Class 13 Control of Movement Smooth Muscle Sp22 PDF

Muscle & Movement PHSL 3051 Dr. Barnett Control of Movement Class 13 Learning Objectives Class 13: The Somatic Nervous System: Control of Movement | Smooth Muscle Derrickson (1st edition: p. 356-359, 412-428, 396-404,2nd edition: p. 425-437, 411-419) 1. Compare and contrast the...

Muscle & Movement PHSL 3051 Dr. Barnett Control of Movement Class 13 Learning Objectives Class 13: The Somatic Nervous System: Control of Movement | Smooth Muscle Derrickson (1st edition: p. 356-359, 412-428, 396-404,2nd edition: p. 425-437, 411-419) 1. Compare and contrast the organization of the somatic nervous system versus the autonomic nervous system. 2. Compare and contrast the structure, anatomical location, and function of muscle spindles and Golgi tendon organs. 3. Describe the series of events initiated by striking the patellar tendon with a percussion hammer that leads to extension of the lower leg (i.e. the knee jerk reflex) 4. Describe the properties of the withdrawal reflex initiated by stepping on a sharp object. 5. List the regions of the brain involved in middle level of motor control and describe the main function that these structures serve. 6. Describe the function of higher centers in motor control. 7. Compare how smooth muscle activation and relaxation differs from the activation and relaxation of skeletal muscle. 8. List the potential sources of calcium that may contribute to smooth muscle activation 2 3 Review: Local Level of Motor Control Communication pathways from peripheral sensors that provide direct inputs to the local motor control centers as well as the higher centers of motor control Facilitates a faster response to changes in the environment May result in either excitation or inhibition of a motor neurons Somatic Reflex Arcs – What do they respond to? The Stretch Reflex – What does it cause? What sensory receptor is involved? The Excess Tension Reflex – What does it cause? What sensory receptor is involved? The Flexor Reflex – What does it cause? What sensory receptor is involved? What makes it different from stretch and tendon reflexes? The Crossed Extensor Reflex – What does it cause? What makes it different from stretch, tendon, and flexor reflexes? 4 Review: Four Sources Of Input To Lower Motor Neurons Somatic motor neurons are also referred to as lower motor neurons Axons of lower motor neurons extend from cranial nerves to innervate skeletal muscles of the face and head and from spinal nerves to innervate skeletal muscles of the limbs and trunk Highest Level of Control Sensory, motor and 2 Upper motor neurons from Intention to move, etc. association cortex cerebral cortex Integration of sensory feedback 3 Basal nuclei Thalamus Neural circuits that regulate lower motor neurons. Middle Level of Control Lower motor neurons receive inputs Motor programs to coordinate 4 Cerebellum movements based on intention, directly from: sensory feedback, etc. 1. Local circuit neurons (purple arrow) and Motor centers Upper motor in brain stem 2. Upper motor neurons in the cerebral 2 neurons from cortex and brain stem (green arrows). brain stem Lowest Level of Control 1 Local circuit neurons in 3. Neurons in the basal nuclei and brain stem and spinal Input from sensory neurons, local interneurons, etc. cord 4. Cerebellar neurons regulate activity of upper motor neurons (red arrows). Lower motor neurons (final common Because lower motor α-motor neurons pathway) neurons provide all output to skeletal muscles, they cell bodies are in the are called the final brain stem and common pathway. spinal cord Skeletal muscles Based on Derrickson Fig.12.1 Can you follow these signals? Raise right arm Raise left arm Raise both arms 6 How does the organization of the nervous system contribute to control of voluntary movements? What part(s) of the nervous system did you use to recognize the signal ? Does that part of the brain control muscle movement? How is this information converted from a request into movements of specific muscles? 7 Four Sources Of Input To Lower Motor Neurons Highest Level of Control Sensory, motor and 2 Upper motor neurons from Intention to move, etc. association cortex cerebral cortex Integration of sensory feedback 1. Local Circuit Neurons 3 Basal nuclei Thalamus Middle Level of Control Local reflexes Motor programs to coordinate Cerebellum movements based on intention, 4 sensory feedback, etc. 2. Upper Motor Neurons Motor centers Upper motor in brain stem Cerebral Cortex 2 neurons from brain stem Brain Stem Lowest Level of Control 1 Local circuit neurons in Input from sensory neurons, local brain stem and spinal interneurons, etc. cord 3. Basal Nuclei Neurons Lower motor neurons (final common 4. Cerebellar Neurons α-motor neurons pathway) Because lower motor neurons provide all output to skeletal muscles, they cell bodies are in the are called the final brain stem and common pathway. spinal cord Skeletal muscles Based on Derrickson Fig.12.1 8 Upper Motor Neurons: Brainstem Indirect Motor Pathways Control of involuntary movements that regulate posture, balance, muscle tone, and reflexive movements of the head and trunk Vestibular Nuclei help control posture and balance Reticular Formation regulates posture and muscle tone during movements during ongoing movements.  