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!
2
Q
The nervous system and the endocrine system work together to
A
monitor external/internal changes and coordinate responses
3
Q
two parts of nercous system
A
1) Central Nervous System (CNS) → Brain & spinal cord
2) Peripheral Nervous System (PNS) → Neurones
4
Q
Messages travel via
A
nerve impulses / action potentials
* Along neurones / nerve fibres
5
Q
Impulse is passed from neurones to
A
target cells via a synapse
* Using neurotransmitters
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
7
Q
A
endocrine gland
8
Q
Exocrine glands
A
- Secretory cells
- Releases secretion into ducts/tubes
(not blood capillaries) - Secretions: Not hormones
- E.g. stomach, salivary glands, pancreas
9
Q
A
exocrine gland
10
Q
Hormones
* Secreted by
A
endocrine glands
11
Q
Hormones can be
A
globular proteins OR steroids
12
Q
protein hormone
A
Insulin
13
Q
steroid hormone
A
Testosterone
14
Q
characteristics of hormones
A
15
Q
nervous system and endocrine system both involve
A
- Cell signalling
- Signal molecule binding to receptor
- Both involve chemicals
16
Q
A
17
Q
Cell body of neurones
A
- Has a nucleus and cytoplasm
- Cytoplasm: Many mitochondria, ribosomes, RER, Golgi
18
Q
Cytoplasmic processes
A
- Thin, cytoplasmic extension of cell body
19
Q
Dendrites
A
- Carry impulses towards the cell body
20
Q
- Axons
A
- Carry impulses away from the cell body
- Some enclosed with myelin sheath
21
Q
Axon terminal / presynaptic knob
A
- Many mitochondria, synaptic vesicles
containing neurotransmitters, voltage
gated Ca2+ channels
22
Q
presynaptic knob is part of a
A
synapse
23
Q
synapse
A
= junction between
neurones / muscles
24
Q
A synapse also includes:
* Synaptic cleft =
A
gap
→ has enzymes to breakdown
neurotransmitters
25
* Postsynaptic membrane
→ has receptor proteins for
neurotransmitters
26
Myelin sheath
* Insulates axons of many neurones
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Myelin sheath function
Speeds up conduction of nerve impulses
28
Myelin sheath made up of
Schwann cells
→ Has nucleus
→ Layers of cytoplasm and plasma membrane spirals around the axon
29
Nodes of Ranvier
Between Schwann cells, no myelin
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3 types of neurones
1. Sensory neurone (afferent)
* Longer sensory axon / dendron
* Shorter axon
3. Motor neurone (efferent)
* Shorter dendrites
* Much longer axon
2. Intermediate / relay neurone
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* Pathway where impulses are carried
along during a
reflex action
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reflex arc example
knee jerk reflex, sneezing
39
advantages of reflex arc
* Fast
* Automatic, involuntary, without
conscious thought
* Innate / instinctive, response is always
the same
* Protects from harm
40
What are impulses?
→Brief changes to the distribution of electrical charge across
membrane (aka membrane potential)
41
At rest:
more negatively charged on inside than outside
* Resting potential = -70mV
42
When impulses are formed:
more positive on inside than outside
* Action potential / depolarization = +30mV
43
roles of sensory receptor cells
1. Detect stimuli
2. Acts as transducers
44
detect stimuli of sensory receptor cellls
* Receptors are specific to one-type
of stimulus
* e.g. chemical, light, heat, sound, pressure
45
transducers of sensory receptor cells
* Converts stimulus energy to electrical energy
* Produce generator / receptor potential
→ Pass impulse along sensory neurone
46
Chemicals act as a
stimulus
47
Diff chemoreceptors are specific for diff
chemicals =
diff tastes
48
salt (NaCl)
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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resting potential =
-70mV
53
At rest =
no stimuli, no impulses formed and transmitted
* Inside of axon more negatively charged than outside
* Neurone is polarized and maintained at -70mV
54
How is a resting potential maintained?
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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Depolarisation (-70 mV → +30mV)
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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Repolarisation (+30mV → -70mV)
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
Hyperpolarisation / Refractory Period
(less than -70mV)
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
Return to Resting Potential (-70mV)
*Na+/K+pump acts again
→ Membrane can be depolarized again
→ Action potential can be generated again
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How action potentials are transmitted
along a non-myelinated axon?
* 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
How action potentials are
transmitted along a myelinated axon?
