrical impulses originating at soma & carried along length of axons -always same regardless of stimulus -primary functional activity of nervous system

Physiological electrical current: -reflects flow of ions rather than electrons -there's a potential on either side of membranes when: 1)concentration of ions different across membrane 2)membrane provides resistance (barrier) to ion flow

Electrical definitions: 1)voltage(V):measure of potential energy generated by separated charge 2)potential difference-voltage measured between 2 points 3)current (I)-flow of electrical charge between 2 points 4)resistance (R)-hindrance to charge flow 5)insulator-substance with high electrical resistance 6)conductor-substance with low electrical resistance

Plasma membrane ion channels: -provide defined path for ions to cross plasma membrane -types of plasma m. ion channels: 1)passive(leak)channels:always open 2)chemically-gated channels: open with binding of specific neurotransmitter 3)voltage-gated channels:open & close in response to membrane potential 4)mechanically-gated channels: open & close in response to physical deformation of channel of membrane

Absolute refractory period: -time from opening of Na+ activation gates through closing of inactivation gates & return to their closed states -it prevents neuron from generating an AP -ensures each AP is separate -enforces one-way transmission of nerve impuses (anteriograde=toward axon terminal) (beginning of AP, includes resting state, depol. & stops once repolarization starts)

Relative refractory period: -interval following absolute refractory period when: 1)VG Na+ channels closed 2)VG K+ channels are in process of closing 3)repolarization is occuring -the threshold level is elevated, so only strong stimuli will cause another action potential (includes beginning of repolarization, hyperpolarization)

electrochemical gradient:the electrical & chemical gradients taken together 1)ions flow with their chemical gradient when they move from an area of high conc. to an area of low concentration 2)ions flow with their electrical gradient when they move toward an area of opposite charge -when gated channels are open: 1)specific ions move quickly across membrane 2)movement is in direction of their electrochemical gradient 3)electrical current is created 4)voltage channels across the membrane

Resting Membrane Potential (Vr): -the potential difference (~-70mV) across membrane of resting neuron -generated by different concentrations of Na+, K+, Cl-, & protein anions (A-) -ionic differences consequence of: 1)diff.permeability of plasma membrane to Na+(low) vs. K+(high) 2)operatin of Na+/K+ATPase pump -Resting membrane potential is~70mV bc: 1)plasma membrane is more permeable to K+(more leaks out) 2)less permeable to Na+ (very little leaks in) 3)Na+/K+ ATPase pumps 3 Na+ out per 2K+ in: -works continuously & uses alot of ATP -primary reason neurons require constant supply of O2 & glucose -most cytoplasmic anions (proteins, phosphates, nucleotides,organic acids) CANNOT LEAK OUT due to size or charge

Efficiency of muscle energy utilization: -only 40% of energy released in muscle activity is converted into work -remaining 60% is given off as heat (to maintain body homeostasis) -dangerous heat levels are prevented by radiation of heat from skin & evaporative cooling (sweating)

Rigor Mortis: stiffening of muscles beginning 3-4hrs after death -stiffness peaks at 12hrs & then declines over next 48 hrs -due to lack of ATP production following death caused by: 1)Ca2+ leaks out of SR into sarcoplasm(no ATP 4 Ca2+ATPase) 2)actin-myosin cross bridges form (but no power strokes bc no ATP) 3)static cross bridges remain until proteases start degrading the myofilament proteins

Skeletal muscle fibers contain 2 sets of intracellular tubules that help regulate muscle contraction: SR & T tubule -sarcoplasmic reticulum(SR): elaborate, smooth endoplasmic reticulum that runs longitudinally & surrounds each myofibril -paired terminal cisternae of SR form perpendicular cross channels @ A-I band junctions & always occur in pairs -functions to regulate intracellular calcium levels (bc calcium provides final "go" signal for contraction) -elongated tubes of sarcolemma called T-tubules penetrate into cells interior at each A-I band junction -T tubules associate w/the paired terminal cisternae to form triad junctions -triads=successive groupings of the 3 membranous structures (terminal cistern, T tubule, & terminal cistern) -T tubule encircle each sarcomere -T tubule=system that ensures that every myofibril in the muscle fiber contracts at the same time & conducts impulses that signal for the release of calcium from the adjacent terminal

