PDBIO 305: Exam 2 Study Guide
PDBIO 305: Exam 2 Study Guide PDBIO305
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This 13 page Study Guide was uploaded by Kirsten Notetaker on Friday October 14, 2016. The Study Guide belongs to PDBIO305 at Brigham Young University taught by David Thomson in Fall 2016. Since its upload, it has received 54 views. For similar materials see Human Physiology in Physiology and Developmental Biology at Brigham Young University.
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Date Created: 10/14/16
PDBIO 305 Exam 2 Study Guide All the notes for this exam in one place, for your convenience Peripheral Nervous System (PNS) Afferent division of the PNS = sensory division Positioning of the spinal cord Dorsal and ventral roots Afferent fibers enter spinal cord via (dorsal root) Efferent fibers leave the spinal cord via (ventral root) Ganglion: collection of cell bodies (term applies outside of CNS) Sensory pathways Stimulus -> receptors -> afferent (1 order) neuron -> spinal cord or brainstem -> 2 nd order neuron -> thalamus -> 3 order neuron -> cortex Sensory intensity Remember – neurons either fire or they don’t, action potentials are all- nothing, NOT “big” or “small” Intense sensory activation doesn’t result in intense action potentials Instead, intensity is coded by the frequency of action potentials (frequency coding) or the number of afferent nerves activation (population coding) Frequency coding Greater stimulus (greater graded potentials) -> greater likelihood of overcoming relative refractory period & reaching threshold -> more frequent action potentials Population coding Greater stimulus -> depolarization (recruitment) of more receptors -> increased frequency on afferent neuron OR depolarization of increased number of afferent neurons -> greater frequency of action potentials arriving in CNS Sensory localization Sensory (receptive) fields overlap When stimulus hits overlapping areas, both neurons fire Lateral inhibition Interneurons at synapse between 1 & 2st ndorder neurons inhibit nearby neurons from transmitting signals (Primary neuron sends EPSP to inhibitory interneuron, which sends IPSP to nearby neurons) Inhibit through neurotransmitters which inhibit calcium channels at synaptic terminals Neurotransmitters used are endogenous opiates, GABA, glycine This means the signal coming from the neuron doing the inhibiting will be relatively stronger arriving in the brain than the signals coming from the nearby inhibited neurons -> helps to pinpoint where stimulus is coming from Presynaptic Inhibition Neurotransmitters (glycine, GABA, etc.) inhibit calcium channels at synaptic terminals -> less calcium enters presynaptic neuron -> less neurotransmitter released -> reduced effect on postsynaptic neuron Types of receptors – mechanoreceptors, thermoreceptors, nociceptors Pain Primarily a protective mechanism meant to bring a conscious awareness that tissue damage is occurring or is about to occur Storage of painful experiences in memory helps us avoid potentially harmful events in future Receptor: nociceptor Two best known pain neurotransmitters Substance P – activates ascending pathways that transmit nociceptive signals to higher levels for further processing Glutamate – major excitatory neurotransmitter Two types of pain, conducted by different afferent fibers Fast pain – sharp, usually temporary, transmitted by fast fibers Slow pain – dull/throbbing/achy, transmitted by slow fibers (C- fibers), persists chronically Gate-control theory Slow pain inhibits inhibitory interneurons Collaterals from other sensory receptors stimulate interneurons, blocking pain transmission Endogenous Opiates Brain has built in analgesic system Suppresses transmission in pain pathways as they enter spinal cord Depends on presence of opiate receptors Endorphins, enkephalins, dynorphin Induced by exercise, stress, acupuncture Prostaglandins Prostaglandin released from damaged tissue greatly enhances receptor response to noxious stimuli Lowers nociceptor’s threshold for activation Some pain relief can be achieved by inhibiting prostaglandin production Non-opioid analgesics (i.e. aspirin) Efferent division = autonomic NS Autonomic Nervous System Autonomic nerve pathways consist of 2 neurons (remember afferent pathways have 3) Preganglionic fiber – cell bodies of preganglionic fiber lie in the spinal cord Postganglionic fiber These fibers synapse within a ganglion Ganglion = cluster of neuron cell bodies outside of CNS Effector organs = skeletal or smooth muscle, glands, adipose tissue, etc. Autonomic neurotransmitters Parasympathic system = “rest & digest” – most activity at mealtimes, during rest & sleep Neurotransmitter – ACh (acetylcholine) Sympathetic system = “fight or flight” – most activity during exercise, fear, flight or fight Neurotransmitters ACh (from preganglionic neurons) Norepinephrine (from postganglionic neurons) Epinephrine (from adrenal medulla) ACh is stimulatory (generates EPSPs) on postganglionic neurons But on target organs it can be stimulatory or inhibitory – depends on receptors Ex: decreases heart rate