Topic 6

Cards (35)

  • Control of heart rate
    1. SAN sends waves of electrical activity over whole of atrial walls, blood forced into ventricles
    2. Waves reach AVN, slight delay to allow atria to empty before ventricles contract
    3. AVN passes activity to bundle of His conducting waves along Purkyne fibres, impulses reach ventricle walls, muscles contract from apex
  • Baroreceptors
    • Detect high and low blood pressure
  • Chemoreceptors
    • Detect changes in oxygen level, CO2 and pH of blood
  • Control of muscle contraction
    1. Impulse from motor neurone cause acetylcholine vesicles to be released into gap
    2. Acetylcholine binds to receptors on sarcolemma causing depolarisation on the membrane
    3. Depolarisation travels down t-tubules
    4. Calcium ions released from sarcoplasmic reticulum
    5. Calcium ions bind to proteins in muscles causing tropomyosin to be pulled away from myosin binding sites leading to muscle contraction
    6. Acetylcholinesterase breaks down acetylcholine and stops contraction
    7. Calcium returned to sarcoplasmic reticulum by active transport
  • Pacinian Corpuscle
    • Rings of connective tissue
    • Deformation cause action potential due to influx of sodium ions through neurones
    • Stretch mediated sodium ion channels present in plasma membrane of sensory neurone
  • Synaptic transmission
    1. Action potential arrives at axon terminal
    2. Voltage gated calcium ion channels open in presynaptic membrane
    3. Calcium ions enter cell by diffusion against concentration gradient
    4. Calcium ions signals to vesicles and fuse to membrane releasing acetylcholine into synaptic cleft
    5. Vesicles move to membrane
    6. Docked vesicles release neurotransmitters by exocytosis
    7. Acetylcholine diffuses across synaptic cleft and binds to receptors in post synaptic membrane
  • Spatial summation
    • A number of different presynaptic neurones all release enough neurotransmitter to exceed threshold and trigger action potential at next neurone
  • Temporal summation
    • One presynaptic neurone releases neurotransmitter many times over a short period of time to exceed threshold and trigger action potential in next neurone
  • Rods
    • More sensitive to light
    • Function better in dim light
    • Absorb all wavelengths of visible light
    • Rhodopsin broken down by light causing generator potential
    • Rhodopsin is a pigment in rods
  • Cones
    • Coloured light will stimulate 3 cells differently
    • Trichromatic theory of colour vision: red light = R cones, yellow light = R and G cones equally, cyan light = B and G cones equally, white light = all 3 cones equally
  • Visual acuity
    • Fovea has high density of cones
    • Each cone has synapse with one neurone
    • Each cone sends impulses to brain
    • High visual acuity
    • Many rods synapse with one bipolar neurone making them more sensitive to low levels of light than cones
  • Positive phototropism
    1. IAA synthesised in shoot tip and transported down shoot
    2. Asymmetric illumination is detected by shoot tip
    3. Causes IAA to move into shaded side
    4. IAA promotes cell elongation on shaded side
    5. Shoot bends towards light source
  • Cell elongation
    1. Auxin binds to receptors in plasma membrane of cells in shoot
    2. Affects transport of ions through cell membrane
    3. Build up of hydrogen ions in cell walls
    4. Low pH activates enzymes that break cross linkages between molecules
    5. Cell takes up water by osmosis, swells and becomes elongated
  • Resting potential
    • Inside of axon always has slightly negative electrical potential compared to outside
    • Potential difference about -70mV
  • Depolarisation
    1. Sodium ion channels in axon membrane open
    2. Sodium ions pass into axon down electrochemical gradient
    3. Reduces potential difference across the axon as inside becomes less negative
    4. Triggers more channels to open allowing more sodium ions to enter = positive feedback
    5. If potential difference reaches around -50mV an action potential is generated
  • Repolarisation and refractory period
    1. All sodium ion voltage gated channel proteins close
    2. Potassium ion voltage gate channel proteins open allowing diffusion of potassium ions out of axon down conc gradient
    3. Returns potential difference to normal
    4. Hyperpolarisation is when the potential difference becomes more negative than resting potential
  • All or nothing principle: an impulse is only transmitted if the initial stimulus is sufficient to increase the membrane potential above a threshold potential
  • If stimulus is below threshold the receptor cells won't be sufficiently depolarised and the sensory neurone will not be activated
  • If stimulus is strong enough to increase the receptor potential above the threshold potential then the receptor will stimulate the sensory neurone to send impulses
  • Structure of thick filaments in myofibril
    • Made up of myosin molecules
    • Fibrous protein molecule with a globular head
    • Fibrous part anchors the molecule into the filament
    • Many myosin molecules lie next to each other with their globular heads all pointing away from M line
  • Structure of thin filaments in myofibril
    • Made up of actin molecules
    • Globular protein molecules
    • Many actin molecules link to form a chain
    • Two actin chains twist to form one thin filament
    • Troponin is attached to the actin chains at regular intervals
  • Muscle contraction
    1. Action potential arrives at motor end plate
    2. Vesicles fuse with presynaptic membrane and release acetylcholine
    3. Acetylcholine diffuses across synaptic cleft and binds with receptors on muscle fibre membrane causing depolarisation
    4. Depolarisation wave travels down tubules
    5. Calcium ions released from stores in sarcoplasmic reticulum
    6. Calcium ions bind to proteins in muscle leading to contraction
    7. Acetylcholinesterase breaks down acetylcholine so contraction only occurs when impulses arrive continuously
  • Fast twitch fibres
    • Contract rapidly
    • More powerful contractions over shorter period of time
    • Intense work eg weightlifting
    • Adapted for intense activities
    • Thicker and more myosin filament
    • High glycogen concentration
    • Store of phosphocreatine to generate ATP
  • Slow twitch fibres
    • Contract slowly
    • Less powerful contractions over longer period of time
    • Endurance work eg marathon running
    • Adapted for aerobic respiration
    • Large store of myoglobin to store oxygen
    • Rich blood supply to supply oxygen for contraction
    • Numerous mitochondria to generate ATP
  • Actin
    • Formed from a helix of actin sub units
    • Each contains a biding site for the myosin heads
    • Tropomyosin - fibrous strand twisted around the actin filament covering myosin binding sites
  • Myosin
    • Formed from a number of myosin proteins wound together
    • Each ends in a myosin head which contains ATP
  • Why is homeostasis important:

    enzyme activity - by maintaining pH and temperature in the body all enzyme linked reactions proceed efficiently
    cell size - changes in water potential of the blood will affect the amount of water in tissue fluid and cells which could cause animal cells to desiccate
    independence from external conditions - animals with constant internal environment can maintain a constant level of activity regardless of their environment
  • Insulin
    • Lowers blood glucose when too high
    • Activates enzymes to convert glucose to glycogen
    • Increases muscle cell rate of respiration of glucose
    • Bind to glycoprotein receptors on target cell causing change in tertiary structure of glucose transport carrier protein = more glucose into cell
    • Increase number of carrier proteins = vesicles fuse with membrane
    • Activation of enzymes converting glucose to glycogen and fat
  • Glucagon
    • Raises blood glucose when too low
    • Activates enzymes to break down glycogen into glucose
    • Cause glucose to be made from glycerol and amino acids
    • Secreted in response to fall in blood glucose concentration by alpha cells
    • Increase blood glucose concentration by attaching glucagon to specific receptors on liver cell membrane
    • Activating enzymes that convert glycogen to glucose
    • Activating enzymes that convert amino acids to glucose
  • Adrenaline
    • Cause increase in blood concentration by attaching to protein receptors in cell surface of target cells
    • Activating enzymes that cause breakdown of glycogen to glucose
  • Second Messenger Model
    1. Adrenaline approaches transmembrane protein
    2. Adrenaline fuses to receptor causing it to change shape activating adenyl cyclase
    3. Adenyl cyclase converts ATP to cyclic AMP
    4. Cyclic AMP changes shape of protein kinase enzyme and activates it
    5. Protein kinase enzyme catalyses conversion of glycogen to glucose
  • Ultrafiltration
    1. Occurs at renal capsule where blood filtered from glomerulus to proximal convoluted tubule
    2. Larger molecules like glucose is filtered out of blood through endothelium of capillary
    3. Smaller molecules like ions are left in the capillary and passed into Bowman's capsule through prodocytes
    4. Blood in glomerulus under higher pressure than Bowman's capsule so pressure pushes fluid into capsule
  • Selective Reabsorption
    1. Occurs in proximal convoluted tubule
    2. Lots of microvilli to increase surface area
    3. Lots of co transporter proteins to transport glucose across membrane by diffusion
    4. Lot of mitochondria in cytoplasm for active transport
    5. Glucose and amino acids completely reabsorbed
    6. Water and ions do decreasing water potential
  • Loop of Henle
    1. Sodium ions actively transported out of ascending tubule into medulla decreasing water potential of medulla
    2. Water move out of descending tubule by osmosis down water potential gradient
    3. Sodium ions diffuse out of lower ascending tubule increasing water potential of filtrate
    4. Filtrate moves down collecting duct, down water potential gradient moving out of collecting duct by osmosis
  • Reabsorption of water by DCT and CD
    1. Fall in water potential detected by osmoreceptors in hypothalamus
    2. Hypothalamus produces anti-diuretic hormone (ADH)
    3. ADH passes to posterior pituitary gland and secreted into bloodstream
    4. ADH transported to kidney binding to specific receptors on cell membrane on DCT and CD
    5. Enzyme activated vesicles containing aquaporins fuse with cell membrane increasing permeability to water