15. Control & Co-ordination Notes Flashcards

In mammals Nervous system: Transmission of nerve impulses 16.02.2021 Synapses 21.02.2021 Muscle contraction 24/26.02.2021 Endocrine system: Human menstrual cycle 24/26.02.2021 In plants Venus fly trap 02.03.2021 Auxin & gibberellin 03/05.03.2021

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1
Q

Structure of a sensory neurone & a motor neurone

Axons carry nerve impulses AWAY from cell body.
Dendrons carry nerve impulses TOWARDS cell body.

Body nervous system:
Central nervous system (CNS) = brain + spinal cord
Peripheral nervous system (PNS)

*Nerve impulse = an electrical signal that passes along a neurone in 1 direction {as a result of rapid movement of Na+ & K+ ions across CSM into/out of axon}

A

Sensory neurone

  1. Cell body, in DORSAL ROOT GANGLION (outside of spinal cord)
    - contains nucleus, mitochondria, rough ER, Golgi body, ribosomes
  2. Dendron is longer than axon, & has dendrites
  3. Has synaptic knobs
  4. Myelin sheath & nodes of Ranvier

Motor neurone

  1. Cell body (inside spinal cord; also Relay neurone)
  2. Has short dendriteS
  3. Axon longer than dendrites
  4. Has synaptic knobs
    - with many mitochondria
    - with many synaptic vesicles that contain neurotransmitters
  5. Myelin sheath & nodes of Ranvier
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2
Q

Functions of sensory, relay and motor neurones in a reflex arc (+ describe)

Importance of reflex arc

  1. Fast and automatic
    - response seen before impulse reaches brain, but impulse still gets transmitted to brain
  2. Protect body from harm, eg. hot/sharp objects
  3. Response is Stereotypic - always the same to each specific stimulus
    eg. knee jerk
A

Reflex arc: the pathway along which impulses are transmitted from a receptor to an effector, w/o involving the conscious regions of the brain
1. Very STRONG stimulus in receptor
eg. light, sound, heat
2. Action potential generated in sensory neurone
3. ❖Sensory neurone transmits impulse from RECEPTOR, through dorsal root of spinal nerve & into spinal cord, to CNS
- Action potential passes to relay neurone
4. ❖Relay neurone transmits impulse from sensory neurone –> motor neurone
5. ❖Motor neurone transmits impulse from relay neurone to EFFECTOR (muscle/gland)
+ impulses to brain
6. Response generated, aka reflex action

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3
Q

Roles of sensory receptor cells in detecting stimuli and STIMULATING the transmission of nerve impulses in sensory neurones

eg. Chemoreceptor cells found in human taste buds
- detect chemical energy {by specific receptor protein}

eg. rods & cones detect light energy

Regardless of intensity of stimulus,
- max action potential is +30mV - fixed size
- speed of transmission of action potential always same
BUT stronger stimulus increases:
- frequency of impulses/action potentials
- no. of neurones transmitting impulse

A
  1. Respond to stimuli (light, sound, touch, pressure, chemicals)
  2. Some receptors are the ends of sensory neurones; some are cells
  3. Are energy transducers: convert stimulus energy to electrical energy
  4. STIMULUS causes Na+ channels to open, Na+ enter cell
  5. Produce RECEPTOR POTENTIAL, depolarisation of membrane
    ❖ If receptor potential greater than threshold, action potential generated - all-or-nothing law
  6. Increased stimulus strength increases frequency of action potential

In receptor cells,
- If receptor potential above threshold, voltage-gated Ca2+ channels open
- Ca2+ enter cell and cause release of neurotransmitter by EXOCYTOSIS
! Neurotransmitter stimulates action potential in sensory neurone, impulse passed along sensory neurone to brain

*if sensory neurone & not separate receptor cell, no need for Ca2+ channels; action potential stimulated by local current flow / local circuit

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4
Q

Transmission of an action potential in a myelinated neurone and its initiation from a resting potential

