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A2 LEVEL 9700 > Control and coordination' > Flashcards

Control and coordination' Flashcards

1
Q

How are messages sent from the receptor to the coordinating
centre, and then to the effector?

A

Through nerve impulses and/or hormones!

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2
Q

The nervous system and the endocrine system work together to

A

monitor external/internal changes and coordinate responses

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3
Q

two parts of nercous system

A

1) Central Nervous System (CNS) → Brain & spinal cord
2) Peripheral Nervous System (PNS) → Neurones

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4
Q

Messages travel via

A

nerve impulses / action potentials
* Along neurones / nerve fibres

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5
Q

Impulse is passed from neurones to

A

target cells via a synapse
* Using neurotransmitters

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6
Q

Endocrine glands

A
  • Secretory cells
  • Releases secretions directly into blood
    capillaries in the glands
  • Secretions: Hormones
  • E.g. pituitary glands, thyroid, adrenal, ovary,
    testes, pancreas
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7
Q
A

endocrine gland

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8
Q

Exocrine glands

A
  • Secretory cells
  • Releases secretion into ducts/tubes
    (not blood capillaries)
  • Secretions: Not hormones
  • E.g. stomach, salivary glands, pancreas
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9
Q
A

exocrine gland

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10
Q

Hormones
* Secreted by

A

endocrine glands

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11
Q

Hormones can be

A

globular proteins OR steroids

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12
Q

protein hormone

A

Insulin

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13
Q

steroid hormone

A

Testosterone

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14
Q

characteristics of hormones

A
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15
Q

nervous system and endocrine system both involve

A
  • Cell signalling
  • Signal molecule binding to receptor
  • Both involve chemicals
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16
Q
A
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17
Q

Cell body of neurones

A
  • Has a nucleus and cytoplasm
  • Cytoplasm: Many mitochondria, ribosomes, RER, Golgi
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18
Q

Cytoplasmic processes

A
  • Thin, cytoplasmic extension of cell body
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19
Q

Dendrites

A
  • Carry impulses towards the cell body
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20
Q
  1. Axons
A
  • Carry impulses away from the cell body
  • Some enclosed with myelin sheath
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21
Q

Axon terminal / presynaptic knob

A
  • Many mitochondria, synaptic vesicles
    containing neurotransmitters, voltage
    gated Ca2+ channels
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22
Q

presynaptic knob is part of a

A

synapse

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23
Q

synapse

A

= junction between
neurones / muscles

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24
Q

A synapse also includes:
* Synaptic cleft =

A

gap
→ has enzymes to breakdown
neurotransmitters

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25
Q
  • Postsynaptic membrane
A

→ has receptor proteins for
neurotransmitters

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26
Q

Myelin sheath

A
  • Insulates axons of many neurones
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27
Q

Myelin sheath function

A

Speeds up conduction of nerve impulses

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28
Q

Myelin sheath made up of

A

Schwann cells
→ Has nucleus
→ Layers of cytoplasm and plasma membrane spirals around the axon

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29
Q

Nodes of Ranvier

A

Between Schwann cells, no myelin

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30
Q
A
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31
Q

3 types of neurones

A
  1. Sensory neurone (afferent)
    * Longer sensory axon / dendron
    * Shorter axon
  2. Motor neurone (efferent)
    * Shorter dendrites
    * Much longer axon
  3. Intermediate / relay neurone
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32
Q
A
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33
Q
A
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34
Q
A
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35
Q
A
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36
Q
A
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37
Q
  • Pathway where impulses are carried
    along during a
A

reflex action

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38
Q

reflex arc example

A

knee jerk reflex, sneezing

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39
Q

advantages of reflex arc

A
  • Fast
  • Automatic, involuntary, without
    conscious thought
  • Innate / instinctive, response is always
    the same
  • Protects from harm
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40
Q

What are impulses?

