TOPIC 6

• The medulla / cardiac control centre sends impulses to the SAN along sympathetic / parasympathetic neurones.: 'This is not wrong, but in the context of controlling heart rate, the emphasis needs to be on the frequency of impulses. When more frequent impulses are sent along sympathetic neurones, heart rate increases. When more frequent impulses are sent along parasympathetic neurones, heart rate decreases.'
• Resting potential


  Inside of axon has a negative charge relative to outside (as more positive ions outside compared to inside)
• How a resting potential is established across the axon membrane in a neurone

  1. Na+/K+ pump actively transports (3) Na+ out of axon AND (2) K+ into axon

  2. Creating an electrochemical gradient: Higher K+ conc. inside AND higher Na+ conc. outside

  3. Differential membrane permeability: More permeable to K+ → move out by facilitated diffusion, Less permeable to Na+ (closed channels)

  
• How changes in membrane permeability lead to depolarisation and the generation of an action potential

  1. Stimulus: Na+ channels open; membrane permeability to Na+ increases, Na+ diffuse into axon down electrochemical gradient (causing depolarisation)

  2. Depolarisation: If threshold potential reached, an action potential is generated, As more voltage-gated Na+ channels open (positive feedback effect), So more Na+ diffuse in rapidly

  3. Repolarisation: Voltage-gated Na+ channels close, Voltage-gated K+ channels open; K+ diffuse out of axon

  4. Hyperpolarisation: K+ channels slow to close so there's a slight overshoot – too many K+ diffuse out

  5. Resting potential: Restored by Na+/K+ pump

  
• All-or-nothing principle


  For an action potential to be produced, depolarisation must exceed threshold potential, Action potentials produced are always same magnitude / size / peak at same potential, Bigger stimuli instead increase frequency of action potentials
• How the passage of an action potential along non-myelinated and myelinated axons results in nerve impulses

  1. Non-myelinated axon: Action potential passes as a wave of depolarisation, Influx of Na+ in one region increases permeability of adjoining region to Na+ by causing voltage-gated Na+ channels to open so adjoining region depolarises

  2. Myelinated axon: Myelination provides electrical insulation, Depolarisation of axon at nodes of Ranvier only, Resulting in saltatory conduction (local currents circuits), So there is no need for depolarisation along whole length of axon

  
• Damage to the myelin sheath

  Less / no saltatory conduction; depolarisation occurs along whole length of axon, So nerve impulses take longer to reach neuromuscular junction; delay in muscle contraction, Ions / depolarisation may pass / leak to other neurones, Causing wrong muscle fibres to contract
• Refractory period


  Time taken to restore axon to resting potential when no further action potential can be generated, As Na+ channels are closed / inactive / will not open
• Importance of the refractory period

  • Ensures discrete impulses are produced (action potentials don't overlap), Limits frequency of impulse transmission at a certain intensity (prevents over reaction to stimulus), Ensures action potentials travel in one direction – can't be propagated in a refractory region
• Factors that affect speed of conductance

  • Myelination: Depolarisation at Nodes of Ranvier only → saltatory conduction, Impulse doesn't travel / depolarise whole length of axon
  • Axon diameter: Bigger diameter means less resistance to flow of ions in cytoplasm
  • Temperature: Increases rate of diffusion of Na+ and K+ as more kinetic energy, But proteins / enzymes could denature at a certain temperature

  
• Cholinergic synapses use the neurotransmitter acetylcholine (ACh).
• Transmission across a cholinergic synapse

  1. At pre-synaptic neurone: Depolarisation of pre-synaptic membrane causes opening of voltage-gated Ca2+ channels, Ca2+ diffuse into pre-synaptic neurone / knob, Causing vesicles containing ACh to move and fuse with pre-synaptic membrane, Releasing ACh into the synaptic cleft (by exocytosis)

  2. At post-synaptic neurone: ACh diffuses across synaptic cleft to bind to specific receptors on post-synaptic membrane, Causing Na+ channels to open, Na+ diffuse into post-synaptic knob causing depolarisation, If threshold is met, an action potential is initiated
• What happens to acetylcholine after synaptic transmission

  It is hydrolysed by acetylcholinesterase, Products are reabsorbed by the presynaptic neurone, To stop overstimulation - if not removed it would keep binding to receptors, causing depolarisation
• How synapses result in unidirectional nerve impulses

  • Neurotransmitter only made in / released from pre-synaptic neurone, Receptors only on post-synaptic membrane

  
• Summation by synapses

  • Addition of a number of impulses converging on a single post-synaptic neurone, Causing rapid buildup of neurotransmitter (NT), So threshold more likely to be reached to generate an action potential

  
• Spatial summation


  Many pre-synaptic neurones share one synaptic cleft / post-synaptic neurone, Collectively release sufficient NT to reach threshold to trigger an action potential

  
• Inhibition by inhibitory synapses

  Inhibitory neurotransmitters hyperpolarise postsynaptic membrane as: Cl- channels open → Cl- diffuse in, K+ channels open → K+ diffuse out, More Na+ required for depolarisation, Reduces likelihood of threshold being met / action potential formation at post-synaptic membranes
• Structure of a neuromuscular junction