Medial reticulospinal tract excites muscles  Lateral reticulospinal tract inhibits muscles Superior Colliculus assists with movements of the head, trunk and saccadic eye movements through the tectospinal tract – responds to sudden/unexpected stimuli Red Nucleus controls precise voluntary movements of the upper limbs through the rubrospinal tract 9 Upper Motor Neurons: Primary Motor Cortex Corticospinal Pathways Voluntary control of skeletal muscles of the body (limbs & trunk) Two Tracts  Lateral Corticospinal Tract - crossesthe midline of the body at the level of the medulla – responsible for precise and agile movements of the hands and feet  Ventral Corticospinal Tract – cross the midline of the body at the level of the spinal cord – responsible for the trunk and proximal parts of the limbs Right cerebral cortex controls muscles on the left side of the body and the left cerebral cortex controls muscles on the right side of the body 10 Upper Motor Neurons: Corticobulbar Pathways RIGHT SIDE OF Primary motor cortex LEFT SIDE OF BODY BODY Voluntary control of muscles in the head Descend from the cerebral cortex Upper motor along the corticobulbar tract neuron Some axons cross over – others do CORTICOBULBAR TRACT not Midbrain Lower motor neuron Control facial expression, chewing, Facial (VII) nerve speech, and movements of the To skeletal muscles of facial eyes, tongue, and neck expression Lower motor neuron Hypoglossal (XII) nerve To skeletal muscle of the tongue 11 Primary Motor Cortex Homunculus Similar to the somatosensory cortex there is a “map” of the body present on the primary motor cortex Each region of the primary motor cortex controls muscle fibers in a different part of the body Which parts of the body have the largest representations? Why does the face have such a large representation in the motor homunculus? A. The face is more sensitive to touch B. The face is emotionally expressive 12 Four Sources Of Input To Lower Motor Neurons Highest Level of Control Sensory, motor and 2 Upper motor neurons from Intention to move, etc. association cortex cerebral cortex Integration of sensory feedback 3 Basal nuclei Thalamus 1. Local Circuit Neurons Middle Level of Control Local reflexes Motor programs to coordinate 4 Cerebellum movements based on intention, sensory feedback, etc. 2. Upper Motor Neurons Upper motor Motor centers in brain stem 2 Cerebral Cortex neurons from brain stem Brain Stem Lowest Level of Control 1 Local circuit neurons in Input from sensory neurons, local brain stem and spinal interneurons, etc. cord 3. Basal Nuclei Neurons Lower motor neurons (final common Because lower motor 4. Cerebellar Neurons α-motor neurons cell bodies are in the pathway) neurons provide all output to skeletal muscles, they are called the final brain stem and common pathway. spinal cord Skeletal muscles Based on Derrickson Fig.12.1 13 The Basal Nuclei Sensory, Association, and Motor Areas of the Cerebral Cortex Anatomy: Made up of several masses of gray matter found deep within the cerebral hemispheres Physiology:  Control the initiation of movement: Cerbral Cortex  Basal Nuclei  Thalamus  Motor Cortex Basal Nuclei  Control the Suppression of Unwanted Movements. Tonic Inhibition of Neurons in the Thalamus  Regulation of Muscle Tone Thalamus Basal Nuclei sends Action Potentials through the Reticulospinal Tracts  Regulation of Non-Motor Processes: Motor Areas of the Cerebral Cortex Helps to initiate and terminate attention, memory, planning, and emotional behaviors (limbic system) Disorders of the Basal Nuclei include:  Parkinson’s Disease Corticospinal and corticobulbar tracts  Huntington’s Disease Initiation of movements  Tourette’s syndrome 14 Four Sources Of Input To Lower Motor Neurons Highest Level of Control Sensory, motor and 2 Upper motor neurons from Intention to move, etc. association cortex cerebral cortex Integration of sensory feedback 3 Basal nuclei Thalamus 1. Local Circuit Neurons Middle Level of Control Local reflexes Motor programs to coordinate 4 Cerebellum movements based on intention, sensory feedback, etc. 2. Upper Motor Neurons Upper motor Motor centers in brain stem 2 Cerebral Cortex neurons from brain stem Brain Stem Lowest Level of Control 1 Local circuit neurons in Input from sensory neurons, local brain stem and spinal interneurons, etc. cord 3. Basal Nuclei Neurons