A

→Brief changes to the distribution of electrical charge across
membrane (aka membrane potential)

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41
Q

At rest:

A

more negatively charged on inside than outside
* Resting potential = -70mV

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42
Q

When impulses are formed:

A

more positive on inside than outside
* Action potential / depolarization = +30mV

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43
Q

roles of sensory receptor cells

A
  1. Detect stimuli
  2. Acts as transducers
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44
Q

detect stimuli of sensory receptor cellls

A
  • Receptors are specific to one-type
    of stimulus
  • e.g. chemical, light, heat, sound, pressure
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45
Q

transducers of sensory receptor cells

A
  • Converts stimulus energy to electrical energy
  • Produce generator / receptor potential
    → Pass impulse along sensory neurone
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46
Q

Chemicals act as a

A

stimulus

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47
Q

Diff chemoreceptors are specific for diff
chemicals =

A

diff tastes

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48
Q

salt (NaCl)

A
  1. Na+ ions diffuse into cell via microvilli
    → Increase in positive charge inside cell
  2. Membrane depolarized
    → Receptor / generator potential generated
  3. Voltage-gated Ca2+ channels open
    →Ca2+ enter cell
  4. Trigger movement of vesicles
    containing neurotransmitters
    → exocytosis occurs
    → neurotransmitter released
  5. Neurotransmitter stimulate action
    potential / impulse in sensory neurone
    → Send impulse to taste centre in brain
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49
Q
A
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50
Q
A
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51
Q
A
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52
Q

resting potential =

A

-70mV

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53
Q

At rest =

A

no stimuli, no impulses formed and transmitted
* Inside of axon more negatively charged than outside
* Neurone is polarized and maintained at -70mV

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54
Q

How is a resting potential maintained?

A
  1. Na+/K+ pump
    * 3 Na+ pumped out, 2 K+ pumped in
    * ATP needed
    * Axon phospholipid bilayer impermeable to K+ / Na+
    * Electrochemical gradient is set up = difference in both charge and chemical
    ions across membrane
    → So K+ diffuse out, Na+ diffuse in
    → via channel proteins
  2. More K+ channels open than Na+ channels
    * Membrane more permeable to K+ than Na+
    * More K+ leaves than Na+ enter
    * Leaking K+ is responsible for resting potential
    →Inside becomes relatively more negative than outside
    P/S: these channel proteins are open all the time. But voltage-gated
    K+ and Na+ channels are closed
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55
Q
A
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56
Q

Depolarisation (-70 mV → +30mV)

A
  1. Voltage-gated K+ channels remain closed
  2. Voltage-gated Na+channels open
    → Channels change shape when membrane potential changes when action
    potential arrives from previous section
    *Na+ enter cell
    *Membrane becomes less negative / depolarized →+30mV
    → Action potential is generated
    * Size of action potentials is fixed at +30 mV
    * The higher the strength/ intensity of the stimulus, the higher the
    frequency of action potentials
    * Also – the more neurones are depolarised
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57
Q
A
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58
Q

Repolarisation (+30mV → -70mV)

A
  1. Voltage-gated Na+ channels close
  2. Voltage-gated K+ channels open
    *K+move out of cell
    *Inside becomes negative /repolarised → -70mV
    Depolarisation spreads to next region due to movement
    of +ve ions to -ve regions. A “local circuit” is set up.
59
Q

Hyperpolarisation / Refractory Period
(less than -70mV)

A
  1. Voltage-gated Na+ channels remain closed
  2. Voltage-gated K+channels close
    *But slight delay so excess K+ions have moved out of axon
    When membrane is hyperpolarized = refractory period
    *Membrane is insensitive to any depolarisation
    *No action potential can be generated
    → Function: ensure one-way transmission
    * Due to the refractory period, action potentials are discrete events /
    do not merge into one another
    → Function: Length of refractory period limits maximum frequency of
    action potentials
    * E.g. longer refractory period = lower maximum frequency
60
Q

Return to Resting Potential (-70mV)

A

*Na+/K+pump acts again
→ Membrane can be depolarized again
→ Action potential can be generated again

61
Q
A
62
Q

How action potentials are transmitted
along a non-myelinated axon?

A
  • Depolarisation spreads to next region due to movement of positive
    ions to negative regions
    →A “local circuit” is set up
    →This causes voltage-gated Na+ channels to open in the next region
    →Causing next action potential
63
Q

How action potentials are
transmitted along a myelinated axon?

