Reflexes and Autonomic Nervous System Objectives | PSL 250, Study notes of Biology

Download Reflexes and Autonomic Nervous System Objectives | PSL 250 and more Study notes Biology in PDF only on Docsity! 1 Reflexes and Autonomic Nervous System (ANS) Objectives 1. A stimulus can be outside or inside the body. Receptors can be distal ends of sensory neurons or separate cells that are associated with sensory neurons. Sensory neurons transmit information to the CNS when a receptor potential produces an action potential. a. Stimuli/stimulus – a change in the environment ( can be internal or external of the body) b. Receptors – i. Peripheral ends of sensory neurons ii. Cells or elaborate structures associated with the sensory neurons 1. Ex: taste buds iii. Specialized – respond best to a particular stimulus (sight, smell, hearing, taste) c. Peripheral Nervous System (PNS) i. Fibers that carry information to and from the CNS – in nerves ii. Divisions 1. Afferent – to the Central Nervous System (CNS) 2. Efferent – from the CNS iii. To make an afferent neuron fire, the stimulus caused a receptor potential which altered the membrane permeability to ions 1. There is a depolarization in the receptor and then we get a local/graded potential. Current flow caused by local potential triggers AP if the membrane next to the receptor is brought to threshold. 2. If the receptor potential causes an AP, then the information goes to the CNS d. Division of CNS i. Brain ii. Spinal cord 2. Sensory information (APs in sensory neurons) can cause an automatic motor response (a reflex). Most reflexes are polysynaptic. a. Knee jerk i. Tap patellar tendon – stretches the quadracep muscle and also the muscle spindles – receptors in muscle ii. Stimulus if gets to membrane threshold, fires APs in afferent (sensory) neuron b. Reflex – automatic (without conscious effort) response to a stimulus has afferent component c. Monosynaptic reflex – one synapse d. Polysynaptic reflex – multiple synapses e. Interneurons are located in the CNS where the reflex is integrated f. 5 components of a reflex i. Receptor (sensor) ii. Afferent pathway (path from sensor to the CNS/control center) iii. Integrating center (control center/CNS) iv. Efferent pathway (path from control center to effector) 1 Nervous System Organization CNSPNS Afferent Efferent (motor) (sensory) Somatic Autonomic (symp and PS) Skeletal Smooth muscle Muscle Cardiac muscle Glands 2 v. Effector – muscle or glands which carry out the orders/cause the effect g. Withdrawal reflex – same reflex as touching a hot stove h. Divergence in CNS of afferent neuron i. Excitatory interneuron – cause EPSPs in motor neuron going to flexor muscle to pull foot away from nail or hand away from hot stove ii. Inhibitory interneurons – cause IPSPs in motor neuron going to extensor muscle. If contracted, would push foot onto the nail. Counterproductive. Need to prevent contraction of the antagonistic muscle 1. Reciprocal innervations – wiring (neuro connections) there so that when you stimulate the agonist (cases the movement) you also inhibit (don’t send impulses to the antagonist due to IPSPs) the antagonist iii. Interneurons of ascending pathway – take information to the bran (can become aware of pain, localize it, and send down impulses to stop the reflex) iv. Interneurons which go to opposite side of the cord and get opposite reaction 3. Reflexes help maintain homeostasis; many reflexes involve autonomic effectors. a. Withdrawal reflex – protects from harm and tissue damage such as severe burn where you would lose a lot of ECF b. Reflex shivering – protects the body temperature c. Reflexes we are not aware of – maintain homeostasis in a BIG way i. Receptors – examples are stretch receptors (sensitive to stretch or deformation), chemoreceptors (sensitive to chemicals), and osmoreceptors (sensitive to osmolarity) in certain organisms like the GI tract ii. Effectors – smooth muscle, cardiac muscle (only found in heart), glands 4. The ANS is part of the efferent division of the peripheral nervous system. It controls smooth muscle, cardiac muscle, and glands. The 2 divisions of the ANS most often have opposite effects on an organ. a. The ANS – part of the nervous system that controls visceral functions, involuntary system, normally ignoring feedback i. Normally functions below conscious level – unaware of controlling stomach secretions, gut movement, blood pressure. ii. Controls visceral effectors – smooth and cardiac muscle and glands