Sliding filament model of contraction: -relaxed state=thin & thin filaments overlap (only at ends of the A band) but are not bound to each other -after the stimulus for contraction, the thin filaments slide past the thick ones so that the actin and myosin filaments overlap increases: -each myosin head binds & detaches to F-actin several times during contraction, acting like a ratchet to generate tension and pull the thin filaments towards the center of the sarcomere ("power stroke") -since the sarcomeres are arranged end to end in the myofibril & this occurs w/all the sarcomeres, the overall muscle generates force & shortens

Duchenne muscular dystrophy (DMD): -carried by females,but expressed almost exclusively in males, (1/3500) inherited, sex-linked recessive disease -usually diagnosed between the ages of 2-10 -victims become clumsy & fall alot as their muscles weaken -progresses from the distal extremities inward, & victims usually die of respiratory failure or cardiac complication in their 20s -cause:lack of cytoskeletal protein called dyastrophin (which helps stabilize sarcolemma, but with DMD patients, sarcolemma tears during contraction allowing excess Ca2+=apoptosis, muscle mass drops) -no cure, but some therapies that show promise

Smooth muscle characteristics: -composed of spindle-shaped fibers w/diameter of 2-10um & length upto a couple hundred um (much smaller than skeletal) -lack coarse connective tissue sheaths of skeletal muscle but have endomysium (fine conn. tissue) -usually 2 sheaths of smooth muscle w/their fibers oriented at right angles to eachother (intestine) (organized into 2 layers= longitudinal & circular of closely apposed fibers)(contract independ.) -found in walls of hollow organs (not heart),in respiratory, digestive, urinary, & reproductive tracts -uses the same contractile proteins (actin & myosin) as skeletal muscle -longitudinal layers=muscle fibers run parallel to long axis of organ. so when fiber contracts, organ dilates & shortens -peristalsis=alternating waves of contraction & relaxation of smooth muscle layers that mix/squeeze through lumen of hollow organs

Cardiac muscle summary: -walls of heart -has pacemaker -branching chains of cells; uni or binucleate; striations -endomysium attached to fibrous skeleton of heart -excitation or inhibition -has T tubule;1 in each sarcomere at Z discs; larger diameter than in skeletal -less SR than skeletal,but has SR;scant terminal cisterns -yes rhythmic contractions -gap junctions at intercalated discs -no neuromuscular junctions -involuntary; intrinsic system regulation & autonomic nervous system controles; hormones;stretch -gets Ca2+ from SR & extracellular fluid -troponin on actin-containing thin filaments -aerobic

Smooth muscle summary: -unitary muscle in walls of hollow visceral organs, multi-unit in intrinsic eye muscles, airways, large arteries -pacemaker in unitary muscle only -single,fusiform,uninucleate; no striations -endomysium -excitation or inhibition -no T tubules;only caveolae -has SR, same amount as cardiac; some SR contacts sarcolemma -rhythmic contractions in unitary muscle -gap junctions in unitary muscle -no neuromuscular junction in unitary muscle, but yes in multi unit muscle -involuntary; autonomic nerves, hormones, local channels, stretch -gets Ca2+ from SR, extracellular fluid -calmodulin in cytosol -mainly aerobic

muscles & aging: -with age, connective tissue increases & muscle fibers decrease, causing muscles to become stringier & sinewy -by age 80,50% of muscle mass is lost -regular exercise minimizes & partially reverses sarcopenia -aging of cardiovascular system affects every organ in body ATHEROSCLEROSIS:may affect distal arteries, leading to intermittent claudication (blockage) & causing severe pain in leg muscles, heart attacks or strokes ARTERIOSCLEROSIS:hardening of arteries; arteries become less elastic & more rigid as smooth muscle is replaced by connective tissue

Summary: Skeletal muscle: -attached to bones or skin -no pacemaker -single,long cylindrical multi- nucleate cells with striations -excitation -epimysium, perimysium & endomysium -has T tubule; 2 in each sarcomere at A-I junctions -has Sarcoplasmic reticulum -no rhythmic contraction -no gap junctions -cells exhibit individual NeuroMuscular junctions -voluntary contraction via axon terminals of somatic nervous syst. -gets Ca2+ from SR -Troponin on actin-containing thin filaments -aerobic & anaerobic