  • action potential at any point in axon triggers production of action potential in adjacent region
  • sodium-potassium pumps & ion channels are in fact still open during depolarisation and repolarisation stages (less significant)
A

❖ Resting potential

  • Axon phospholipid bilayer impermeable to K+ & Na+
    1. In a resting axon, SODIUM-POTASSIUM PUMPs (in CSM of neurone) actively pump 3 Na+ ions out and 2 K+ ions into axon
  • active transport, lots of ATP needed
    2. CSM also has ion channels for facilitated diffusion (passive) across membrane
  • less Na+ channels & more K+ channels
  • more K+ ions diffuse out, less Na+ ions diffuse into axon
    3. ∴ inside of axon more negative than outside; resting potential ≈ -70mV –> axon membrane is POLARISED
  • Voltage-gated channels closed

❖ Depolarisation

  1. If resting potential above threshold potential -55mV, VOLTAGE-GATED sodium ion channels open, Na+ enter axon
  2. Inside of axon becomes less negative –> depolarised
  3. Na+ continue to enter until potential difference raised to +30mV
  4. Voltage-gated sodium ion channels close

❖ Repolarisation

  1. VOLTAGE-GATED potassium ion channels open, K+ move out of axon
  2. Inside of axon becomes more negative again - repolarised

❖ Hyperpolarisation

  1. K+ continue to exit until potential difference is very negative -80mV –> hyperpolarised
  2. Voltage-gated potassium ion channels close
  3. Sodium-potassium pumps restore p.d. by pumping out Na+ and pumping in K+
  4. Resting potential -70mV achieved again; action potential can occur again
  • Myelin sheath insulates axon & prevents ion movement
  • Action potential ONLY occurs at nodes of Ranvier
  • LOCAL CIRCUITS set up between nodes {movement of Na+ from +ve to -ve region, across axon}
  • saltatory conduction occurs, in which action potential jumps from node to node
  • One way transmission of action potential due to…
  • …Refractory period at previous node

^action potential only generated ahead, NOT behind it
^region that has just had action potential cannot trigger a new action potential for a short time (in recovery)

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5
Q

Importance of the myelin sheath (saltatory conduction) in determining the speed of nerve impulses and the refractory period in determining their frequency

+ larger diameter / thicker axons transmit impulses faster than thin ones, due to lower resistance

A
  • Uncovered areas between Schwann cells = nodes of Ranvier
  • Schwann cells contain a nucleus
  • not all axons and dendrites have myelin sheath
  • Made up of Schwann cells that wrap around axons (and dendrons, but axons more important )
  • Sheath mainly lipid {+ some proteins}
    1. Insulate axons & Prevent ion movement (b/c impermeable to Na+ & K+)
    2. Action potentials/Depolarisation can ONLY occur at nodes of Ranvier
    3. LONGER local circuits set up between nodes; nodes are 1-3mm intervals apart {Na+ move from +ve to -ve region, across axon}
    4. Saltatory conduction occurs, action potentials jump from node to node
    5. Speed of transmission of impulse in myelinated neurone 100ms-1, approx. 50x faster than unmyelinated
    6. Speed in unmyelinated neurone 0.5ms-1
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6
Q

Structure of a cholinergic synapse and explain how it functions

*nerve impulses cannot jump across synapses; signals passed across by chemicals called neurotransmitters

A

Structure
1. Synaptic cleft = gap between two neurones
2. Vesicle containing neurotransmitter
3. Neurotransmitter receptor proteins
4. Synaptic knob has many mitochondria to produce ATP for:
- neurotransmitter synthesis
- vesicle formation
- vesicle movement
- exocytosis
+ removal of Ca2+ from pre- neurone by active transport