iii. Purely motor (efferent) – defined that way, consists of motor/efferent neurons iv. Sensory afferent neurons important component of autonomic reflexes but are not considered part of the ANS v. Autonomic reflexes – effectors are in internal organs and the neurons to them are autonomic b. 2 divisions of the ANS i. Sympathetic (symp) ii. Parasympathetic (PS) c. Sympathetic – Thoracolumbar division – fibers (preganglionic fibers) emerge from thoracic and lumbar segments of the spinal cord (from T1 – L2 spinal cord segments) 2 5 iv. Gut: PS – speeds peristalsis (ring of contraction of the smooth muscle that moves down the gut). Symp – slows peristalsis (contracts sphincters) v. Dual innervation with autonomic antagonism allows precise and quicker control over an organ 1. Decrease HR – decrease symp activity (# of impulses from neuron) – this takes a while, it’s like taking your foot off the accelerator a. Can decrease HR faster if also increase PS impulses – it’s like using the brake vi. Not always opposite effects though 1. Salivary glands – both divisions cause secretion, but each division causes a different type 5. The sympathetic nervous system prepares the body for emergency. Hormones from the adrenal medulla reinforce sympathetic neural effects. a. “Fight or Flight” reaction (stress or alarm reaction) – symp response to emergency i. only occurs in extremely stressful situations b. With fight or flight, you are ready for intense muscular activity so the best physical reaction can occur i. Increase glucose levels in the blood for a quick energy source ii. Increase heart rate, increase metabolic rate from NE or adrenaline iii. Increase lung tubes/airways (dilate, sphincters relax) iv. Pupils are dilated (hold in the middle of the iris is larger) v. Increase mental activity/awareness vi. Stimulates the adrenal medulla (adrenal gland is like a cap on the kidney, medulla is the in the gland) 1. Adrenal medulla – exception of the 2 neuron chain rule 2. Preganglionics reach medulla, no postganglionics from medulla (none emerge from medulla) 3. Medulla modified postganglionic neurons that don’t develop long axons 4. Adrenal medulla (an endocrine gland) secretes 20% NE and 80% epinephrine (epi, adrenaline) into the blood vii. Adrenal hormones last longer (removed from blood slower) 1. (seconds vs. milliseconds) 2. Hormones reinforce symp neural effects and can reach cells without innervation (without nerve cells going to the cells); essentially can reach all cells of the body since hormones transported basically everywhere except the eye c. The symp nervous system can be less active i. Can be on but not in full effect, like for an exam that you are well prepared for. You are still nervous so it may only be 1/8 on ii. Only take effect one organ and not others 1. Walk into a dark room, pupils dilate, HR stays the same because the situation is not suspenseful 5 6 6. The parasympathetic nervous system gets the routine, everyday work done (when we’re not confronted with emergencies) a. PS nervous system does more ‘internal housekeeping’ or ‘rest and digest’ i. Everyday internal work like digestion 1. GI tract – increased activity with increased PS impulses, now not stressful so can process food and get rid of waste 2. Defecation, urination are PS reflexes b. PS system dominant during rest. ( sitting in an easy chair by the fire reading a mellow book after a great dinner) – both systems are still active, but PS is more active 7. Specific effects of the ANS are made easier if one remembers the general functions of the 2 systems: Emergency vs. Routine Work Sympathetic (guy down a dark alley with knife) Parasympathetic (mellow situation with no stress) A. Smooth Muscle Eye Iris Muscle that focuses eye (lens) Dilates pupil; contracts radial fibers of iris (occurs in fight or flight reaction) Adjusts for far vision Constricts pupil; contracts circular fibers of iris (reflex in bright light) keeps out too much light. Happens when reading a book with light Adjusts for near vision Arrector pili muscle (attached to hair follicles) Contracts – hair on end, ‘goosebumps’ --------------------------------- Bronchial tubes/airways Dilate – relax the cicrcular muscle, increase air flow Slight constriction of circular muscles, don’t need high air flow GI tract Decrease peristalsis Increase contraction of sphincters Less movement thru tract Increase peristalsis Increase relaxation of sphincters More movement thru tract Urinary Bladder Relaxes muscle of the