Nerve muscle physiology1 /certified fixed orthodontic courses by Indian dental academy


Published on

The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.

Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit ,or call

  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Nerve muscle physiology1 /certified fixed orthodontic courses by Indian dental academy

  1. 1. INDIAN DENTAL ACADEMY Leader in continuing dental education Nerve Muscle Physiology
  2. 2.      Sensation Awareness of internal and external events Perception Assigning meaning to a sensation Central Nervous System The brain and spinal cord Peripheral Nervous System All nervous system structures outside the CNS; i.e. nerves the cranial nerves, ganglia and sensory receptors Neuroglia (neuro = nerve; glia = glue) Nonexcitable cells of neural tissue that support, protect, and insulate neurons
  3. 3.    Neuron Cell of the nervous system specialized to generate and transmit nerve impulses Dendrite (dendr = tree) branching neuron process that serves as a receptive or input region Axon (axo = axis) Neuron process that conducts impulses
  4. 4.      Myelin Sheath Fatty insulating sheath that surrounds all but the smallest nerve fibers Sensory Receptor Dendritic end organs, or parts of other cell types, specialized to respond to a stimulus Resting Potential The voltage difference which exists across the membranes of all cells due to the unequal distribution of ions between intracellular and extracellular fluids Graded Potential A local change in membrane potential that declines with distance and is not conducted along the nerve fiber Action Potential A large transient depolarization event, which includes a reversal of polarity that is conducted along the nerve fiber
  5. 5.     Saltatory Conduction Transmission of an action potential along a myelinated nerve fiber in which the nerve impulse appears to leap from node to node Synapse (synaps = a union) Functional junction or point of close contact between two neurons or between a neuron and an effector cell Neurotransmitter Chemical substance released by neurons that may, upon binding to receptors or neurons or effector cells, stimulate or inhibit those cells Sensory Transduction Conversion of stimulus energy into a nerve impulse
  6. 6.  NEURONS:      Are highly specialized Are one of a few types of excitable cells (able to fire action potentials) in the body Conduct messages in the form of action potentials (nerve impulses) from one part of the body to another Are amitotic; they can not replace themselves; they do, however, have extreme longevity Have a high metabolic rate and can not survive for more than a few minutes without oxygen
  7. 7.  Have a cell body or soma and numerous thin processes (extensions)  Most cell bodies of neurons are located in the CNS where they are protected by the cranium and vertebral column  Within cell bodies all standard organelles are contained
  8. 8.   Dendrites are processes that receive information, they are input regions of the neuron but they do not have the ability to generate action potentials. Axons are processes that can generate and conduct action potentials, they arise at an area associated with neuron's soma called the axon hillock or spike initiation zone (trigger zone); they may be very short or very long depending on where they are conducting information; can give off branches called axon collaterals; finally they form synapses at their terminals.
  9. 9. MYELlNATED AND UNMYELINATED NERVE FIBERS The large fibers are myelinated, and the small ones are unmyelinated. The average nerve trunk contains about twice as many unmyelinated fibers as myelinated fibers.  The central core of the fiber is the axon, and the membrane of the axon is the actual conductive membrane for conducting the 'action potential. The axon is filled in its center with axoplasm, which is a viscid intracellular fluid.  Surrounding the axon is a myelin sheath that is often thicker than the axon itself, and about once every 1 to 3 millimeters along the length of the axon the myelin sheath is interrupted by a node of Ranvier.
  10. 10.    The myelin sheath is deposited around the axon by Schwann cells Saltatory conduction in myelinated fibers from node to node -action potentials are conducted from node to node electrical current flows through the surrounding extracellular fluids outside the myelin sheath as well as through the axoplasm from node to node, exciting successive nodes one after another.
  11. 11.
  12. 12. Velocity of Conduction in Nerve Fibers   The velocity of conduction in nerve fibers varies from as little as 0.25 m/sec in very small unmyelinated fibers to as high as 100 m/sec (the length of a football field in 1 second) in very large myelinated fibers. The velocity increases approximately with the fiber diameter in myelinated nerve fibers and approximately with the square root of fiber diameter in unmyelinated fibers.