Function

  1. When action potential reaches synaptic knob, VOLTAGE-GATED calcium ion channels open in presynaptic membrane
  2. Ca2+ enter {diffuse} synaptic knob & induce vesicles containing acetylcholine (ACh) to move towards PREsynaptic membrane
  3. Vesicles fuse with pre- membrane & release Ach into synaptic cleft (exocytosis)
  4. Ach DIFFUSEs across synaptic cleft & binds to complementary receptor on POSTsynaptic membrane
  5. Ligand-gated sodium ion channels open & Na+ enter post- neurone
  6. Postsynaptic membrane is depolarised
  7. Action potential generated in postsynaptic neurone
  • synaptic cleft contains ACETYLCHOLINESTERASE; hydrolyse ACh –> acetate + choline
  • stops continuous production of action potentials in post- neurone
  • choline combines with acetyl CoA –> Ach again in presynaptic neurone (ATP needed)
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7
Q

4 roles of synapses in the nervous system

A

❖Ensure transmission in 1 direction
- vesicles containing neurotransmitters ONLY in presynaptic neurone & receptor proteins ONLY in postsynaptic membrane

❖Allow interconnections of many nerve pathways
- allows wide range of responses

  1. Involved in memory and learning
    - due to new synapses being formed
    - summation
  2. Filter out less frequent impulses / low level stimuli (to avoid overloading neurones)
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8
Q

Ultrastructure of striated muscle with particular reference to sarcomere structure

  • striated muscle cells / muscle fibres / myofibres
  • multinucleate syncytium
A
  1. Sarcolemma - equivalent of CSM
  2. Sarcoplasm - equiv. of cytoplasm; many mitochondria
  3. Sarcoplasmic reticulum *equiv. of ER but diff. function
    - stores high conc. of Ca2+ ions
    - many protein pumps on its membrane for active transport of Ca2+
  4. T tubules (transverse system tubules)
    - infolding of sarcolemma
    - usually close to a sarcoplasmic reticulum
  5. In a muscle fibre, many myofibrils made of actin + myosin

❖Actin: THIN filament attached to Z lines/discs
- globular protein
- has binding site for myosin head
- troponin & tropomyosin attached
❖Myosin: THICK filament attached to M lines
- fibrous protein w/ globular protein head (ATPase)

❖Sarcomere: distance between Z lines

  1. I band - only actin (lightest)
  2. H band - only myosin (lighter)
  3. A band
    - overlapping regions of actin + myosin (darkest & thickest)
    - includes H band
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9
Q

Roles of neuromuscular junctions, transverse system tubules and sarcoplasmic reticulum in STIMULATING contraction in striated muscle

  • Neuromuscular junction = junction between motor neurone & muscle fibre
A

Action potential reaches NEUROMUSCULAR JUNCTION / motor end plate, same events as in synapse earlier (eg. synaptic cleft)… then

  1. Acetylcholine binds to receptors in SARCOLEMMA, Na+ channels open, Na+ enter muscle fibre
  2. Sarcolemma is DEPOLARISED (& initiates action potential)
  3. Depolarisation spreads down T TUBULES
    * sarcoplasmic reticulum near T tubules
  4. Induce calcium ion channels on membrane of sarcoplasmic reticulum to open
  5. Ca2+ diffuse out of SARCOPLASMIC RETICULUM
  6. Ca2+ bind to troponin
  7. Troponin changes shape & tropomyosin moves, exposing myosin-binding site on actin
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10
Q

Sliding filament model of muscular contraction
including the roles of troponin, tropomyosin, calcium ions and ATP

  • If Q asks about role of Ca2+ in the coordination of muscle contraction:
    1. when impulse arrives at neuromuscular junction, voltage-gated Ca2+ channels open; Ca2+ enter; stimulate vesicles to fuse with pre- membrane; impulse in sarcolemma/T-tubules stimulates release of Ca2+ from sarcoplasmic reticulum
    2. bind to troponin… when no action potential, Ca2+ pumped back into sarcoplasmic reticulum
A
  1. Ca2+ released from sarcoplasmic reticulum
  2. Ca2+ bind to troponin
  3. Troponin changes shape & moves tropomyosin, exposing binding site on actin
  4. Myosin head binds to site & forms CROSS BRIDGE
  5. Myosin head has ATPase; hydrolyses ATP –> ADP + Pi
  6. When ATP binds to myosin head, myosin head detaches from actin
  7. When ATP hydrolysed, myosin tilts head
  8. Myosin head binds to actin again
  9. When ADP + Pi released, POWER STROKE occurs, in which myosin head pulls actin & goes back to previous orientation
    - each power stroke moves 10nm; combined effect of power stroke allows contraction
  10. Process repeated
  11. Sarcomere shortens (A band remains same length)