EPSPs:(Excitatory) -graded potentials that help initiate action potential on postsynaptic neuron -use only chemically gated channels -a single EPSP is a sub-threshold stimulus IPSPs:(Inhibitory) -neurotransmitter binding a receptor @inhibitory synapses 1)causes postsynaptic membrane to become more permeable to K+ & Cl-ions 2)makes charge on inner surface of membrane more negative (hyperpolarization) 3)inhibits postsynaptic neurons ability to generate an action potential

Summation of EPSPs & IPSPs: -a single EPSP cannot induce an AP -EPSPs must summate temporally or spatially to induce an AP -temporal summation=presynaptic neurons transmit impulses in rapid fire (high frequency) -spatial summation=postsynaptic neuron is stimulated by large number of presynaptic terminals at the same time -IPSPs can also summate with EPSPs, effectively canceling each other out

Saltatory conduction: -current passes through myelinated axon only at nodes of ranvier (gaps between ends of schwann cells_ -VG Na+ channels are concentrated at these nodes -action potentials triggered only at nodes & jump from 1 node to the next -much faster than conduction along unmyelinated fibers

Synapse: -a junction that mediates information transfer from one neuron to either: 1)another neuron 2)an effector cell -presynaptic neuron: conducts impulses toward the synapse -postsynaptic neuron:transmits impulses away from synapse

Myofilaments: -think filaments=extend the entire length of an A band (contain myosin protein) -contected to the sarcolemma & hold in alignment at the Z discs & M lines -thin filaments=extend across the I band & part way into the A band (contain actin) -Z disc=coin shaped sheet of connective tissue that anchors the thin filaments & connects myofibrils to one another -elastic filaments=stretch from z-disc through the thick filament to the M line & made from huge protein called titin -titan holds thick filaments in place & helps the muscle cell spring back into shape after stretching -thin filaments dont overlap thick fils in the lighter H zone -H zone of the A bands is less dense bc the thin filaments do not extend into it I band=thin filaments only H zone=thick filaments only M line=thick filaments linked by accessory proteins Outer edge of A band=thick & thin filaments overlap -the central portion of a thick filament (H zone) is smooth, but the ends are studded with staggered array of myosin heads

Thick Vs. Thin filaments 1)Thick filaments (myosin): -composed of 200-500 myosin protein molecules -each myosin has a rodlike tail & 2 globular heads -tails=2 interwoven, heavy protein/polypeptide chains -heads=2 smaller,light protein chains (during contraction heads link the thick & thin filaments together, forming cross bridges that act as motor neurons to generate force) -arranged in a bundle w/the heads protruding outward in a spiral pattern around bundles tails 2)Thin Filaments(actin): -primary contractile protein is F-actin, a double helical polymer of individual subunits called G-actin -Each G-actin subunit contains an active site to which a myosin head attaches during contraction -tropomyosin=filamentous protein bound in the grooves of the F-actin helix & blocks the myosin binding site in relaxed muscles so that myosin heads on thick filaments bind to the thin filaments -troponin=regulatory protein complex bound to F-actin & tropomysin & binds calcium ions -both troponin & tropomyosin help control the myosin-actin interactions involved in contraction -sliding of the thin filaments past the thick produces muscle shortening -in the sarcomere center, thick filaments lack myosin heads, which are only present in areas of myosin-actin overlap

Two types of smooth muscle: 1)single unit (unitary)-smooth muscle cells, commonly called visceral muscle: -contract rhythmically as a unit(innervated by varicosities) -electrically coupled to one another via gap junctions -often exhibit spontaneous action potentials -arranged in opposing sheets (longitudinal & circular) -found in digestive tract, most blood vessels, uterus, & urinary bladder -respond to various chemical stimuli

Two types of smooth muscle: 2)multi-unit (like skeletal muscle): -electrically & structurally independent muscle fibers (so act independently of each other) -infrequent spontaneous depolarizations -rich supply forms motor units -graded contractions in response to neural stimuli (that involve recruitment) -found in large airways to the lungs, large arteries, arrector pili muscles (attached to hair follicles), & in internal eye muscles -multi unit muscle & unitary smooth muscle is innervated by autonomic(involuntary) division & also responds to hormones (skeletal muscle served by somatic [voluntary] division of nervous syst.

