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Other names for______ in muscle: -Plasma membrane -Cytoplasm -Endoplasmic Reticulum |
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Definition
-Sarcolemma -Sarcoplasm -Sarcoplasmic Reticulum |
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Sarcomere: Z line to Z line Middle of Sarcomere: M line A-Band- Dark due to myosin H-zone- Lighter part of A-band, no overlap I-band- light due to Actin |
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Made up of G actin(Globular) A bunch of G actin makes an F actin which is a double helix |
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protein that lies in the groove of the F actin, spans 7 G actin molecules |
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Contains Ca2+ ATPase: pumps Ca from ICF to reticulum Calsequestrin binds up to 43 Ca Ryanodine receptor: Ca release channel |
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Extensions of sarcolemma that go all the way through the cell |
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Contains 2 sarcoplasmic reticulum and 1 T-Tubule Also has dihydropyridine receptor(voltage receptor that pulls open Ryanodine Receptor) |
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A motor neuron and all the muscle fibers it innervates. There can be many(gross muscle movement) or few(fine muscle control. |
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Consists of motor neuron end-terminal, synaptic cleft, and motor end plate of muscle cell. |
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Arranged in synaptic folds with concentrated acetylcholine receptors. -End Plate potential is always excitatory |
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Muscle depolarization events |
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Depolarized T-tubule causes conformational change to dihydropyridine receptor, causes ryanodine receptor to open and release Ca, which initiates sliding filament mechanism. |
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Only ATP can be used. Phosphocreatine can give a little Glycolysis(Anaerobic) provides enough for a 1.3-16 minutes of max muscle usage Oxidative Metabolism- provides the most for sustained physical activity. |
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Pathophysiology of Muscle |
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Definition
-Botulinum toxin- messes with Atch, results in paralysis -Myasthenia gravis-autoimmune, autoantiboies attack Atch receptors -Muscular Dystrophy- genetic disease, messed up dystrophin, muscles are replaced with fatty fibrous tissue. |
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Cardiac Muscle Characteristics |
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Definition
smaller, one nuclei, intercalated disks, dyads w/one T-tubule, |
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Specialized Cardiac muscle cells |
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Atrial/Ventricular myocytes Purkinje fibers- less actin/myosin, larger diameter SA/AV node |
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Cardiac Muscle generates 2 types of AP: |
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Definition
Fast Response: A/V myocytes & Purkinje fibers
Slow Resonse: SA/AV node |
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Cardiac Muscle Contraction -iNa -iCa -ito -iK1 -iK |
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Definition
-iNa-opens briefly and initiates depolarization -iCa- allows slow influx of Ca -ito-allows slow efflux of K -iK1-Generally only open while resting, aids in repolarization -iK-mainly in charge of repolarization |
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Fast Na channels open, depolarizing cell. iK1 gates close |
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Initial repolarization occurs through i-to channels. These channels don't close until end of P2 |
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Plateau happens due to Ca entering through iCa and K entering through iK and iK. |
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K out overpowers Ca in. iK lets more out, iK1 starts to let more K out. i-to no longer contributes. |
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Na-K and Ca pumps activated. |
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Not a rapid upstroke. Upstroke mediated by iCa, Ca blockers can affect |
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Mediated by K leaving through iK |
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-There is a spontaneous depolarization due to iF. -Slow depolarization activates iCaT which aids in depolarization. iCaT not blocked by Ca blockers. -L-type Ca-in charge of depolarization, can be blocked. |
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Cardiac excitation: dihydropyridine receptor |
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Definition
activates Ryanodine receptor through chemical no mechanical process like in skeletal muscle |
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Myocyte contraction directly proportional to: |
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Catecholamine affect on myocytes |
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Definition
increases cAMP, which increases PKA, which phosphorylates iCaL channels. This all allows in more Ca. -They also increase rate of relaxation by phosphorylating phospholamban, which pumps Ca out faster. |
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Catecholamine affect on SA node |
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Definition
funny channels have increased slope of depolarization. |
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-Also called Digitalis -Block Na-K pump. less Na inside cell. -Slows Ca-Na pump which usually puts Ca out and Na in. |
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Acetylcholine one heart muscle |
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Definition
-Only decreases atrial mycytes, not ventricular myocytes. -Decrease formation of cAMP -Puts more K out, hyperpolarizes and takes longer to reach threshold. -Also makes funny channels take longer |
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-Most have gap junctions(unitary) -Smaller than skeletal -No sarcomeres, not striated -Myosin regulated contraction -No T-tubules, but have caveoli |
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-Twice as much actin that are long and skinny -Actin originates from dense body -Dense bodies make up dense bands -No troponin in smooth muscle |
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Smooth Muscle Contraction |
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-Most Ca comes from outside cell -Ca binds to calmodulin -Calmodulin activates myosin light chain kinase(MLCK) -MLCK phosphorylates regulatory myosin light chain. -Then crossbridges with actin form |
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Hormone affect on smooth muscle |
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Definition
-Increases DAG and IP3 -IP3 acts on Sarc.Ret to release Ca -DAG increases PKC which increases contractibility |
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Smooth muscle innervated by autonomic nervous system |
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-Nerves terminate in varicosities, like beads on a string. |
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Possible due to latch mechanism |
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specific type of sensation that can be detected by a sensory receptor |
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Electrotonic, graded, not propagated. Similar to EPSP |
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Involves a receptor, afferent sensory neuron, efferent motor nerve, end organ |
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-A monosynaptic reflex -Sensory receptor is a muscle spindle |
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-3-12 narrow muscle fibers -These are called intrafusal fibers -Wrapped in primary afferent neurons |
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Alpha- neuron that comes from muscle spindle Gamma-neuron that activates stretch reflex |
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-Activated by tension -activates inhibitory interneurons -Prevents extreme contraction |
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Dorsal Column-Medial Lemniscal System |
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-2 Pt discrimination, vibratio, proprioception -Large and myelinated -Crosses between medulla and midbrain -Needed for localizing pain/temp, not for sensing them. |
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-Small diameter -Crosses in the spinal cord immediately -Neospinothalamic-fast pain -Paleospinothalamic-slow pain |
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-Descend from the cerebral cortex -Release enkephalin which inhibits incoming painful stimuli -Morphine and naloxone are similar drugs |
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Primary cortex
Supplementary cortex |
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Primary- makes sure that was is suppose to happen happens
Supplementary- organizing and planning a sequence of muscle activation |
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Control of rapid muscle movements -Knows the plan and receives info on what is actually happening to make sure the 2 line up. -Stops movement when a target is reached -Necessary for balance |
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-Ipsilateral loss of function -Past pointing- overshooting an object -Intention tremor-absent at rest -Ataxi-uncoordinated movements -Decomp of movement- steps instead of fluid -Slurred speech- dysarthria |
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Direct Pathway- excitatory
Indirect Pathway- inhibits |
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-Voluntary tremors due to lack of dopamine -scarcity of movement -Treated with L-Dopa |
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-Destruction of inhibitory neurons -Distortion of movement(chorea) |
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