Roles
❖Troponin has binding site for Ca2+
❖Tropomyosin covers/uncovers binding site on actin

When there is no action potential,
> Ca2+ channels on membrane of sarcoplasmic reticulum close
❖Ca2+ pumped back into sarcoplasmic reticulum by active transport using ATP
- Ca2+ are removed from troponin
- Tropomyosin moves & blocks binding site on actin
> No cross bridge between actin and myosin - muscle relaxes

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11
Q

Compare the nervous and endocrine systems as communication systems that co-ordinate responses to changes in the internal and external environment

3 similarities + 7 differences

A

Similarities

  1. Both involve cell signalling
  2. Chemicals (neurotransmitters/hormones)
  3. Signalling molecules bind to receptors
Differences 
✦ form & mode of transmission 
- Electrical impulses travelling along neurones
vs Chemicals called hormones travelling in blood
✦ nature of communication
- Electric and chemical vs Chemical 
✦ response destination
- Muscle/gland vs Target organs
✦ effect is...
- Localised vs Widespread
✦ transmission speed
- Faster vs Slower
✦ longevity of effect response
- Short-lived vs Long-lived
✦ receptor location
- On CSM vs Either on CSM or within cell
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12
Q

Human menstrual cycle
roles of the hormones FSH, LH, oestrogen and progesterone in controlling changes in the ovary and uterus

≈ 28 days; 1st day = start of menstruation
1st half of cycle (follicular phase) - secondary oocyte produced
2nd half of cycle (luteal phase) - uterus prepares for implantation

FSH & LH secreted by pituitary gland
oestrogen & progesterone secreted by ovaries

*endometrium = uterus lining

A
  1. Hypothalamus releases GnRH (gonadotrophin releasing hormone) to pituitary gland
    - so anterior pituitary gland secretes FSH into blood
    ✦target: ovary, to stimulate development of a primary follicle
  2. As follicle develops, it secretes oestrogen into blood
    - [oestrogen] increases
    3 targets:
    ✦uterus: repair & thicken endometrium, increase in blood vessels
    ✦anterior pituitary gland: inhibit FSH & LH at LOW level of oestrogen (negative feedback)
    ✦hypothalamus: inhibit GnRH
    - oestrogen level high just before ovulation
    - HIGH level of oestrogen triggers FSH & LH secretion
  3. LH & FSH released in a SURGE
    ✦ovary: LH triggers ovulation (day 14) - release of secondary oocyte from ovarian follicle/Graafian follicle
    - Remains of ovarian follicle develop into a corpus luteum
  4. Corpus luteum secretes progesterone & oestrogen (lower level)
    3 targets of progesterone:
    ✦uterus: maintain endometrium
    ✦anterior pituitary gland: inhibit FSH & LH secretion
    ✦hypothalamus: inhibit GnRH
  5. If fertilisation does not occur,
    - Corpus luteum degenerates b/c production of FSH & LH, which are needed to survive, are inhibited by progesterone & oestrogen
    - As corpus luteum degenerates, levels of oestrogen & progesterone decrease
    - Endometrium not maintained & breaks down –> menstruation occurs
    - FSH no longer inhibited, so can stimulate development of new primary follicle
    Cycle can start again

If fertilisation occurs,

  • Corpus luteum receives hCG (human chorionic gonadotrophin) hormone from implanted embryo
  • hCG allows corpus luteum to sustain w/o FSH & LH
  • Corpus luteum continues to secrete progesterone & oestrogen to maintain endometrium (until placenta develops and secretes progesterone throughout pregnancy)
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13
Q