  13. 13. BASIC PRINCIPLES OF ELECTRICITY    All cells in the body have an unequal distribution of ions (concentration gradient) and charged molecules (electrical gradient) across their membranes. all have a net negative balance inside relative to outside (differences are always expressed as inside relative to outside). Because opposite charges attract, there is a driving force which would lead to ions flow if not for the presence of the membrane. This represents a potential energy, which is called the potential difference or membrane potential, the measure of this potential energy is called voltage and is expressed in volts or millivolts.
  14. 14.   This membrane potential is present in all cells, including neurons and muscle cells when they are at rest (are not firing action potentials), and is called the resting membrane potential, or resting potential. The size of resting potential ranges from -20 to -200 millivolts in different cells, in neurons it ranges from -50 to -100 millivolts and in muscles it averages about - 70 mV. neurons and muscle cells are unique. Unlike all other cells, they have the ability to actively change the potential across their membranes in a rapid and reversible way. The rapid reversal of membrane potential is referred to as an action potential.
  15. 15.       Source of the potential difference is primarily due to: 1) Imbalance of Na+ and K+ across the membrane 2) Differences in the relative permeability of the membrane to these two ions Almost all membranes are more permeable to potassium since there are a large number of K+ leak channels that are always open 3) There are relatively few such channels for sodium   Na+/K+ pump- a carrier protein found in the membrane transports 2 K+ ions into the cell and 3 Na+ ions out, with the expenditure of one ATP
  16. 16.  1) Depolarization: membrane potential decreases (becomes less negative)  2) Hyperpolarization: membrane potential increases (becomes more negative)
  17. 17.     Whether an action potential (AP) is generated or not depends on the strength of depolarizing stimulus. Stimuli can be: 1. Subthreshold 2. Threshold 3. Suprathreshold
  18. 18. Molecular Events Underlying the Action Potential :     The membrane of all excitable cells contains two special gated channels. One is a Na + channel and the other is a K + channel and both are VOLTAGE GATED . At rest, virtually all of the voltage-gated channels are closed, potassium and sodium can only slowly move across the membrane, through the passive "leak" channels The first thing that occurs when a depolarizing graded potential reaches the threshold is that the voltage gated Na + channels begin to open and Na + influx into the cell exceeds K + efflux out of the cell
  19. 19. Two things happen next:  1) As the membrane depolarizes further and the cell becomes positive inside and negative outside, the flow of Na+ will decrease. 2) Even more importantly, the voltage- gated Na+  channels close When the inactivation gates close, Na+ influx stops and the repolarizing phase takes place.
  20. 20.   Next, the voltage gated K + channels are activated at the time the action potential reaches its peak. At this time, both concentration and electrical gradients favour the movement of K+ out of the cell.  These channels are also inactivated with time but not until after the efflux of K+ has returned the membrane potential to, or below the resting level (after hyperpolarization /positive afterpotential ).
  21. 21.    All-or-none Phenomenon  Because the series of events becomes selfperpetuating once the membrane is depolarized past threshold, and because all action potentials are of the exact same size, it is said to be an all-or-none event.  If threshold is reached, you get an action potential that is always the same. Therefore, both the threshold and suprathreshold stimuli can generate only one response - an action potential.
  22. 22.   As a result, the membrane cannot be excited to generate another action potential at this site until the ongoing event is over. This period during which the membrane is completely unexcitable is the absolute refractory period .  Once the membrane potential has returned to resting conditions, another action potential can be generated. However, before it happens there is a short period during which the voltage gated K+ channels are still open producing hyperpolarization, during which the membrane potential is further from threshold and during which a larger than normal stimulus is required to generate an action potential. This is the relative refractory period .
  23. 23.      Synapses are the junctions between neurons and the structures they innervate.  Electrical Synapses: There are some specialized neurons, which are connected by gap junctions, and through which ions can flow and, hence, across which action potentials can be directly propagated. these are relatively uncommon in the nervous system they are extremely important in the cardiac muscle tissue Chemical Synapses: Most neurons are separated from the object that they innervate by a short gap. These gaps or junctions are very narrow but the action potential cannot jump across them. Instead, electrical activity is usually transferred from the axon terminal to the next cell by a chemical messenger - a neurotransmitter, such transfer can occur in only one direction.