Lower motor neurons (final common Because lower motor 4. Cerebellar Neurons α-motor neurons cell bodies are in the pathway) neurons provide all output to skeletal muscles, they are called the final brain stem and common pathway. spinal cord Skeletal muscles Based on Derrickson Fig.12.1 The Cerebellum 1. Monitors intention for movement 2. Monitors actual movement 3. Compares command signals with sensory information 4. Sends out corrective feedback 16 Smooth muscles Cells are 30 – 200 µm long and 3 – 8 µm in diameter Cells are spindle-shaped, thicker in the middle and tapered toward each end One centrally located nucleus Thick and thin filaments but no myofibrils Thick filaments have myosin crossbridges along their entire length (no bare zone at the center) Thin filaments composed of actin and tropomyosin, but no troponin Thin filaments are bound to membrane anchored protein assemblies called dense bodies (no Z- lines) Dense bodies are also linked by intermediate filaments as part of the cytoskeleton Cells are physically attached to one another by desmosomes in their cell membrane. 17 Where is smooth muscle found? Smooth Muscle lines hollow structures and organs such as: Arteries – regulate blood pressure Arterioles (small arteries) – regulate distribution of blood flow Airways – regulate airflow in the bronchi of the lungs Stomach – mix contents with secretions Stomach Intestines – move contents from stomach to rectum Urinary bladder – store and expel urine Uterus – expel baby 18 The Role of Ca2+ in Muscle Contraction:  Skeletal muscle – the amount of Ca2+ released from the SR as a result of an action potential is sufficient to briefly saturate all of the troponin Ca2+ binding sites. (resulting in a twitch)  Smooth muscle - Cytosolic Ca2+ concentration can be increased in a graded manner (i.e. concentration can change by different amounts depending on the stimulus)  The amount of tension generated in muscle cells is determined by the concentration of Ca2+ in the cytosol  There are many ways in which cytosolic Ca2+ in smooth muscle can be increased  The sarcoplasmic reticulum (SR) does not contain as much calcium as the SR in skeletal muscle and provides a small percentage of the calcium required for contraction 19 Where does the Ca2+ come from for Smooth Muscle Contraction? Extracellular Ca2+ can enter the cell down its huge gradient (10,000 times higher concentration outside the cell than inside) via: Voltage-gated Ca2+ channels Ligand-gated Ca2+ channels Stretch-activated cation (Na+ and Ca2+) Release of Ca2+ from intracellular stores (sarcoplasmic reticulum) G-protein coupled receptors 20 Smooth Muscle Contractile Proteins Troponin – No! Role as calcium sensor is replaced by Calmodulin Calmodulin – Calcium sensor in smooth muscle  Ca2+ bound calmodulin complex binds to Myosin Light-Chain Kinase, thereby activating the kinase Tropomyosin – Yes.  However, without Troponin to lock its position it cannot block myosin’s binding to actin as strongly as it does in skeletal muscle Actin – Yes! Still provides the cable for myosin to pull along. Myosin – must be phosphorylated by the action of myosin light-chain kinase to be able to bind to actin and start cross bridge cycling Myosin Light Chain Kinase (MLCK)  activated by Ca2+-calmodulin  Phosphorylates Myosin’s Regulatory Light Chain when active. Myosin Light Chain Phosphatase (MLCP) Dephosphorylates Myosin’s Regulatory Light Chain to relax smooth muscle. 21 Smooth Muscle Contraction Cells have both Thick (myosin-based) and thin (actin-based) filaments, biochemically similar to those in Sarcolemma skeletal muscle fiber Dense body Intermediate Myosin crossbridge interaction with filament actin to cause smooth muscle contraction. Length-tension relationship – the optimum length that permits Nucleus maximum tension generation is found over broader range than skeletal muscle. Thick filament Because activation and relaxation Thin filament occur more slowly smooth muscle maintains a tone (partially contracted state) that allows for steady pressure Relaxed Contracted on the structures it surrounds Figure 11.25 22 Smooth Muscle Activation 1. Calcium (Ca2+) binds to calmodulin in the cytoplasm. Sarcoplasm of smooth muscle fiber 2. Ca2+-calmodulin complex binds to MLCK Ca2+ (inactive) and activates Myosin Light Chain Kinase (MLCK). 1 2 3. Activated MLCK phosphorylates the Calmodulin Ca2+–calmodulin myosin regulatory light chain (RLC) complex by transferring a phosphate from MLCK ATP. Myosin (inactive) (active) 4. Phosphorylated myosin heads bind 3 P Phosphate group to actin and begin contraction by P MLCP crossbridge cycling. 4  Contraction is triggered by calcium induced Myosin-binding site of an actin changes to the thick filament molecule  Contractions start more slowly and last longer P than skeletal muscle contractions 5. Relaxation involves a decrease in Tropomyosin Thin filament sarcoplasm calcium levels and dephosphorylation of myosin by myosin Based on Figure 11.26 light chain phosphatase (MLCP). 