Autonomic receptor types Cholinergic receptors – receive ACh Nicotinic receptors – open cation channels (lots of Na+ + comes in, some K released -> depolarization -> excitation) Muscarinic receptors – initiate cell signaling cascades, several subtypes ACh binds to receptor -> G-protein subunits dissociate -> G- protein binds to K channel -> hyperpolarization -> less excitation Adrenergic receptors (for NE) Activated by epinephrine & norepinephrine 2 major classes: α and β Two subtypes of each: α1, α2 and β1, β2 Alpha 1 Alpha 2 Beta 2 Adenylate cyclase converts ATP into cAMP Acetylcholinesterase breaks down ACh into acetate & choline Choline is recycled to make more ACh Norepinephrine is recycled directly back into the releasing cell Effect of sympathetic (S) vs. parasympathetic (P) stimulation on various organs Heart: S increases HR (mainly beta-1), P decreases HR (HR = heart rate) Blood vessels: S vasoconstriction (alpha-1), P vasodilation (of penis & clitoris vessels only) Stomach, intestines: S decreases activity (alpha-1), P increases activity Lungs: S bronchioles dilate (beta-2), P bronchioles constrict Adrenal medulla: S releases epinephrine Liver: S glycogenolysis (glycogen -> glucose, alpha-1 & beta-2) Adipose tissue: S lipolysis Agonists & antagonists Sympathetic agonist = drugs that mimics effect of norepinephrine Sympathetic antagonist = drugs that block effect of norepinephrine Parasympathetic agonist = drugs that mimic effect of acetylcholine Parasympathetic antagonist = drugs that block effect of acetylcholine Voluntary vs. autonomic pathways Voluntary: motor neuron goes straight from spinal cord or brain to muscle Autonomic: preganglionic neuron goes from spinal cord or brain to ganglion, postganglionic neuron goes from ganglion to organ Skeletal Muscle Basic skeletal muscle structure Muscles are made up of many fascicles which are made up of many muscle fibers (AKA myofibers, AKA muscle cells) Myofibers are multinucleated (have many nuclei) but don’t divide Each muscle cell has many myofibrils (different from myofiber – don’t get confused) Sarcolemma = cell membrane of myofiber, sarcoplasm = cytoplasm, sarcoplasmic reticulum = endoplasmic reticulum Each muscle fiber (or cell) is connected to one motor neuron Connection is called a neuromuscular junction Neuromuscular Junction Type of synapse between motor neuron & postsynaptic site on muscle fiber (called motor end plate) Action potential causes voltage-gated Ca channels to open -> causes exocytosis of ACh from synaptic vesicles -> ACh binds to nicotinic receptors on motor end plate (Na/K ion channels) -> Cell becomes depolarized with influx of Na into cell -> action potential Nicotinic receptors cause ions channels to open -> depolarization of end plate, T-tubules & sarcoplasmic reticulum Once generated at the neuromuscular junction, the action potential spreads over the muscle fiber sarcolemma in all directions T-tubules = invaginations in the sarcolemma that extend deep into the muscle cell, running along the myofibrils Sarcoplasmic reticulum = specialized ER, stores calcium Action potentials & calcium release As action potentials run along sarcolemma, they dive down into the muscle along the T-tubule system When motor end plate receives stimulus it will always create an action potential (graded potentials in this place will always reach threshold) Called end plate potentials Dihydropyridine (DHP) receptors change conformation w/ depolarization When DHP receptors shift, they “pull” ryanodine receptors (calcium channels) into a new conformation, opening them When ryanodine receptors open, calcium flows out of SR (from lateral sacs) The sarcomere Under microscope, skeletal & cardiac muscle cells are “striated” or striped Due to alternating A bands (dark) and I bands (light) A band – defined by presence of thick filament (myosin) I band – defined by presence of thin filament (actin) but NO thick filament H zone – portion of the A band w/ only thick filament (NO thin filament) M line – anchors thick filaments Z line – anchors thin filaments Sarcomere: functional unit of skeletal muscle, runs from Z line to Z line Thick filament = myosin Made of many myosin proteins Myosin has ATPase activity – breaks down ATP, releases energy Myosin can bind to actin in thin filament (six thin filaments surround each thick filament) Two “heads” poke out from myosin molecule, cocked at an angle, each have ATPase site & actin-binding site Thin filament = actin Made of many actin, troponin, & tropomyosin proteins Actin – globular protein, each has a binding site for myosin Tropomyosin – strand-like protein; in resting muscle, covers myosin- binding sites on actin molecules Troponin – complex of 3 subunits; one binds calcium, one binds actin, one binds tropomyosin The sarcomere during contraction (see pictures on Learning Suite) I band & H zones shorten, but A band remains the same length -> distance between Z lines shortens This occurs as filaments slide past each other (sliding filament theory) During maximal contraction, filaments have slid past each other so much that I band is totally gone & thick filaments