  24. 24. Neurotransmitters:  At present there are over 100 chemical substances believed to act as neurotransmitters in different parts of the nervous system. Many neurons make more than one transmitter and may release more than one transmitter upon the arrival of a single action potential at the axon terminal.   The main neurotransmitters of the peripheral NS. are:•        Acetylcholine (Ach) ACh is the primary neurotransmitter of the somatic NS and the parasympathetic division of the ANS.   •        Norepinephrine (NE).  NE is the primary neurotransmitter of the sympathetic division of the ANS 
  25. 25. Skeletal muscle  40% of adult body weight  50% of child’s body weight  Muscle contains: 75% water  20% protein  5% organic and inorganic compounds   Functions: Movement  Maintenance of posture 
  26. 26. Whole muscle  Separate organ  Encased in connective tissue – fascia  Functions of fascia Protect muscle fibers  Attach muscle to bone  Provide structure for network of nerves and blood/lymph vessels 
  27. 27. Layers of fascia  Epimysium Surface of muscle  Tapers at ends to form tendon   Perimysium  Divides muscle fibers into bundles or fascicles  Endomysium  Surrounds single muscle fibers
  28. 28. PHYSIOLOGIC ANATOMY OF SKELETAL MUSCLE     skeletal muscles are made of numerous fibers  ranging from 10 to 80 micrometers in diameter. Each of these fibers in turn is made up of  successively smaller subunits In most muscles, the fibers extend the entire  length of the muscle; except for about 2 per cent  of the fibers, each is innervated by only one nerve ending,  located near the middle of the fiber.
  29. 29.  Organization of skeletal muscle, from the gross to the molecular level..
  30. 30.    SARCOLEMMA. The sarcolemma is the cell.  Membrane of the muscle fiber.  It  consists of a true cell membrane, called the  plasma membrane, and an outer coat made up of a  thin layer of polysaccharide material that contains  numerous thin collagen fibrils. At the end of the muscle fiber sarcolemma fuses  with a tendon fiber, and the tendon fibers in turn  collect into bundles to form the muscle tendons  and thence insert into the bones.
  31. 31. Sarcoplasm – cytoplasm of muscle cell  Sarcotubular system  Sarcoplasmic reticulum  Sarcotubules and transverse tubules  Ca++ uptake, regulation, release and storage 
  32. 32. SARCOPLASM.    The myofibrils are suspended inside the muscle  fiber in a matrix called sarcoplasm, which is  composed of usual intracellular constituents,  The fluid of the sarcoplasm contains large  quantities of potassium, magnesium, phosphate,  and protein enzymes. There are tremendous numbers of mitochondria that lie between and parallel to the myofibrils, it  indicates the great need for large amounts of  adenosine triphosphate (ATP) for the contracting  myofibrils..
  33. 33.      MYOFIBRILS; ACTIN AND  Troponin Tropomyosin(thin) MYOSIN FILAMENTS.(thick) Each muscle fiber contains several hundred to  several thousand myofibrils.  Each myofibril in turn has, lying side by side,  about 1500 myosin filaments and 3000 actin filaments, which are large polymerized protein  molecules that are responsible for muscle  contraction.
  34. 34.     The thick filaments are myosin and the thin  filaments are actin. myosin and actin filaments partially interdigitate  and thus cause the myofibrils to have alternate  light and dark bands.  The light bands contain only actin filaments and  are called I bands because they are isotropic to  polarized light.  The dark bands contain the myosin filaments as  well as the ends of the actin filaments where they  overlap the myosin and are called A bands because  they are anisotropic to polarized light..
  35. 35.