23 Autonomic Innervation & Single-Unit vs. Multi-unit Smooth Muscle Smooth muscles are regulated by the autonomic nervous system but individual cells do not have neuromuscular junctions. Instead the autonomic nerves release transmitter molecules from varicosities along the axon. The transmitter molecules then bind to receptors on smooth muscle cells. Single-unit Smooth Muscles (common) are connected by gap junctions so that excitation of one cell results in the excitation of the entire collection of interconnected muscle cells. Multi-unit Smooth Muscles (rare) activate individually after reception of the activating signal. For both cell types, physical interconnections by desmosomes in the cell membrane facilitate the development of tension through the smooth muscle tissue. Ciliary bodies are part of the iris and Stomach Eye contraction reshapes the lens for focus on near objects Autonomic neuron Autonomic neuron Gap junction varicosity varicosity (a) Single-unit smooth muscle (b) Multi-unit smooth muscle 24 Comparison of the activation sequence of smooth and skeletal muscles ↑ Cytosolic Ca2+ ↑ Cytosolic Ca2+ Ca2+ binds to Ca2+ binds to calmodulin in troponin on thin cytosol filaments Ca2+ -calmodulin complex binds to myosin light-chain kinase Conformational change in troponin moves Myosin light-chain kinase tropomyosin out of the uses ATP to blocking position phosphorylate myosin crossbridge RLC Phosphorylated Myosin crossbridges bind to actin crossbridges filaments bind to actin Crossbridge Crossbridge cycle produces cycle produces tension and tension and shortening shortening 25 Autorhythmic Cells: Pacemakers Depolarizing Repolarizing phase of action phase of action potential potential Membrane potential (mV) Threshold Pacemaker cells have an unsteady resting membrane potential, this is sometimes Pacemaker due to “leaky” ion channels potential When threshold for voltage- Time (min) gated Ca2+-channels is Mechanism involved reached the cells depolarize Pacemaker potential: An increase in Ca2+ movement into the cell Repolarization requires or a decrease in K+ movement out of the cell closing of the Ca2+-channels Depolarizing phase: L-type voltage-gated Ca2+ channels open and opening of voltage-gated K+-channels Repolarizing phase: L-type voltage-gated Ca2+ channels close; voltage-gated K+ channels open (a) Pacemaker potential and action potential in an autorhythmic smooth muscle fiber 26 Autorhythmic Cells: Slow waves Depolarizing phase Repolarizing phase of action potential of action potential A different type of Membrane potential (mV) autorhythmic behavior is the undulating membrane Threshold potential known as a slow wave. A stimulus will only reach Slow-wave threshold when the potential underlying slow wave is Time (min) near the crest of a cycle. Mechanism involved The result is a periodic Slow-wave potential: Fluctuations in Na+ movement out of the cell due to periodic changes in Na+/K+ pump activity contraction pattern timed to match the frequency of Depolarizing phase: L-type voltage-gated Ca2+ channels open the slow waves Repolarizing phase: L-type voltage-gated Ca2+ channels close; voltage-gated K+ channels open (b) Slow-wave potential and action potential in an autorhythmic smooth muscle fiber 27 Excitation-Contraction Coupling in Smooth Muscle can Contract: Smooth Muscle  When there is an action Ca2+ potential Neurotransmitter or hormone Ca2+  When there is a subthreshold Neurotransmitter Ligand-gated channel G protein Ion channel Neurotransmitter depolarization Ca2+ L-type voltage-gated Receptor or hormone Ca2+ channel Receptor  When there is no change in G protein Phospholipase C membrane potential Sarcoplasm Changes in calcium Ca2+ Sarcoplasmic reticulum concentration can be due to Trigger Ca2+ the action of: IP3 DAG  Voltage-gated channels Ca2+-induced Ca2+  Calcium release channels release (CICR) Ca2+ release IP3-gated  Receptor-activated channels channel channel Mechanically-gated  IP3 – gated channels Smooth muscle fiber channel  Store-operated channels Store-operated Stretch channel Ca2+  Mechanically gated-channels Ca2+ 28 Cardiac Muscle 29 EC-Coupling Cardiac Style Sarcolemma Muscle action potential Transverse Sarcoplasm tubule Sarcoplasmic Ca2+ reticulum Ca2+ Trigger Ca2+ Ca2+-induced Ca2+ release (CICR) The increased Ca2+ concentration in the sarcoplasm starts muscle contraction. Key: L-type voltage-gated Ca2+ channel (dihydropyridine receptor) Ca2+ release channel (ryanodine receptor) 30 Cardiac AP Membrane potential (mV) Action Tension potential developed Tension (g) Refractory period Time (msec) 31 Next: Cardiovascular Physiology Dr. Wu