A

But with the MYELIN SHEATH… there is an increased speed of conduction!
* Myelin insulates axon
→ Does not allow movement of ions
→ Lengthens local circuits
* Passage of ions only at nodes of Ranvier
→ Action potential / depolarization only at nodes of Ranvier
→Local circuit is set up between nodes
→Action potential ‘jumps’ from node to node
→This is called saltatory conduction

64
Q

Saltatory Conduction

A

Faster transmission because myelin sheath insulates axons
→Local circuit is set up between nodes
→Action potential ‘jumps’ from node to node

65
Q

Threshold Potential (-50mV)

A
  • Minimum potential needed for action potential to be generated
    → Only depolarisation that reaches threshold produces an action potential
66
Q

If depolarisation <-50mV

A

action potential is not generated
→ only local depolarisation occurs

67
Q

Only if depolarisation >= -50mV,

A

action potential is generated
→ Size of action potential is fixed at +30mV
→ all-or-nothing law

68
Q
A
69
Q
A
70
Q

synapse=

A

junction between neurones
/ muscles

71
Q
  • Presynaptic knob
A

→ Many mitochondria, synaptic vesicles
containing neurotransmitters, voltage
gated Ca2+ channels

72
Q

Synaptic cleft

A

= gap
→ has enzymes to breakdown
neurotransmitters

73
Q

Postsynaptic membrane

A

→ has receptor proteins for
neurotransmitter

74
Q

role of synapses

A
  1. Ensure one-way transmission
  2. Allow interconnection of nerve
    pathways
  3. Involved in memory and learning
  4. Filter out low-level stimuli
75
Q

how do synaspses Ensure one-way transmission

A
  • Receptors only on postsynaptic neurone
  • Neurotransmitter vesicles only on
    presynaptic neurone
76
Q

how do synapses allow interconnection of nerve apthways

A
  • Nerve impulses can diverge / integrate
  • Allow wider range of behaviour / action in
    response to a stimulus
77
Q

how are synapses involved in memory and learning

A
  • Due to new synapses being formed
78
Q

how do synapses Filter out low-level stimuli

A
  • Weaker stimulus cause release of low
    quantities of neurotransmitters
  • No impulse generated in postsynaptic
    neurone →brain
  • Prevent brain from being overloaded with
    sensory information
79
Q

The Cholinergic Synapse

A

Neurotransmitter = acetylcholine (ACh)
1. Action potential reaches presynaptic
membrane
2. Voltage-gated Ca2+ channels open
→ Presynaptic membrane becomes
more permeable to Ca2+
→ Ca2+ ions enter presynaptic neurone
3. Vesicles containing ACh move towards
and fuse with presynaptic membrane
→ Exocytosis occurs
→ ACh released into synaptic cleft
4. ACh diffuse across synaptic cleft
5. ACh binds with receptor proteins
on postsynaptic membrane
6. Receptor proteins change shape and
Na+ channels open
→ Na+ enter postsynaptic neurone
* Postsynaptic neurone depolarized
* Action potential is generated
* As long as ACh binds with receptors,
Na+ channels will stay open
→ Continuous transmission of action
potential
→ Can cause synaptic fatigue / paralysis
7. ACh breakdown by acetylcholinesterase at synaptic cleft
* ACh→ acetate & choline
* ACh is recycled (ATP needed)
* Depolarisation stops in
postsynaptic membrane
→ stop continuous action potential

80
Q
A
81
Q

3 types of muscles

A

cardiac
skeletal
smooth

82
Q

2 types of striated muscle

A

cardiac and skeletal

83
Q
A
84
Q

Striated Muscles

A
  • Striated = striped under microscope
  • Attached to bones by tendons
  • Many long, cylindrical muscle fibres
    →Multinucleated
    →Each muscle fibre is made up of myofibrils
85
Q
A
86
Q
A
87
Q

Muscle fibres have

A
  • Plasma membrane = sarcolemma
  • Cytoplasm = sarcoplasm
  • Specialised ER = sarcoplasmic reticulum
88
Q

muscle fibres have Plasma membrane = sarcolemma

A

→ sarcolemma infoldings = transverse
system tubules (T-tubules)
→ can conduct action potentials

89
Q

muscle fibres have Cytoplasm = sarcoplasm

A

→ Many parallel myofibrils
→ Fibres are multinucleated
→ Manymitochondria

90
Q

muscle fibres have Specialised ER = sarcoplasmic reticulum

A

→ have protein pumps
→ have a lot of Ca2+

91
Q
A
92
Q
A
93
Q
A
94
Q
A
95
Q

Two types of myofilaments:

A
  • Thick filaments = made of myosin
  • Thin filaments = made of actin
96
Q
  • Thick filaments = made of myosin
A

→fibrous protein with globular
protein head
→ Attached to M line

97
Q

Thin filaments = made of actin

A

→chain of globular protein molecules
→ has binding site for myosin
→ troponin and tropomyosin is
attached to actin
→ Attached to Z line