  36. 36.  small projections from the sides of the  myosin filaments are cross-bridges. They  protrude from the surfaces of the myosin  filaments along the entire extent of the  filament except in the very center.   Interaction between these cross- bridges  and the actin filaments causes contraction
  37. 37.    ends of the actin filaments are attached to Z disc. From this disc, these filaments extend in both  directions to interdigitate  with the myosin  filaments.  The Z disc is composed of filamentous proteins  different from the actin and myosin filaments  the entire muscle fiber has light and dark bands,  as do the-individual myofibrils. These bands give  skeletal and cardiac muscle their striated  appearance.
  38. 38.   The portion of a myofibril that lies between two  successive Z discs is called a sarcomere, When the muscle' fiber is at its normal, fully  stretched resting length, the length of the  sarcomere is about 2 micrometers. At this length,  the actin filaments overlap the myosin filaments  and are just beginning to overlap one another.
  39. 39. Neuronal Control of Muscle Contraction  Movement requires contraction of many fibers within a muscle & of many muscles within the body – correctly timed with one another & regulating the strength of contraction  Coordination generated within NS = most muscle contract only when APs arrive at Neuromuscular Junction
  40. 40. TRANSMISSION OF IMPULSES FROM NERVES TO SKELETAL MUSCLE FIBERS:NEUROMUSCULAR JUNCTION   The nerve ending makes a junction, called the  neuromuscular junction, with the muscle fiber  near the fiber's midpoint, and the action potential  in the fiber travels in both directions toward the  muscle fiber ends. With the exception of about 2  per cent of the muscle fibers, there is only one  such junction per muscle fiber.
  42. 42.  The nerve fiber branches at its end to form a  complex of branching nerve terminals, which invaginate into the muscle fiber but  lie outside the muscle fiber plasma  membrane. The entire structure is called the  motor end plate.
  43. 43. End Plate Potential And Excitation Of The  Skeletal Muscle Fiber    sudden insurgence of sodium ions into the muscle  fiber when the acetylcholine channels open causes  the internal membrane potential in the local area of the end plate to increase in the positive  direction as much as 50 to 75 millivolts, creating a  local potential called the end plate potential. end plate potential created by the acetylcholine  stimulation is normally far greater than enough to  initiate an action potential in the muscle fiber.
  44. 44. Safety Factor For Transmission At  The  Neuromuscular Junction   Each impulse that arrives at the neuromuscular junction causes about three times as much end plate potential as that required to stimulate the muscle fiber therefore the normal neuromuscular junction is said to have a safety factor repeated stimulation diminishes the number of vesicles of acetylcholine released with each impulse so much that impulse fails to pass into the muscle fiber – FATIGUE
  45. 45.    A new action potential cannot occur in an excitable fiber as long as the membrane is still depolarized from the preceding action potential. shortly after the action potential is initiated, the sodium channels (or calcium channels, or both) become inactivated, and any amount of excitatory signal applied to these channels at this point will not open the inactivation gates. The only condition that will re-open them is for the membrane potential to return to the original resting membrane potential level.
  46. 46.   The period during which a second action potential cannot be elicited, even with a strong stimulus, is called the absolute refractory period. This period for large myelinated nerve fibers is about 1/2500second.. After the absolute refractory period is a relative refractory period, lasting about one quarter to one half as long as the absolute period. During this time, stronger than normal stimuli can excite the fiber.
  47. 47. The cause of this relative refractoriness are: (1) During this time, some of the sodium channels still have not been reversed from their inactivation state, and (2) the potassium channels are usually wide open at this time, causing greatly excess flow of positive potassium ion charges to the outside of the fiber opposing the stimulating signal 
  48. 48. Steps in muscle contraction  Excitation Action potential traverses nerve  Neurotransmitter released into neuromuscular junction - Ach  Muscle fiber depolarization   Sarcolemma to transverse tubules – Ca++ release from sarcoplasmic reticulum
  49. 49.  Coupling  Ca++ binds to troponin-tropomyosin complex
  50. 50.  Contraction Ca++ binding moves troponin-tropomyosin complex  Myosin heads attach to actin    Crossbridge formation Crossbridge cycling  Moves the myosin heads along the actin and shortens the sarcomere
  51. 51.  Relaxation Ca++ removed from troponin-tropomyosin complex  Cross bridge detachment  Ca++ pumped into SR – active transport  Sarcomere lengthens 
  52. 52. Excitation-contraction coupling
  53. 53.