are overlapping Sliding filament theory (lots of questions about this on the test!) (also called cross-bridge cycle) At rest: myosin binding sites on actin are covered by tropomyosin, myosin head is “cocked” or in an energized state, ADP + inorganic phosphate (Pi) is bound to myosin head Calcium released from SR: calcium binds to troponin, which shifts tropomyosin off from myosin-binding sites on actin Myosin bind to actin: myosin heads bind to myosin-binding sites on actin, causes release of Pi from the ATP binding site Power Stroke: Loss of Pi leads to conformational change in myosin head, pulling actin along; ADP is released from myosin head Actin-Myosin Detachment: Binding of a fresh ATP to the myosin head causes detachment of the myosin head from actin “Cocking”: ATP is hydrolyzed & the energy is used to “cock” the myosin head; as long as calcium is present the cross-bridge cycle will repeat over and over to pull actin in toward the M-line It’s like a big tug of war – many different heads grab, pull & let go at different times, so tension is not lost Excitation-Contraction coupling = whole process from stimulus of motor end plate through activation of cross-bridge cycle Relaxation = no more action potentials DHP receptor closes ryanodine receptor -> no release of calcium ATPase pumps use energy from breaking down ATP to pump calcium back into lumen of lateral sac + These pumps are referred to as Ca ATPase pumps or SERCA pumps (Sarcoplasmic Endoplasmic Reticulum Calcium ATP pumps) Calsequestrin stores calcium in lateral sacs Think “sequester” = separating or setting something apart, keeping something contained Binds to Ca w/in lateral sac – Ca bound to something doesn’t effect concentrations -> pumps don’t have to work as hard to pump against Ca concentration gradient ATP is required for muscle relaxation 1. To provide energy for Ca pumps to pump Ca back into the lateral sacs of the SR and away from the myofibrils 2. To bind to myosin head pieces, allowing them to release from actin Muscle twitch 1 action potential on a muscle fiber results in a muscle twitch (quick, weak contraction) Delay between the start of the action potential & the start of the twitch is called the “latent period” Force production by individual muscle fibers Determined by frequency of stimulation, fiber length, & fiber diameter Frequency of stimulation Twitch summation Twitches last much longer than action potentials If a second action potential occurs before twitch finishes, calcium release exceeds removal from cytosol -> increased calcium in cytosol Increased calcium -> increased force production Complete (fused) tetanus = action potentials rapid enough to prevent dip in calcium/force between twitches Incomplete (unfused) tetanus = action potentials rapid enough to keep average tension constant, but there are slight dips in calcium/force Fiber length Optimal overlap between myosin heads and actins results in optimal force production If the fibers are too tight together or too stretched out, force production decreases Fiber diameter Increased diameter -> increased myofibrils in parallel -> increased force production Skeletal muscle fiber type & plasticity Motor unit summation (spatial summation) Motor unit = one motor neuron + all the muscle fibers that it innervates Note: every muscle fiber is only innervated by 1 neuron, but a motor neuron may innervate many muscle fibers The muscle fibers in 1 motor unit are spread out in the muscle, not right next to each other As increased force is required, more motor units are recruited Orderly recruitment of motor units Motor neurons that innervate many muscle fibers are bigger than those that innervate only a few fibers Small neurons are easier to depolarize than big ones Recruitment of motor units occurs based on size, small -> medium -> large, depending on magnitude of drive from the CNS Isotonic contraction = muscle is allowed to shorten (or lengthen) as it contracts with tension being held constant Usual muscle movement, i.e. walking, lifting things, etc. Concentric contraction – muscle shortens as you exert force on something (i.e. bicep curls w/ weights) Eccentric contraction – muscle lengthens because weight/ gravity is greater than force you’re able to exert of the object (i.e. your biceps are curled and someone hands you a weight too heavy for you to hold -> you uncurl your biceps because you aren’t strong enough to hold it there) Isometric contraction = muscle is not allowed to shorten so tension will vary throughout contraction Muscle activity to maintain posture, pushing or holding things Skeletal muscle fiber type Muscles are typically classified based on their: Speed of contraction – fast or slow Major pathway of ATP production – glycolytic (glucose) or oxidative (fat) Isometric contractions of fast & slow twitch muscles Ex: extraocular muscle twitch = 7-8 msec, while soleus twitch = 90 msec Thus, extraocular muscle has more fast fibers while soleus has more slow fibers Gastrocnemius = 40 msec, so it has a good mix of fast & slow fibers Classified as Type 1, Type 11A, or Type 11X fibers Type I Type IIA Type IIX