98
Q

Sarcomere

A

Interdigitation of thick and thin filaments give striated appearance

99
Q
A
100
Q

Myosin attached to

A

M line

101
Q

Actin attached to

A

Z line

102
Q

scaromere between

A

2 Z lines

103
Q
  • Distance between Z line decreases
A

during muscle contraction

104
Q

I band

A

light band
* Only thin filaments
* Shortens during muscle contraction

105
Q

H band

A

light band at centre of dark
band
* Only thick filaments
* Shortens during muscle contraction

105
Q

A band =

A

dark band
* Overlap of thick and thin filaments
* Stays the same during muscle contract

106
Q
A
107
Q
A
108
Q
A
109
Q

Muscle Contraction begins at

A

neuromuscular junction
→ Cholinergic synapse between a motor neurone and a muscle fibre
* Terminal knobs of motor neurone = motor end plate
* Neurotransmitter = acetylcholine (Ach)

110
Q
A
111
Q
A

neuromuscular junction

112
Q
  1. Cholinergic synapse of neuromuscular junction
A
  • Action potential arrives the presynaptic membrane
  • Voltage-gated Ca2+ channels open
  • Ca2+ enter presynaptic knob
  • Vesicles containing ACh fuse with presynaptic
    membrane
  • AChreleased by exocytosis into synaptic cleft
  • ACh diffuses across synaptic cleft
  • AChbind to receptors on sarcolemma
    (muscle cell membrane)
  • Na+ channel opens
  • Na+ ions enter sarcoplasm of muscle cell
    sarcolemma
  • Sacrolemma depolarised
113
Q
  1. Depolarisation and Ca2+
A
  • Depolarisation spreads via T-tubules → sarcoplasmic reticulum (ER)
  • Sarcoplasmic reticulum depolarized
  • Voltage-gated Ca2+ channels open
  • Ca2+ diffuse out from sarcoplasmic reticulum → sarcoplasm
  • Ca2+ initiates muscle contraction
114
Q

When muscle is relaxed:

A
  • Troponin = attached to tropomyosin
  • Tropomyosin = blocks myosin-binding
    site on actin
115
Q

When muscle contracts:

A
  • Ca2+ in sarcoplasm bind to troponin
    → Troponin changes shape and moves tropomyosin
    → Exposes myosin-binding site on actin
    → Allows myosin head to attach and form cross-bridge with actin
116
Q

Sliding Filament Model

A

1) Myosin head with ADP and Pi form
cross-bridges with actin
→ Pi is released
2) Myosin head tilts and pulls actin
→ Power stroke moves actin towards M line
→ Myofibril / sarcomere shortens
→ ADP released from myosin head
3) ATP binds to myosin head
→ ATPase hydrolyses ATP into ADP and Pi
→ Myosin head lets go of actin
→ Myosin moves back to original position
4) Process repeated at site further along actin molecule

117
Q

Sarcomere shortens during

A

muscle contraction
* H band shortens
* I band shortens
* A band remains the same

118
Q
A
119
Q
A
120
Q

Muscle Relaxation
When action potential stimulation
stops….

A
  • Ca2+ is actively pumped into
    sarcoplasmic reticulum
    → Ca2+ do not bind to troponin on
    actin filament
    → Tropomyosin moves to block
    myosin-binding sites on actin
    filament
    → Filaments slide back to original
    position
    → Muscle relaxes
121
Q

Muscles uses a lot of

A

ATP
* Only small amount of ATP present in muscle

122
Q

More ATP is synthesized by….

A
  1. Aerobic respiration in mitochondria
  2. Lactate pathway in sarcoplasm
  3. Creatine phosphate in sarcoplasm
    * Immediate source of energy once ATP is used up
123
Q
A
124
Q

Similarities between mammals and plants about electrical coomunication

A
  • Have electrochemical gradients
  • Plant cells have sodium-potassium pumps
  • Have resting potential
  • Membrane depolarises → action potentials
125
Q