bladder wall Contracts the muscle of the bladder wall, urination is a PS reflex Blood Vessels Overall effect is constriction except to muscles, the blood vessels dilate to get more blood there Mostly ------ except special places Erection is PS reflex with NO(nitric oxide) transmitter B. Cardiac Muscle Heart Increase activity Increase HR Increase force of contraction Decrease activity Decrease HR Not an important effect on force of contraction C. Glands Salivary Glands Thicker secretion, more mucus (stressed, dry mouth) Watery secretions with enzymes for digestion Intestinal Glands (for digestion) Decrease secretion Increase secretion Liver Increase glucose released for more energy -------------------------- Adrenal Medulla Increase release of epinephrine and NR -------------------------- a. Effect on organs if symp stimulates PS inhibits (and vice versa) b. Symp neurons (postganglionic) release NE at effector organs (almost always) c. PS neurons (postganglionic) release ACh at effector organs 8. There are different types and subtypes of adrenergic receptors. Drugs can stimulate or block receptors and can cause or prevent responses and are used clinically a. Adrenergic receptors – receptors for NE and epi. One organ can have different effects of symp stimulation because there are different adrenergic receptors 6 7 i. Alpha – α1 (receptors on blood vessels) and α2 ii. Beta 1. β1 – receptors on the heart. Stimulation increases hear rate and force on contraction like NE and epi would 2. β2 – receptors on lung airways. Stimulation dilates lung tubes/airways, relaxes circular muscles b. Phenylephrine stimulates alpha-1 receptors – reduces nasal congestion because it constricts blood vessels in the nose) decrease blood flow, decrease congestion c. Agonist – binds to receptor and acts like the natural agen, stimulates the receptor, mimics the natural chemical and triggers the cell’s response i. Pheylephrine α1 agonist – stimulates alpha-1 receptors like NE would d. Antagonist – blocks receptors; binds to receptor but doesn’t cause response, so competes with natural chemical and sits in the way of NE and epi from getting to the receptor and having an effect. i. Propranolol – beta blocker (blocks both beta-1 and beta-2) used as an anti- hypertensive drug (blocks NE and epis effect on the heart and lowers blood pressure) ii. Atenol – Beta-1 antagonist (selective Beta-1 blocker) blocks Beta-1 receptors on heart but not the Beta-2 receptors on the lung tubes/airways e. Alpha-1 receptors on blood vessels: activation causes constriction of vessel f. Beta-1 receptors on heart: activation increases activity of the heart (hear rate and force of constriction) g. Beta-2 receptors on lung tubes: activation causes dilation of the airway 9. There are different types of cholinergic receptors a. Cholinergic receptor – ACh receptor b. Examples: i. Muscarinic – activated by muscarine (poison in toad stoles) 1. Found on effector cell membranes of smooth and cardiac muscles and glands ii. Nicotinic – activated by nicotine (in tobacco) 1. Found at autonomic ganglias, on cell bodies/dendrites of postganglia neurons c. Antagonists of Cholinergic receptors i. Atropine – blocks muscarinic receptors ii. Curare – blocks nicotinic receptors on skeletal muscle 10. There are important areas in the brain that affect autonomic function. a. Medulla – autonomic control centeres here like cardiovascular and digestive center i. Afferent impulses from receptors  goes to medulla  to the autonomic centers  sends out a command via ANS fibers = efferent b. Hypothalamus – affects autonomic control centers in medulla i. Fear excites hypothalamus, acts on cardiovascular center in medulla to increase HR and increase BP 7 10 2. Botulism – blocks ACh release (breaks down proteins on membrane needed for exocytosis of ACh). Can be used clinically to prevent involuntary contractions/spasms. Also used for wrinkles (Botox) iii. Inhibit acetylcholinesterase – continual depolarization of membrane 1. Nerve gases for warfare 2. Insecticides (type called organophosphate) iv. Disease – 1. Myasthenia gravis (severe muscle weakness) making antibodies against your own ACh receptors and destroys the receptors (autoimmune disease) 2. ACh cant find a receptor because the number of ones that work are limited, therefore resulting in muscle weakness 2. Muscle cells contain specialized structures for contraction. a. Muscle Fiber (see figure on pg 93) i. Sarcolemma – cell membrane ii. Sarcoplasm – muscle