Muscle fatigue:muscle is in a state of physiological inability to contract (even though muscle is receiving stimuli) -intense rapid exercise produces rapid muscle fatigue with rapid recovery (mostly due to ionic imbalances resulting in problems with EC coupling) -low-intensity exercise produces slow developing fatigue with slower recovery (maybe due to damage to SR resulting in decreased Ca2+ release) -Normally, fatigue is not due to muscle running out of ATP since its continuously being regenerated

Vigorous exercise causes dramatic changes in muscle chemistry -4 muscle to return to resting state 1)oxygen reserves (in myoglobin) must be replenished 2)lactic acid must be reconverted to pyruvic acid 3)glycogen stores must be replenished 4)ATP & CP(creatine phosphate) reserves must be restored -EPOC (excess postexercise oxygen consumption) = the extra amount of oxygen needed for the above restorative processes -all anaerobic sources of ATP used during muscle activity contribute to EPOC

Motor units: -1 motor neuron & all of the muscle fibers it supplies -each muscle has many motor units that are activated independently -the myocytes of a motor unit are distributes throughout the muscle -when a sub-maximal amount of force generation is needed, only a subset of motor units are activated: +the total force of contraction of a muscle is the summation of all the active motor units (spacial summation) +the motor units which are actively contracting can take turns & allow for a sustained long-term contraction w/out muscle fatigue -smaller motor units(few myocytes innervated by a motor neuron) are found where fine control is required (eye,finger, & larynx muscles), allows talking -large motor units(hundreds of myocytes per motor neuron) are found in large muscles (back,hip,leg) & movements less precise -muscle fibers in a single motor unit are not clustered together but spread throughout the muscles, as a result, stimulation of a single motor unit causes weak contraction of the entire muscle

When an AP reaches the end of an axon @the neuromuscular junction: 1)voltage-regulated Ca2+ channels open & allow Ca2+ to enter the axon terminal 2)Ca2+ inside the axon terminal causes axonal vesicles containing Ach to fuse with axonal membrane 3)this fusion releases ACh into the synaptic cleft via exocytosis 4)ACh diffuses across the synaptic cleft to ACh receptors on the sarcolemma 5)binding of the ACh to its receptos initiates an AP on the sarcolemma & causes a contraction 6)ACh in the synaptic cleft is chemically degraded by the acetylcholinesterase enzyme, which turns off signal & causes relaxation (Acetylcholinesterase breaks down ACh into its building blocks acetic acid & choline) -removal of ACh prevents continued (& usually undesirable) muscle fiber contraction in the absence of additional nervous system stimulation

arrangement of fascicles of muscles: fascicles are bundles of myocytes surrounded by perimysium membrane `parallel:fascicles run parallel to muscle long axis (sartorius) `fusiform:spindle shaped muscles (biceps brachii) `pennate:short fascicles that attach obliquely to a central tendon insertion (rectus femoris) `convergent:converge from broad origin to single tendon insertion (pectoralis major) `circular:arranged in concentric rings (orbic. oris) `multipennate (deltoid) `bipennate(rectus femoris) `unipennate(enxt.dig.longus)

attachment: usually to bone 1)direct attachment: -epimysium of muscle continuous with periosteum of bone 2)indirect attachment: -epimysium collects into a tendon or aponeurosis that attaches to periosteum via perforating fibers -most common(biceps brachii, gastrocnemius, etc) Intrinsic vs extrinsic muscles: 1)intrinsic: muscles contained within region that is moved by their contraction 2)extrinsic: muscles move body parts outside region where they are found

skeletal muscle tissue: -packaged into skeletal muscles that attach to & cover the bony skeleton -cells have obvious stripes called striations -controlled voluntarily (by conscious control) or reflexes -contracts rapidly but tired easily -provides the force responsible for overall body movement -very adaptable (exert force to pick up paper clip or a heavy book)

cardiac muscle tissue: -found only in heart -striated, but not voluntary -involuntary neural control allows heart to respond to changes in body requirements for oxygen & fuel delivery -contracts at rate set by body's pacemaker