differences between mammals and plants about electrical coomunication

A
126
Q
A
127
Q

venus fly trap

A
  1. Sensory hair cell is receptor and detects touch
    * If 2 hairs are touched / 1 hair is touched twice within 35 seconds…
    * Ca2+ ion channels open @ cells at base of hair
    * Ca2+ flow in
    * Cell membrane depolarised
    → Action potential occurs
    * Depolarisation spreads over leaf / lobe
    → to midrib / hinge cells
  2. Acid growth @ hinge cells
    * H+ pumped out of cells into cell walls
    * Cross-links in cell wall broken
    * Calcium pectate of middle lamella dissolves
    * Cell wall loosens
    * Ca2+ enter hinge cells
    * Water enters hinge cells by osmosis
    * Cells expand / become turgid
    * Lobes change from convex to concave
    * Trap shuts quickly in 0.3s
    * Elastic tension released
  3. Further deflections of sensory hairs
    * Trigger action potentials → seal trap
    * Stimulate entry of Ca2+ into gland cells
    * Ca2+ stimulate exocytosis of vesicles containing digestive enzymes
    * Trap stays shut for up to 1w for digestion
  4. After digestion, cells of upper surface of midrib grow slowly
    * Leaf reopens and elastic tension builds in the cell walls of midrib
128
Q

Venus Fly Trap
Two adaptions to conserve energy and avoid closing unnecessarily:

A
  1. Stimulation of single hair does not trigger closure
    → At least two hairs must be touched OR one hair touched twice
    within 35 seconds
    → Prevent trap from closing when raining or when debris fall into trap
  2. Gaps between stiff hairs allow very small insects to crawl out
    →No energy wasted on digesting a very small meal
129
Q

Chemical Communication in Plants

A
  • Plant hormones/plant growth regulators
  • Produced in a variety of plant tissues
  • Not in endocrine glands
  • Plant hormones interact with receptors
    inside/outside cell and initiate a signaling cascade
130
Q

Movement of plant hormones:

A

a) Directly from cell to cell
→By active transport or diffusion
b) Via phloem/xylem vessels
E.g. Auxins, gibberellins, abscisic acid

131
Q

Auxins (IAA) short

A
  • Growth by cell elongation at tips of roots and shoots
  • Inhibits lateral growth / branching– i.e. apical dominance
  • Via acid growth hypothesis
  • Group of several chemicals
  • Main auxin = IAA (indole 3-acetic acid)
  • Synthesized in growing tips of shoots & roots
    → Aka apical meristems where there is active mitosis
132
Q
  1. Gibberellins (GA) short
A
  • Seed germination
  • Stem elongation
  • Causes breakdown of DELLA proteins, which are inhibitors of cell growth
    and seed germination
  • Plant growth regulator / plant hormone
  • Synthesized in young leaves, seeds & stems
133
Q
  1. Abscisic acid (ABA) short
A
  • Respond to water stress
  • Stimulate closure of stomata
  • Uses Ca2+ as second messenger
134
Q

Role of auxin

A
  1. Stimulate cell elongation
  2. Inhibits lateral growth / branching – i.e. apical dominance
    → Cause plants to grow taller towards light
    P/S: Auxin not solely responsible for apical dominance
    * There is interaction between auxin and other plant growth regulators
    * Gibberellin enhances IAA
135
Q

Role of Auxin in Cell Elongation
The Acid Growth Hypothesis

A
  1. Auxin binds to receptors in cell surface membrane
  2. Stimulates proton pumps in cell surface membrane
    * By active transport
    * H+ from cytoplasm into cell wall
    * Cell wall become more acidic
  3. pH-dependent enzymes (expansins) activated to weaken cell wall
    * By breaking H bonds between cellulose microfibrils
    * Cell wall loosens → more elastic, can stretch
  4. Ions enter cell and water potential of cell decreases
    * Water enter cell by osmosis
    * Increase in turgor pressure
    * Cell wall expands
    * Cause elongation of cell
136
Q

why is the acid growth hypothesis supported

A

Hypothesis supported bcs….
1. Cell elongation can be prevented by neutralising the acidity of cell
wall using a buffer
2. Can cause cell elongation by acids
3. Protons released from cells in response to auxin

137
Q
A
138
Q

Uneven distribution of auxin can cause

A

stem / root to bend in
respond to stimuli
→ Higher concentration of auxin, more cell elongation
→ E.g. auxin causes shoots to bend towards sunlight
* Auxin inhibits lateral growth at
growing tips of shoots
→ The act of pruning removes auxin
→ Allows branching and produces bushier plants

139
Q

roles of GA

A
  1. Seed germination
  2. Stimulates cell division and cell elongation in stem
140
Q

Gibberellin enhances

A

IAA

141
Q

for seed germination to happen

A
  • Seed is dormant / metabolically inactive
    →DELLA proteins act as inhibitors of cell growth and seed germination
    →Maintain seed dormancy
142
Q
A
  1. Seed absorbs water by osmosis
    →Water stimulates production of gibberellin by embryo

A2 LEVEL 9700 (6 decks)

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