cytoplasm iii. (SR) Sarcoplasmic reticulum (specialized endoplasmic reticulum (ER)) – formed by the fusion of cells. This is how you have many nuclei, many mitochondria (‘powerhouse’ of cell, produces ATP for cell work, like muscle contraction) iv. Fiber jam-packed with myofibrils (myofibrils take up about 80% of the cell) v. Muscle striated – striped, light then dark bands because myofibrils are striated (because of arrangement of actin and myosin) vi. Myosin filament – thicker, causing dark stripes vii. Actin filament – thinner, causing lighter stripes viii. Myofibril – made up of repeating units called sarcomeres 3. Muscles shorten when filaments slide past each other a. Sarcomere – unit of contraction. Contraction of the sarcomere causes contraction of the muscle. The sarcomere is the smallest unit that performs the function of contraction. Its boundary is from z-line to z-line. i. A-band and I-band (since 1 I-band is in 2 different sarcomeres, the z-line goes thru the I-band) also H-zone is in the middle of an A-band. 10 11 ii. Only myosin is in the H-zone, NO actin! iii. I-band contains only actin iv. Z-line – goes through the middle of I-band; actin filaments attach to Z-line (anchoring pt. for the actin filaments) on one end, extend toward middle of sarcomere v. M-line – in middle of H-zone, supports myosin filaments vi. See figure on page 94 b. Muscle contraction occurs via a sliding filament mechanism – individual filament lengths do not change instead filaments slide! i. Actin slides past myosin ii. A-band length is constant iii. I-band length gets narrower and narrower as thin filaments slide past myosin towards the center of the sarcomere iv. H-zone gets smaller and can disappear when/if actin filaments meet at the center of the sarcomere, but it doesn’t always happen v. Sarcomere shortens, Z-lines get closer vi. Myosin cross bridges are essential for moving actin past myosin, act as something to grab actin with c. Filament structure made up of myosin filament – about 200 golf club shaped molecules i. 2 headed shaft – helix, shafts arranged lengthwise (bundled together) ii. ½ of filament molecules in one direction, ½ in the other direction 1. The center has the heads/cross bridges sticking out 2. There are no cross bridges in the center of the filament iii. Cross bridges are a site for ATP to bind d. Actin filament – actually contains 3 different proteins (actin, tropomyosin, troponin) i. Actin molecules are the primary structure, ‘the backbone’ ii. Actin molecules are spherical in shape and for 2 chains twisted like 2 strands of pearls. iii. Each actin has a myosin cross bridge binding site where the head of myosin attaches during contraction e. Tropomyosin and troponin are regulatory proteins that make sure myosin binds to actin at the correct time i. Tropomyosin – rod or threadlike molecule, lies on surface of actin strand believed to physically prevent myosin CBs from attaching (covers the myosin CB site) ii. Troponin – globular 3 units; 1 binds actin, 1 binds tropomyosin, 1 binds Ca++ 1. Binding of Ca++ to troponin is what turns ‘on’ muscle contraction 4. Changes in Ca++ concentration in the cytosol turn contraction on and off. ATP is needed for contraction-relaxation. a. Muscle Contraction 11 12 i. On – when Ca++ binds to troponin and pulls on tropomyosin which is pulled into the groove, away from the blocking position it was in before. The CB binding sites on actin are uncovered, and myosin can attach to actin. ii. Off – removal of Ca++ (or decreasing ICF cytosol Ca++ concentration) 1. Troponin loses Ca++, regulatory proteins move back to the blocking position and the contraction is turned off and the muscle relaxes 2. Whether the contraction is turned on or off depends on Ca++ concentration in the cytosol a. Cytosol – the fluid that surrounds the organelles b. ICF = cytosol + fluid in organelles b. Increased Ca++ concentration in the cytosol and the cross bridges move actin past myosin (assuming that tropomyosin is out of the way, then myosin’s head can attach to actin which causes myosin’s head to tilt). Head then detaches and reattaches at a point further down on actin strand, tilts, detaches, reattaches, tilts and on and on… i. Like little oars moving actin towards the center  c. Power Stroke – tilt or movement of myosin’s head/CB d. ATP is needed for muscle contraction ATP  ADP + P + energy i. ATP is not split during power stroke. It is split before myosin attaches to actin ii. ATPase on myosin’s head will split the ATP into ADP and P before actin is attached iii. Myosin is then a highly charged molecule containing stored energy and the head is then brought to a 90° angle. iv. Charged state of myosin is attached to actin, energy released, CB moves (power stroke) v. New ATP is needed for detachment of actin and myosin. When then ATP is bound, the actin/myosin rigor complex is broken and the process begins again e. So far ATP is needed for 2 functions. 