Most axons in PNS myelinated: -white,fatty protein (20% protein/80% lipid), segmented sheath of schwann cells surrounding axons -functions to: 1)protect axon 2)electrically insulate fibers from one another 3)increase speed of nerve impulse transmission In CNS: -both myelinated & unmyelinated fibers present -myelin sheaths formed by oligodendryocytes instead of schwann cells

conduction speed of nerve impulses depends on: 1)diameter of axon (larger=faster) 2)myelination state (myelinated=faster) -example of conduction speedL 1)small unmyelinated fibers ~2.0m/second 2)small myelinated fibers ~15.0m/second 3)large myelinated fibers ~120m/second Relationship of speed of function: -fast signals: motor neuron signaling to skeletal muscle, sensory afferent signaling to CNS -slow signals: motor neuron signaling to visceral organs (stomach, intestines, etc)

Contractile characteristics of smooth muscle: -whole sheets of muscle exhibit slow, synchronized contraction -cells contract in unison, reflecting their electrical coupling with gap junctions (APs are transmitted directly from cell to cell)=specialized cell connections -some smooth muscle, certain cells act as pacemakers & set the contractile pace for whole sheets of muscle (like fibers in the stomach & small intestine) -are self-excitatory & depolarize w/out external stimuli -gap junctions allow muscles to transmit APs from fiber to fiber

contraction mechanism similarities in smooth & skeletal muscle: -actin & myosin interact via sliding filament mechanism -the final trigger for contraction is rise in intracellular Ca2+ -ATP energizes sliding process -both relax when intracellular Ca2+ levels drop (but process more complex in smooth muscle) DIFFERENCES: -Smooth muscle: Ca2+ is released from the SR & enters from extracellular space -Ca2+ interacts with calmodulin & myosin light chain kinase (MLCK) to activate myosin -in skeletal, Calciumions activate myosin by binding to troponin

chapter 10: muscular system: -skeletal muscle works together or in opposition (to eachother) [whatever one muscle or group of muscles does, another/others undoes -muscles only pull (never push) -as muscles shorten, insertion moved toward origin ~600 muscles in human body

functions of muscles: -move body parts -move contents of organs (smooth & cardiac muscles) -maintain posture & prevent movement -communication (speech, expressions, & writing) -control body openings -heat production

Regeneration: -cardiac & skeletal muscle become amitotic in adulthood, but can lengthen & thicken -myoblast-like satellite cells in skeletal muscle show very limited regenerative ability (significant only in childhood) -cardiac cells lack satellite cells -smooth muscle has good regenerative ability

gender differences: biological basis for greater strength in men vs women: -women skeletal muscle makes up 36% of body mass -men skeletal muscle makes up 42-45% of their body mass -differences due primarily bc of male sex hormone:testosterone -with more muscle mass, men generally stronger than women -body strength per unit muscle mass same in both sexes

grouping of muscles by function: 1)prime movers-provide major force for producing specific movement 2)antagonists-oppose or reverse a particular movement 3)synergists-add force to movement, reduce desirable or unnecessary movement, -fixators=synergists that mobilize a bone or muscle's origin

muscular system naming: -location of muscle: bone or body region associated w/muscle -shape: ex.deltoid (delta= triangle) -relative size: ex.maximus (largest) or minimus(smallest),longus(long) -direction of fibers: ex. rectus (fibers run straight), transversus, & oblique (fibers run at right angles to a defined axis) -number of origins: ex.biceps (two origins), triceps (3 origins) -location of attachments:named according to point of origin or insertion -action:ex.flexor or extensor, muscles that flex or extend