  Very similar to a synapse except: Receptors are on muscle fibre instead of postsynaptic membrane and there are more, Muscle fibre forms clefts to store enzyme eg. acetylcholinesterase to break down neurotransmitter
• Effect of drugs on a synapse

  • Some drugs stimulate the nervous system, leading to more action potentials, eg. Similar shape to neurotransmitter, Stimulate release of more neurotransmitter, Inhibit enzyme that breaks down neurotransmitter → Na+ continues to enter
  • Some drugs inhibit the nervous system, leading to fewer action potentials, eg. Inhibit release of neurotransmitter eg. prevent opening of calcium ion channels, Block receptors by mimicking shape of neurotransmitter
• Skeletal muscles work in antagonistic pairs - one muscle contracts (agonist), pulling on bone / producing force, one muscle relaxes (antagonist).
• Gross and microscopic structure of skeletal muscle

  • Made of many bundles of muscle fibres (cells) packaged together, Attached to bones by tendons, Muscle fibres contain: Sarcolemma (cell membrane) which folds inwards (invagination) to form transverse (T) tubules, Sarcoplasm (cytoplasm), Multiple nuclei, Many myofibrils, Sarcoplasmic reticulum (endoplasmic reticulum), Many mitochondria
• Ultrastructure of a myofibril

  Made of two types of long protein filaments, arranged in parallel: Myosin - thick filament, Actin - thin filament, Arranged in functional units called sarcomeres: Ends – Z-line / disc, Middle – M-line, H zone – contains only myosin

  
• Myofibril

  • Arranged in functional units called sarcomeres
  • Ends – Z-line / disc
  • Middle – M-line
  • H zone – contains only myosin
• 1. bands

  • Dark bands containing thick myosin filaments (and some actin filaments)
  • H zone contains only myosin
  • Darkest region contains overlapping actin and myosin

  
• Muscle contraction


  1. Myosin heads slide actin along myosin causing the sarcomere to contract

  2. Simultaneous contraction of many sarcomeres causes myofibrils and muscle fibres to contract

  3. When sarcomeres contract (shorten): H zones get shorter, I band get shorter, A band stays the same, Z lines get closer
• Roles in myofibril contraction

  • Actin (A)
  • Myosin (M)
  • Calcium ions (C)
  • Tropomyosin (T)
  • ATP

  
• Phosphocreatine


  • A source of inorganic phosphate (Pi) → rapidly phosphorylates ADP to regenerate ATP
  • Runs out after a few seconds → used in short bursts of vigorous exercise
  • Anaerobic and alactic
• Properties of slow and fast skeletal muscle fibres

  • Slow twitch
  • Fast twitch
• Slow twitch muscle fibres


  • Specialised for slow, sustained contractions
  • Obtain ATP mostly from aerobic respiration → release energy slowly
  • Fatigues slowly
• Fast twitch muscle fibres

  • Specialised for brief, intensive contractions
  • Obtain ATP mostly from anaerobic respiration → release energy quickly
  • Fatigues quickly due to high lactate conc.
• Location of slow and fast twitch muscle fibres

  • Slow twitch: High proportion in muscles used for posture eg. back, calves, legs of long distance runners
  • Fast twitch: High proportion in muscles used for fast movement eg. biceps, eyelids, legs of sprinters
• Slow twitch muscle fibre structure

  • High conc. of myoglobin → stores oxygen for aerobic respiration
  • Many mitochondria → high rate of aerobic respiration
  • Many capillaries → supply high conc. of oxygen / glucose for aerobic respiration and to prevent build-up of lactic acid causing muscle fatigue
• Fast twitch muscle fibre structure

  • Low levels of myoglobin
  • Lots of glycogen → hydrolysed to provide glucose for glycolysis / anaerobic respiration which is inefficient so large quantities of glucose required
  • High conc. of enzymes involved in anaerobic respiration (in cytoplasm)
  • Store phosphocreatine
• Homeostasis is the maintenance of a stable internal environment within restricted limits
• Homeostasis


  Physiological control systems (normally involve negative feedback)
• Examples of homeostasis


  • Core temperature
  • Blood pH
  • Blood glucose concentration
  • Blood water potential
• Importance of maintaining stable core temperature

  • If too high: Hydrogen bonds in tertiary structure of enzymes break, enzymes denature, fewer enzyme-substrate complexes
  • If too low: Not enough kinetic energy so fewer enzyme-substrate complexes
• Importance of maintaining stable blood pH

  Above or below optimal pH, ionic / hydrogen bonds in tertiary structure break, enzymes denature, fewer enzyme substrate complexes
• Importance of maintaining stable blood glucose concentration

  • Too low (hypoglycaemia): Not enough glucose (respiratory substrate) for respiration, less ATP produced, active transport etc. can't happen → cell death, water potential of blood decreases, water lost from tissue to blood via osmosis, kidneys can't absorb all glucose → more water lost in urine causing dehydration
  • Too high (hyperglycaemia): Water potential of blood decreases, water lost from tissue to blood via osmosis, kidneys can't absorb all glucose → more water lost in urine causing dehydration
• Negative feedback in homeostasis

  1. Receptors detect change from optimum

  2. Effectors respond to counteract change

  3. Returning levels to optimum / normal