1 ATP can be used to do both, but there are 2 separate actions of ATP) i. Break down of ATP to charge the myosin head ii. Binding, but not break down of ATP to detach myosin from actin to break the rigor complex f. Rigor mortis – ‘stiffness’ ‘death’ i. Because there is no ATP production after death, the myosin cannot detach from actin, therefore remaining in a stiff state 5. Describe how contraction is turned on a. T tubules – transverse tubules – run deep into fiber (relatively large cells) i. Invaginations or inturnings of cell membrane. Continuous touch with sarcolemma b. Sarcoplasmic Reticulum (SR) – surrounds each myofibril (sealed double sheet, lacy, totally continuous, no big holes, but there are channels that can open) i. Next to T tubule SR forms lateral sacs ii. Each T tubule flanked on either side by 2 lateral sacs 12 15 ii. Few motor neurons active. Weak contraction iii. Many motor unites active. Strong contraction c. Asynchronous recruitment of motor units (take turns) prevents fatigue (decreased response of the muscle because of previous activity). i. Happens with posturous muscles during long term contractions, subconscious switching of motor units 13. Though skeletal muscle length is limited in the body, starting length of the muscle affects force of contraction a. Stretching muscle so that there is NO overlap of myofilaments. i. There is no tension generated because the CBs cannot attach and no overlap of myosin and actin. b. Compress muscle so there is too much overlap of myofilaments i. Actin overlaps itself and does not allow for the maximum number of attachments with CBs c. Maximum CB binding i. When actin only overlaps myosin and the greatest number of CBs can be attached d. Skeletal muscle attachment to bones keeps them near optimal length for optimal CB attaching 14. Hypertrophy – increased size of an organ by increasing the cell size 15. Types of muscles produced by… a. Aerobic exercise does not increase the muscle mass by very much. It does however increase the number of oxidative fibers that use aerobic pathways. b. Anaerobic exercise increases muscle mass (hypertrophy) 16. There are different muscle fiber types Muscle Fiber Types Slow Oxidative (red) Breaks down ATP slowly, slow CB cycling. Use aerobic pathway Fast Glycolytic (white) Breaks down ATP quickly, fast CB cycling. Use anaerobic pathway Myoglobin Lots (this causes the red) Little (this causes the white) Glycolytic enzymes Low High activity and lots of them Mitochondria, Capillaries Lots Little (rely on stored nutrients and don’t need O2) Glycogen (storage compound for glucose) Little because nutrients are delivered Lots – use glycogen up for contraction Twitch Rate Slow Fast Fatigue Resistance High (fatigue slowly) Low (fatigue quickly, but recover quickly) ATPase activity Low. Contraction is slow. Split ATP slow. Slow CB cycling High. Contraction is fast. Split ATP fast. Fast CB cycling Muscle Cell Diameter Small Large – lots of myofibrils 17. Atrophy – decrease in muscle size, cells shrink a. Denervation atrophy – cut nerve to muscle (or disease (polio) of nerve) i. So that losing nerve stimulation – muscles need to keep happy and healthy b. Disuse atrophy – not used for a period of time i. Immobilized in a cast for a period of time. Leg in the cast is smaller and can reverse it by using that muscle 15 16 Smooth Muscle and Cardiac Muscle Objectives 1) Smooth muscle cells are smaller than skeletal muscle cells. Smooth muscle has myofilaments but they are not arranged the same way they are in skeletal muscle. Activation of the cross bridges (which allows myosin to bind to actin) is different in smooth muscle (compared to skeletal muscle). a) Smooth Muscle i) Location – the calls of hollow (tubes) organs such as GI tract, blood vessels, airways, uterus ii) Innervation – ‘involuntary’ muscle in ANS iii) Size – much smaller than skeletal muscle fibers. 