  54. 54. GENERAL MECHANISM OF MUSCLE CONTRACTION The initiation and execution of muscle contraction occurs in following sequential steps. 1. An action potential travels along a motor nerve to its endings on muscle fibers. 2. At each ending, the nerve secretes a small amount of the neurotransmitter substance acetylcholine. 3. The acetylcholine acts on a local area of the muscle fiber membrane to open multiple acetylcholine-gated channels through protein molecules in the muscle fiber membrane.
  55. 55. 4. Opening of the acetylcholine channels allows large quantities of sodium ions to flow to the interior of the muscle fiber membrane at the point of the nerve terminal. This initiates an action potential in the muscle fiber. 5. The action potential travels along the muscle fiber membrane in the same way that action potentials travel along nerve membranes. 6. The action potential depolarizes the muscle fiber membrane and also travels deeply within the muscle fiber Where it causes the sarcoplasmic reticulum to release into the myofibrils large quantities of calcium ions that have been stored within the reticulum.
  56. 56.   7. The calcium ions initiate attractive forces between the actin and myosin filaments, causing them to slide together, which is the contractile process. 8. After a fraction of a second, the calcium ions are pumped back into the sarcoplasmic reticulum, where they remain stored until a new muscle action potential comes along; this removal of the calcium ions from the myofibrils causes muscle contraction to cease.
  57. 57. Sliding Filament Theory  during contraction, thick and thin filaments do not change their length, but slide past each other (overlapping further) as a result, individual sarcomeres shorten ,myofibrils shorten, the entire cell shortens
  58. 58. Muscle contraction  Types  Isometric or static Constant muscle length  Increased tension   Isotonic Constant muscle tension  Constant movement  – Concentric - shortening – Eccentric - lengthening
  59. 59.
  60. 60.    It demonstrates that maximum contraction occurs when there is maximum overlap between the actin filaments and the cross-bridges of the myosin filaments, the greater the number of cross-bridges pulling the actin filaments, the greater the strength of contraction. when the muscle is at its normal resting length, which is at a sarcomere length of about 2 micrometers, it contracts with maximum force of contraction.
  61. 61.   If the muscle is stretched to much greater than normal length before contraction, a large amount of resting tension develops in the muscle even before contraction takes place; this tension results from the elastic forces of the connective tissue, blood vessels, nerves, and so forth. the increase in tension during contraction, called active tension, decreases as the muscle is stretched much beyond its normal length
  62. 62. Relation of Velocity of Contraction to LOAD A muscle contracts extremely rapidly when it contracts against no load-to a state of full contraction in about 0.1 second for the average muscle. When loads are applied, the velocity of contraction becomes progressively less as the load increases
  63. 63. ATP & Muscle Contraction Muscle contraction is absolutely dependent on ATP for 3 processes (Myosin ATPase breaks down ATP as fiber contracts) : 1) hydrolysis of ATP energizes the myosin head which begins the “power stroke” of the cross-bridge cycle 2) attachment of ATP to myosin facilitates the dissociation of the actomyosin complex allows for continues x-bridge cycling and further shortening Each x-bridge cycle shortens the muscle 1% of its resting length 3) Ca++ reuptake into the SR occurs through an ATP dependent pump 
  64. 64. Sources of ATP for Muscle Contraction
  65. 65. Summation   contraction of individual muscle fibers is allor-none - any graded response must come from the number of motor units stimulated at any one time summation = adding together of individual muscle twitches to make a whole muscle contraction - accomplished by increasing number of motor units contracting at one time (spatial summation) or by increasing frequency of contraction of individual muscle contractions (temporal summation)
  66. 66.
  67. 67.    Summotion means the adding together of individual twitch contractions to increase the intensity of overall muscle contraction. Summation occurs in two ways: (1) by increasing the number of motor units contracting simultaneously, which is called multiple fiber summation,and (2) by increasing the frequency of contraction, which is called frequency summation and can lead to tetanization.
