Chap 15: Control and Coordination

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Created by
Mae Jian

Cards (19)

  • How myelin sheath increases the speed of conduction of nerve impulses.
    • Myelin insulates axon
    • Action potential (AP) only at nodes of Ranvier 
    • Local circuits set up between nodes
    • Saltatory conduction → AP/impulses jump from node to node
  • Importance of the myelin sheath in the transmission of action potentials:
    • Myelin sheath insulates axon, preventing ions from passing through
    • Allows for saltatory conduction, where the impulse travels/jumps from node to node
    • Action potential only occurs at the node of Ranvier
    • Transmission of impulses is faster
    • Longer local circuits are produced between nodes
  • Events at a synapse leading to the release of acetylcholine:
    • Action potential occurs at the presynaptic membrane
    • Ca2+ channels open, allowing Ca2+ ions to enter the presynaptic neuron through facilitated diffusion
    • Vesicles containing acetylcholine (ACh) move and fuse to the presynaptic membrane
    • Exocytosis of ACh releases it into the synaptic cleft
  • Role of acetylcholinesterase in the synapse:
    • Breaks down ACh in the synaptic cleft and recycles them
    • ACh leaves the binding site, stopping depolarization in the postsynaptic membrane
    • Stops continuous action potential
  • Roles of synapses in the nervous system:
    • Ensures one-way transmission of impulses
    • Interconnects nerve pathways
    • Integrates impulses
    • Involved in memory and learning
  • How an action potential arriving at the neuromuscular junction can result in depolarization of the sarcolemma:
    • Ca2+ channels open in the presynaptic membrane
    • Ca2+ enters the presynaptic neuron
    • Vesicles containing ACh/neurotransmitters move towards and fuse with the presynaptic membrane
    • ACh is released through exocytosis and diffuses across the synaptic cleft
    • ACh binds to receptors on the sarcolemma
    • Na+ channels open, allowing Na+ to enter the sarcoplasm and causing depolarization
  • Describe how the response of the sarcoplasmic reticulum to the arrival of an AP leads to the contraction of striated muscle.
    1. When sarcoplasmic reticulum (SR) is depolarised
    2. Voltage gated Ca2+ channels open
    3. Ca2+ diffuses down the concentration gradient
    4. Binds to troponin which changes shape
    5. Tropomyosin is displaced/moves
    6. Binding sites are exposed
    7. Allows globular heads of myosin to bind to actin (cross bridges formation)
    8. Power stroke → myosin moves and pulls actin
  • Main features of thick and thin filaments in the sarcomere
    Thick filaments
    • Myosin
    • Fibrous protein
    • Globular heads
    • M lines
    Thin filaments
    • Actin
    • Globular protein
    • Consists of troponin and tropomyosin
    • Z lines
  • Describe how tropomyosin and myosin are involved in the sliding filament model of muscle contraction.
    Tropomyosin:
    1. Covers myosin binding sites on actin
    2. When calcium ions bind to troponin/tropomyosin → moves/changes shape
    3. Allows myosin to bind to actin → forming cross bridges
    Myosin:
    1. ATP hydrolysis
    2. Myosin head pivots 
    3. Myosin heads binds to actin and forms cross links with actin
    4. ADP and Pi detaches 
    5. Myosin head returns to previous position
    6. Actin is moved
    7. New ATP binds
    8. Myosin detaches from actin and cross bridges break
  • Explain the role of ATP in the contraction of striated muscle.
    1. Myosin head binds to actin → forms cross bridges
    2. ADP released causes motion of myosin heads
    3. Actin moves - power stroke
    4. ATP binds to myosin heads
    5. Myosin head detaches from actin
    6. Myosin head moves back to original position
    7. ATP needed to pump Ca2+ back into SR
  • Describe the role of calcium ions in the contraction of striated muscles.
    1. Voltage gated Ca2+ channels open 
    2. Ca2+ diffuses out of SR and into sarcoplasm
    3. Ca2+ binds to troponin which causes it to change shape 
    4. Tropomyosin moves/displaces
    5. Exposes myosin-binding sites
    6. Globular heads of myosin binds to these site (actin) and cross links 
    7. Power stroke, myosin moves and pulls actin → contraction of muscle
  • Describe how the production of AP in the leaf cells of the Venus fly trap can result in the leaves closing and trapping the cell. [5]
    • AP reaches lobe - hinge cells
    • H+ pumped out of the cell/into the cell wall
    • Cell wall loosens and cross-links are broken
    • Calcium pectate dissolves
    • Ca2+ enters cell, decreases WP
    • Water enters through osmosis
    • Cells expand and become turgid
    • Leaves become concave
  • Describe how venus fly trap produces AP to digest insects.
    1. 2 sensory hairs stimulated within 30 seconds // 1 sensory hair stimulated twice 
    2. AP travels
    3. Ca2+ channels open → Ca2+ diffuses into gland cells
    4. Stimulates vesicle-containing digestive enzymes to move and fuse to CSM
    5. Exocytosis of digestive enzymes → digest insects
  • Describe sequence of events that follows the uptake of water by grain wheat
    1. Embryo produces/releases gibberellin
    2. Gibberellin moves into aleurone layer
    3. Gibberellin stimulates production of amylase
    4. Amylase moves into endosperm
    5. Hydrolyse/break down starch to maltose
    6. Maltose converted to glucose
    7. Glucose moves into embryo
    8. For respiration/ATP production
    9. For growth
  • Describe how auxin contributes to elongation growth.
    1. Auxin binds to receptors on CSM
    2. Stimulates ATPase proton pumps to pump H+ ions → from cytoplasm to cell wall
    3. Acidify cell wall, decreasing pH
    4. Activates expansins → loosen bonds between cellulose microfibrils
    5. K+ channels open, K+ diffuses in → Influx of K+
    6. Decrease WP, increase osmosis of water through aquaporins
    7. Cell elongates due to an increase in internal pressure
  • How is resting potential maintained?
    • Sodium-potassium pumps in axon membrane - 3 Na+ out, 2 K+ in
    • Many large, negatively charged molecules in axon - attracts K+ ions
    • Impermeability of axon membrane - Na+ cannot diffuse through axon membrane when neurone is at rest
    • Closure of voltage gated channels
  • How membrane potential changes
    • Impulse reaches threshold potential (-50mV)
    • Depolarisation
    • Repolarisation
    • Hyperpolarisation
    • Refractory period
    • Resting state
  • When action potential is stimulated:
    • Sodium channel proteins open
    • Na+ ions pass into the axon down electrochemical gradient
    • Depolarisation: decreases potential difference, inside becomes less negative/more positive and reaches threshold potential (-55mV)
    • All or nothing principle
    • Positive feedback - triggers more voltage gated sodium channels to open, more Na+ enters - reaches 30mV
    • Action potential is generated
  • Repolarisation and refractory period
    • After 1 ms, all Na+ voltage gated channels close
    • K+ voltage gated channels open - K+ diffuses out
    • Repolarisation: returns to potential difference (-70mV)
    • Short period of hyperpolarisation
    • K+ voltage gated channels close, refractory period - recovery and unresponsive