1 smooth muscle cell diameter is about equal to 1 myofibril diameter iv) Anatomy – spindle shaped, single nucleus. v) Lack striations – no sarcomeres (which cause striations), no myofibrils b) Smooth muscle has myofilaments – actin and myosin i) Myosin is longer in smooth muscle than in skeletal muscle ii) Actin is anchored to dense bodies and act like Z-lines iii) Arranged in a diagonal pattern to the long axis of the cell iv) There is no troponin to activate CBs v) Phosphorylation of myosin activates CB by Kinase (1) Kinase is an enzyme that puts a phosphate group on myosin to allow for the rigor complex vi) Contraction turned off by the removal of phosphate group by phosphotase vii) Turn on CB cycling by putting a phosphate group on myosin, occurs with increase [Ca++] in cytosol viii) Turn off CB cycling by removing a phosphate group off myosin, occurs with decrease [Ca++] in cytosol ix) Smooth muscle – change in myosin activates CBs x) Skeletal muscle – change in actin activates CBs c) Ca++ comes from outside and inside the cell to turn on contraction in smooth muscle i) Smooth muscle lacks T tubules because the cells are small and don’t need a quick switch for contraction like in skeletal muscle (SR not well developed) ii) Ca++ trigger to turn on contraction comes from 2 sources: (1) ECF (2) Not so developed SR d) Smooth muscle responds to more than neural input; some inputs inhibit or decrease the contraction of smooth muscle i) Membrane activation – effecting contractile activity, multiple inputs for contraction, can increase or decrease contraction ii) Skeletal muscle – 1 input – somatic/motor neuron always excitatory iii) Smooth muscle – many inputs – all alter concentration of Ca++ in the cytosol (increase and decrease [Ca++] in the cytosol (1) Doesn’t necessarily have to be an AP that causes the contraction (2) If it is AP, then Ca++ goes into cell during depolarization during AP 16 17 (3) More depolarization, increased [Ca ++ ] in cytosol, more contraction (4) More hyper polarization, decreased [Ca ++ ] in cytosol, decreased contraction (5) Can have contraction with NO change in membrane potential – example: hormone binds to one receptor and causes second messenger inside cell and causes [Ca++] release from SR e) Smooth muscle is better than skeletal muscle for surrounding hollow organs i) The length of contractions and twitches in smooth muscle (3-5 seconds) are longer than that of skeletal(0.1 seconds) and cardiac muscle(0.3 seconds) ii) Sustained contractions with less ATP used (1) Myosin can stay attached to actin in a latched state (rigor-like) and can maintain tension with low ATP use which makes it economical and useful because lots of smooth muscle contracts for long periods iii) Ca++ pump on SR and on cell membrane (because Ca++ comes from SR and ECF) – on both places, slow – Ca++ spends more time in cytosol therefore longer twitches f) Smooth muscle tone i) Basal Degree of tone (tension) – arterioles (type of blood vessel), gut smooth muscle (encircles tube). If have a low level of tension normally, can increase contraction or decrease contraction. (1) Increase contraction  constrict (2) Decrease contraction  dilate g) Smooth muscle develops tension over greater range of starting lengths than skeletal muscle i) If stretched 2 times normal length, can still develop tension, actin still overlaps myosin which is longer in smooth muscle. ii) This is really good for the urinary bladder because when it becomes full and muscle is stretched it can still contract and empty, skeletal muscle would not let it contract once stretched h) Smooth muscle can all by itself cause APs in the smooth muscle cell i) Unstable membrane potentials in some (single unit) smooth muscle – spontaneous electrical activity – changes in membrane potential on its own – without stimulus from outside the muscle (extrinsic stimulus) ii) Slow waves – gradual oscillations in membrane potential (1) An increase in nerves (ANS) and hormones might depolarize to threshold iii) Pacemaker Potentials – spontaneous depolarization of single cell, if it reaches threshold it causes an AP then repolarizes and starts to depolarize again (1) Acts as a ramp to threshold, shoots it there (2) Common in the gut and other tubes in the body i) Autonomic nerves and hormones can stimulate (increase Ca++ in cytosol) or inhibit (decrease Ca++ in cytosol) smooth muscle (increase/decrease(increase relaxation) contraction) i) Gut sphincters – symp increases, PS decreases contraction ii) Gut wall – sym decreases, PS increases contraction iii) Uterus smooth muscle – estrogen increases, progesterone decreases contraction 17