Twitch speed Slow Fast Fast Myosin ATPase activity Low High High Sarcoplasmic reticulum density Sparse Dense Dense Calcium ATPase activity Low High Highest Fatigue resistance Very high High Low Creatine kinase activity Low High High Glycolytic potential Low High Very high Glycogen content Low High Very high Mitochondrial density Very high High Low Oxidative potential Very high High low Triglyceride content Very high High Low Capillary density Very high High Low Myoglobin content High High Low Color Red Red White Recruitment order 1 2 3 Darker muscle (w/ more mitochondria) is slower, fast muscle contracts quicker but has much less endurance Denser SR -> faster twitch because calcium can diffuse more easily & is closer to myofibrils More calcium pumps -> faster twitch because calcium is taken up more quickly -> end of twitch Creatine kinase makes ATP very quickly -> faster twitch Glycolysis is fast, but doesn’t make very much ATP -> faster twitch Why does oxidative potential & triglyceride content go along with more mitochondria? Fat can only be used for energy through beta-oxidation, which requires mitochondria Glycolysis which does not progress to the Krebs cycle/oxidative phosphorylation doesn’t require mitochondria Lots of capillaries provide myoglobin w/ needed nutrients Recruitment order – type 1 recruit first because they are used more often -> more endurance Type IIx recruit third – these pathways are used less often -> less endurance Muscle biopsy Needle used to obtain small bit of muscle Muscle is frozen, sliced, stained, & examined under microscope Fiber type stain – different types of fibers stain different colors When are different types of muscles recruited? Type I (Slow-oxidative): posture & endurance Type IIA (Fast-oxidative): endurance (walking, jogging) Type IIX (Fast-glycolytic): max effort, sprint-type activity What determines fiber type? Genetics determine which motor neurons innervate our individual muscle fibers Muscle fibers become specialized according to the type of neuron that stimulates them Endurance training & muscular inactivity may result in small changes in the percentage of IIA & IIX fibers (won’t completely change the type of muscle, though – changes aren’t big enough for that) Intense training will increase amount of IIA fibers (IIX fibers increase in endurance) Aging may result in changes in the percentage of FT to ST fibers due to loss of FT fibers Potential causes of muscle fatigue ATP use exceeds ATP production (local ATP depletion) + Lactic Acid (H ) accumulation interferes w/ ATP production & muscle contraction Glycogen depletion during long-term exercise; hypoglycemia may also occur Inhibition of excitation-contraction coupling (i.e. inhibition of release of calcium from the lateral sacs) Skeletal muscle training Training different fiber types Types I and IIA fibers are used during jogging or moderate intensity running Type IIB fibers are only recruited during high intensity activities (hill running, sprinting) With intense training, IIX fibers can turn into IIA fibers With more mitochondria, trained muscle can make ATP faster An increase in mitochondria allows higher rates of ATP production with less lactate accumulation in the muscle During long-term exercise glycogen depletion in muscle -> fatigue Working muscles can use both fatty acids & glycogen Increased capacity of trained muscle to use fat allows sparing of glycogen & delays time to fatigue How does muscle grow? Hypertrophic stimulus/damage -> mTOR/S6k activation -> increased protein synthesis -> muscle hypertrophy/repair OR… Hypertrophic stimulus/damage -> satellite cell activation -> muscle fiber hypertrophy/myogenesis -> muscle hypertrophy/repair Satellite Cells Skeletal muscle cells (fibers) are multinucleated Satellite cells lie between the muscle cell membrane & the basal lamina Once activated they proliferate and then differentiate into myonuclei May not be required for muscle growth, but are required for muscle repair/regeneration Muscle growth Protein synthesis must occur at a greater rate than protein degradation Controlled by signaling pathways Hypertrophic stimulus (weight lifting, amino acids, insulin, growth factors, etc.) -> mTOR -> other factors are stimulated -> increased protein translation Endurance vs. resistance exercise With endurance exercise the cell experiences a prolonged consistent increase in Ca++ as well as energetic stress which activates AMPK (AMP kinase) AMPK and Ca++ drive an increase in mitochondrial biogenesis by activating the transcription of mitochondrial genes AMPK activates mitochondrial biogenesis -> increased mitochondria, increased fat oxidation, blocks protein synthesis In resistance exercise, the tension drives the activation of the mTOR pathway, which increases protein synthesis to support growth of the muscle AMPK opposes or blocks the activity of mTOR, so the two types of exercise generate opposing adaptations in the muscle Perhaps partially explains why elite endurance athletes look the way they do, while elite strength athletes look very different
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