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
Saltatory Conduction
Faster transmission because myelin sheath insulates axons
→Local circuit is set up between nodes
→Action potential ‘jumps’ from node to node
65
Threshold Potential (-50mV)
* Minimum potential needed for action potential to be generated
→ Only depolarisation that reaches threshold produces an action potential
66
If depolarisation <-50mV
action potential is not generated
→ only local depolarisation occurs
67
Only if depolarisation >= -50mV,
action potential is generated
→ Size of action potential is fixed at +30mV
→ all-or-nothing law
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synapse=
junction between neurones
/ muscles
71
* Presynaptic knob
→ Many mitochondria, synaptic vesicles
containing neurotransmitters, voltage
gated Ca2+ channels
72
Synaptic cleft
= gap
→ has enzymes to breakdown
neurotransmitters
73
Postsynaptic membrane
→ has receptor proteins for
neurotransmitter
74
role of synapses
1. Ensure one-way transmission
2. Allow interconnection of nerve
pathways
3. Involved in memory and learning
4. Filter out low-level stimuli
75
how do synaspses Ensure one-way transmission
* Receptors only on postsynaptic neurone
* Neurotransmitter vesicles only on
presynaptic neurone
76
how do synapses allow interconnection of nerve apthways
* Nerve impulses can diverge / integrate
* Allow wider range of behaviour / action in
response to a stimulus
77
how are synapses involved in memory and learning
* Due to new synapses being formed
78
how do synapses Filter out low-level stimuli
* 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
The Cholinergic Synapse
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
81
3 types of muscles
cardiac
skeletal
smooth
82
2 types of striated muscle
cardiac and skeletal
83
84
Striated Muscles
* Striated = striped under microscope
* Attached to bones by tendons
* Many long, cylindrical muscle fibres
→Multinucleated
→Each muscle fibre is made up of myofibrils
85
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87
Muscle fibres have
* Plasma membrane = sarcolemma
* Cytoplasm = sarcoplasm
* Specialised ER = sarcoplasmic reticulum
88
muscle fibres have Plasma membrane = sarcolemma
→ sarcolemma infoldings = transverse
system tubules (T-tubules)
→ can conduct action potentials
89
muscle fibres have Cytoplasm = sarcoplasm
→ Many parallel myofibrils
→ Fibres are multinucleated
→ Manymitochondria
90
muscle fibres have Specialised ER = sarcoplasmic reticulum
→ have protein pumps
→ have a lot of Ca2+
91
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93
94
95
Two types of myofilaments:
* Thick filaments = made of myosin
* Thin filaments = made of actin
96
* Thick filaments = made of myosin
→fibrous protein with globular
protein head
→ Attached to M line
97
Thin filaments = made of actin
→chain of globular protein molecules
→ has binding site for myosin
→ troponin and tropomyosin is
attached to actin
→ Attached to Z line
98
Sarcomere
Interdigitation of thick and thin filaments give striated appearance
99
100
Myosin attached to
M line
101
Actin attached to
Z line
102
scaromere between
2 Z lines
103
* Distance between Z line decreases
during muscle contraction
104
I band
light band
* Only thin filaments
* Shortens during muscle contraction
105
H band
light band at centre of dark
band
* Only thick filaments
* Shortens during muscle contraction
105
A band =
dark band
* Overlap of thick and thin filaments
* Stays the same during muscle contract
106
107
108
109
Muscle Contraction begins at
neuromuscular junction
→ Cholinergic synapse between a motor neurone and a muscle fibre
* Terminal knobs of motor neurone = motor end plate
* Neurotransmitter = acetylcholine (Ach)
110
111
neuromuscular junction
112
1. Cholinergic synapse of neuromuscular junction
* 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
2. Depolarisation and Ca2+
* 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
When muscle is relaxed:
* Troponin = attached to tropomyosin
* Tropomyosin = blocks myosin-binding
site on actin
115
When muscle contracts:
* 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
Sliding Filament Model
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
Sarcomere shortens during
muscle contraction
* H band shortens
* I band shortens
* A band remains the same
118
119
120
Muscle Relaxation
When action potential stimulation
stops….
* 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
Muscles uses a lot of
ATP
* Only small amount of ATP present in muscle
122
More ATP is synthesized by….
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
124
Similarities between mammals and plants about electrical coomunication
* Have electrochemical gradients
* Plant cells have sodium-potassium pumps
* Have resting potential
* Membrane depolarises → action potentials
125
differences between mammals and plants about electrical coomunication
126
127
venus fly trap
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
Venus Fly Trap
Two adaptions to conserve energy and avoid closing unnecessarily:
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
Chemical Communication in Plants
* 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
Movement of plant hormones:
a) Directly from cell to cell
→By active transport or diffusion
b) Via phloem/xylem vessels
E.g. Auxins, gibberellins, abscisic acid
131
Auxins (IAA) short
* 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
2. Gibberellins (GA) short
* 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
3. Abscisic acid (ABA) short
* Respond to water stress
* Stimulate closure of stomata
* Uses Ca2+ as second messenger
134
Role of auxin
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
Role of Auxin in Cell Elongation
The Acid Growth Hypothesis
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
why is the acid growth hypothesis supported
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
138
Uneven distribution of auxin can cause
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
roles of GA
1. Seed germination
2. Stimulates cell division and cell elongation in stem
140
Gibberellin enhances
IAA
141
for seed germination to happen
* Seed is dormant / metabolically inactive
→DELLA proteins act as inhibitors of cell growth and seed germination
→Maintain seed dormancy
142
1. Seed absorbs water by osmosis
→Water stimulates production of gibberellin by embryo
A2 LEVEL 9700
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