  68. 68.  To the left are displayed individual twitch contractions occurring one after another at low frequency of stimulation. Then, as the frequency increases, there comes a point when each, new contraction occurs before the preceding one is over. This is called tetanization.
  69. 69.   CHANGES IN MUSCLE STRENGTH AT THE ONSET OF CONTRACTION- THE STAIRCASE EFFECT (TREPPE). When a muscle begins to contract after a long period of rest, its initial strength of contraction may be as little as one half its strength 10 to 50 muscle twitches later. That is, the strength of contraction increases to a plateau, a phenomenon called the staircase effect or treppe.
  70. 70.  Reflects the amount of Ca2+ available in the sarcoplasm and more efficient enzyme activity as the muscle liberates heat - Principal behind warming-up before physical activity
  71. 71.  Muscle fatigue –Prolonged strong contractions leads to fatigue due to inability of contractile & metabolic processes to supply adequately to maintain the work load - nerve continues to function properly passing AP onto the muscle fibers but contractions become weaker due to lack of ATP  Hypertrophy - increase in muscle mass caused by forceful muscular activity – increase power of muscle contraction  Atrophy - when a muscle is not used for a length of time or is used for only weak contractions
  72. 72.    HYPERPLASIA OF MUSCLE FIBERS. Under rare conditions of extreme muscle force generation, the numbers of muscle fibers increase, but by only a few percentage points, in addition to the fiber hypertrophy process. This increase in fiber numbers is called fiber hyperplasia. it occurs by the mechanism of linear splitting of previously enlarged fibers.
  73. 73. Effects of Muscle Denervation     When a muscle loses its nerve supply, it no longer receives the contractile signals that are required to maintain normal muscle size. atrophy begins almost immediately. After about 2 months, degenerative changes also begin to appear in the muscle fibers themselves. If the nerve supply grows back to the muscle, full return of function usually occurs in about 3 months, but from that time onward, the capability of functional return becomes less and less, with no return of function after 1 to 2 years.
  74. 74. Satellite Cells: repair and regeneration   Satellite cells play a critical role in repairing or replacing myofibrils which have been damaged Proliferation and differentiation of satellite cells -Migrate into cytoplasm (near point of damage) - Fuse together to form myotubes and align themselves within existing fiber, or become a new fiber May play a role in stretch induced muscle growth
  75. 75. Muscle Fiber Types
  76. 76. Contract or Relax? Effect of type of stimuli
  77. 77.
  78. 78. Receptors in Muscle: Feedback to CNS     Muscle contains receptors that provide sensory information regarding: – Chemical changes (i.e., O2, CO2, H+): chemoreceptors – Tension development: Golgi Tendon Organs (GTO’s) – Muscle length: Muscle spindles Information from these receptors provides information about the energetic requirements of exercising muscle and about movement patterns
  79. 79. Muscle spindle – Detect dynamic and static changes in muscle length– Stretch reflex • Stretch on muscle causes reflex contraction  Golgi tendon organ (GTO) – Monitor tension developed in muscle – Prevents damage during excessive force generation • Stimulation results in reflex relaxation of muscle 
  80. 80.    Muscle spindles respond to muscle stretch Gamma motor neurons are coactivated during contraction – Causing contraction of fibers within muscle spindle – Deviations in consistency signal excessive stretch
  81. 81. Golgi Tendon Organ  Located in tendon Monitor muscle tension Activation causes inhibition of alphamotor neuron “Safety mechanism” against excessive force during contraction
  82. 82. Role of spindles and GTO’s in muscle stretch and spasm    Reduced pliability of the myotendinous regions(golgi receptors) of skeletal muscle may increase risk of injury – Effective stretching techniques are designed to inhibit muscle spindles and to activate GTO’s Muscle cramps/spasms may be caused by overactive spindles and underactive GTO’s in fatigued skeletal muscle
  83. 83.  Myotactic reflex  Clasp knife reflex
  84. 84.
  85. 85. Thank you For more details please visit