Biological basis of contraceptive pills containing oestrogen and/or progesterone

A
  1. Synthetic hormones used, as they do not get broken down quickly
    - taken daily for 21 days then stop for 7 days to allow menstruation
  2. Oestrogen & progesterone conc. remain high
  3. Negative feedback on anterior pituitary gland to Inhibit secretion of FSH & LH
  4. Ovarian follicle does not develop & ovulation is inhibited
  5. Thickens CERVICAL mucus to prevent entry of sperm
  6. Endometrium is thin, so prevents implantation
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14
Q

Rapid response of the Venus fly trap to stimulation of hairs on the lobes of modified leaves + how the closure of the trap is achieved

  • live where soil conditions lack nitrogen; so obtain nitrogen for growth by trapping and digesting insects
  • lobes are connected by hinge cells in the middle
  • each lobe has 3 sensory/trigger HAIRS

(Electrical communication in plants)

A
  1. Mechanical energy converted to electrical…
  2. …by sensory hair cells - receptors that detect touch
  3. Cell membrane depolarises {b/c Ca2+ channels open, Ca2+ enter, generate receptor potential}
  4. If (at least) 2 hairs touched within 35 seconds OR 1 hair touched twice within 35 seconds,
  5. Action potential occurs & spreads over leaf/lobe, to HINGE cells {spread through leaf cells via plasmodesmata; plants do not have neurones}
  6. H+ pumped out of cells into cell walls
  7. Cell wall loosens (due to low pH)
  8. CALCIUM PECTATE dissolves in the middle lamella
  9. Ca2+ ions enter cells & water enters cells by OSMOSIS, down the ψ gradient
  10. (hinge) Cells become turgid and expand
  11. Lobes change from convex to CONCAVE
  12. Trap shuts quickly in 0.3s
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15
Q

Role of auxin in (cell) elongation growth by stimulating proton pumping to acidify cell walls

(Chemical communication in plants)

*Auxin, gibberellin = plant growth regulators

A
  1. based off Acid-growth hypothesis
  2. Auxin binds to a receptor on the CSM
  3. Auxin stimulates proton pumps in CSM…
  4. …To pump H+ (from the cytoplasm) into the cell wall by active transport
  5. pH of cell wall decreases
  6. pH-dependent enzymes - EXPANSINS - activated
  7. Bonds between cellulose microfibrils broken
  8. Cell wall loosens & becomes more elastic
  9. More water enters cell & turgor pressure increases
  10. so Cell wall expands
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16
Q

Control of gibberellin synthesis + Role of gibberellin in stem elongation

A

Control

  1. Gibberellin synthesis controlled by Le/le gene
  2. Dominant allele Le gives functional enzyme
  3. Enzyme converts inactive to active gibberellin {GA}

Stem elongation

  1. w/o gibberellin, DELLA protein binds to PIF transcription factor
  2. Gibberellin binds to receptor & activates an enzyme
  3. Causes breakdown of DELLA protein
  4. PIF binds to promotorer region of DNA
  5. Transcription of growth genes occurs
  6. Causes CELL DIVISION & CELL ELONGATION
    * similar to role of auxin
  7. Loosens cell walls
  8. so Cells can expand when water enters
17
Q

Explain why the side shoots increase in length when the terminal buds are removed. [3m]

Describe the part played by auxins in APICAL DOMINANCE in a plant shoot. [7m]

A
  1. apical bud is source of auxin
  2. auxin inhibits growth of side shoot
    * so that plant can grow in a pyramidal shape, which allows maximum light exposure
  3. remove bud & auxin conc. falls
  4. this allows CELL division & cell elongation to take place in side shoots
  5. Plant growth regulator
  6. Synthesised in apical buds
  7. Moves by diffusion / active transport, from cell to cell
  8. Also mass flow in phloem
  9. Stimulates CELL elongation
  10. Inhibits lateral buds growth
  11. Plant grows upwards
  12. Auxin not solely responsible; Interaction between IAA and other plant growth regulators