Muscles of back: -prime mover of back extension is erector spinae -erector spinae has 3 columns on each side of vertebrae (total of 6 columns, 3 on each side): iliocostalis, longissimus, & spinalis -lateral bending of back done by unilateral contraction of these muscles -other deep back extensors are semispinalis muscles & quadratus lumborum

muscular system: THORAX: primary function of deep thoracic muscles is to promote movement for breathing 1)external intercostals-more superficial layer that lifts rib cage & increases thoracic volume to allow inspiration 2)internal intercostals-deeper layer that aids in forced expiratio 3)diaphragm-most important for inspiration at rest

muscular system: ABDOMINAL WALL: composed of 4 paired muscles (internal & external obliques, transversus abdominis, & rectus abdominis), their fasciae, & their aponeuroses -fascicles of these muscles run at right angles to one another, giving abdominal wall added strength -in addition to forming abdominal wall, these muscles involved in: lateral flexion & rotation of trunk, and helps promote urination, defecation, childbirth, vomiting, coughing, & screaming

muscular system:SHOULDER: -prime movers of shoulder elevation are trapezius & levator scapulae -9 muscles cross shoulder joint & insert into humerus -prime movers include: 1)pectoralis major-arm flexion 2/3)latissimus dorsi & posterior fibers of the deltoid-arm extension 4)middle fingers of deltoid-arm abduction -rotator cuff muscles: supraspinatus, infraspinatus, teres major, & subscapularis 1)function to reinforce shoulder capsule 2)act as synergists & fixators

Termination of neurotransmitter signaling: -NM bound to postsynaptic neuron produces continuous postsynaptic effect & must be removed from its receptor in order to stop signal -removal of neurotransmitters occurs when they: 1)are degraded by enzymes 2)are reabsorbed by astrocytes or presynaptic terminals 3)diffuse out of synaptic cleft

postsynaptic potentials: -neurotransmitter receptors mediate changes in membrane potential according to: 1)amount of neurotransmitter released 2)length of time neurotransmitter is bound to receptors 3)type of receptor to which neurotransmitter is bound -2 types of postsynaptic potentials: 1)EPSP-excitatory postsynaptic potentials 2)IPSP-inhibitory postsynaptic potentials

Stimulation strength: -Threshold stimulus:stimulus strength when 1st observable muscle contraction occurs -beyond threshold, muscle contracts more vigorously as stimulus strength increased -force of contraction precisely controlled by multiple motor unit summation=recruitment, which brings more & more fibers into action -sub-threshold/below stimulus contractions produce no observable contractions in laboratory situation

real life:motor control regions in brain(motor cortex)signals amount of motor neurons to active& send APs to their myocytes(i.e.how many motor units become activated) -increasing the stimulus intensity beyond maximal stimulus doesnt produce a stronger contraction -recruitment process isnt random= size principal of recruitment: -motor units w/smallest muscle fibers activated 1st bc controlled by smallest most excitable motor neurons and as larger motor units, containing large coarse muscle fibers, have more contractile strength & controlled by largest/ least excitable(highest-threshold) neurons

contraction:activation of myosin cross bridges so force (tension) developed in muscle (when lengthen muscle, still generating force) -muscle tension:force exerted by contracting muscle on an object -load:opposing force exerted on muscle by weight of object to be moved (two types of isotonic cont): 1)shortening(concentric contraction) occurs when tension generated by cross bridge exceeds load & muscle decreases in length(muscle shortens & does work, ex. kick ball or pick up book) 1)eccentric contraction occurs when load is greater than muscle force generation & muscle lengthens during contraction(muscle generates force as it lengthens, more forceful & delayed-onset muscle soreness,ex.calfs day after hiking up steep hill) -contraction ends when cross bridges become inactive

two types of muscle contractions: 1)isometric:muscle does not always shorten & move load, if muscle tension develops but load is not moved=isometric (same measure) -ex. trying to life 2000lb truck -muscle doesnt shorten/lengthen -when you stimulate muscles to contract, doesnt move weight -increasing muscle tension is measured 4 isometric contractions, whereas amount of muscle shortening(distance in mmeters) is measured for isotonic contractions) -cross bridges generate force but dont move the thin filaments 2)isotonic:thin filaments slide, muscle tension developed overcomes load (same tension) & muscle shortening occurs ex. lifting 5lb sack of sugar -so muscle length changes & moves a load. once sufficient tension developed to move load, tension remains relatively constant throughout contractile period