TOPIC 10:

Coordination
TOPIC 10 : COORDINATION
Subtopic:
10.1 Nervous System
10.2 Mechanism of Muscle Contraction
10.3 Hormones in Mammals
10.4 Photoperiodism

10.1 Nervous System

Objective:
a. State the organisation of the nervous system.
b. Explain formation of resting and action potential.
c. Describe the characteristics of nerve impulse.
d. Describe the structure of synapse.
e. Explain the mechanism of synaptic transmission across synapses.
f. Compare the transmission of impulse across synapse and along
the axon.
g. Explain the mechanism of action of drugs (e.g. cocaine) on the
nervous system.

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 I. CENTRAL NERVOUS SYSTEM
• consists of the brain & spinal cord.
• integration centre.
• interpret sensory input followed by appropriate responses of
the body.

II. PERIPHERAL NERVOUS SYSTEM

• Consists of:
i. Sensory receptors
ii. Nerves that link sensory receptor with the CNS
iii. Nerves that link the CNS with the effectors (muscles and
glands)
• carries information from sensory receptors to the CNS – use
afferent neurons.
• & carries command signals from the CNS to effector cells – use
efferent neurons.

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• divided into 2 functional divisions:
i. somatic nervous system (SNS)
ii. autonomic nervous system (ANS)

i. SOMATIC NERVOUS SYSTEM (SNS):

• Helps body response to changes in external environment.
• involves in voluntary actions.
• Its effectors are skeletal muscles.

ii. AUTONOMIC NERVOUS SYSTEM (ANS):

• Maintain homeostasis in the internal environment despite
changes.
• Works automatically without voluntary input (involves • Most autonomic pathways consist of a chain of 2 motor
involuntary activities). neurons:
• Its effectors are smooth muscle, cardiac muscle and – preganglionic neurons
glands.
– postganglionic neurons
• Regulated by the medulla oblongata & hypothalamus.
• The synapse & cell body between the 2 neurons is found
• Nerves of ANS originate from the lower brain & spinal within a ganglion (a cluster of nerve cell bodies)
cord
• Preganglionic neurons
– Neuron that carried signals from CNS to ganglion
• Postganglionic neurons
– Neuron that carried signals from the ganglion to the
effector (target organ)

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• The autonomic nervous system, and its motor functions
are split into two divisions:
– Sympathetic systems
– Parasympathetic systems
• They often have antagonistic effects.
• In each system 2 neurones (preganglionic and
postganglionic neurons) make up the pathway from the
CNS to the organs.
SYMPHATETIC SYSTEM
• Signals carried by sympathetic nerves generally enhance
activities that consume energy.
• Often referred to as the ‘fight or flight response’.
• Sympathetic nerves emerge from middle spinal cords (thoracic &
lumbar) regions.
PARASYMPHATETIC SYSTEM
• Signals carried by parasympathetic nerves generally enhance
activities that gain & conserve energy.

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• Parasympathetic nerves emerge from the lower brain & sacral EXPLAIN THE FORMATION OF RESTING AND ACTION
region of spinal cord. POTENTIAL.
Membrane potential
• All living cells have an electrical charge difference across the
plasma membranes
• WHY?
– Because of the difference in the ion concentration inside &
outside the cells.
• This difference in electrical or voltage is known as the membrane
potential.

Resting Potential
• The potential of nerve membrane which exists when inside of the
membrane is more negative & the outside is more positive.

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 2. Membrane of the axon is more permeable to K+ than to Na+
• Due to the presence of more non-gated K+ channel (potassium
channel) compared to non-gated channel Na+ (sodium channel)

3. Presence of anions e.g. proteins in the cell which too large to

• If a neuron is not transmitting any electrical signal / diffuse out
impulse, the neuron is in  resting state • [A-] organic anions remain inside the cell
• The membrane potential of an unstimulated neuron is called
 the resting potential 4. Closing of voltage-gated ion channel

– measures about -70 mV Na

+
Outside cell
• The inner membrane is more negative, the outer membrane ++ +++ +++
Voltage-gated Axon
is more positive ++ +++ +++ membrane
ion channels
Resting potential is maintained by: -- --- ---
+ Inside cell
K
1. The sodium-potassium pump
• always brings out 3 Na+ and brings in 2 K+
• The net result is:
– The outside of the membrane is more positive compared to
the inside of the membrane which is more negative.
– The cell membrane of the neuron is said to be polarised.

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 Action potential
1. Action potential is the membrane potential of a neuron when it is
stimulated by a strong stimulus that cause depolarisation of
membrane that exceeds threshold potential and triggers the
opening of more Na+ voltage gated channel.

2. Stimulus: any disturbance in the external / internal environment

– which changes the potential difference across a membrane
– may be chemical, thermal or electrical.

3. Consists of
– depolarisation phase
– repolarisation phase
– hyperpolarisation phase

Generation of an action potential

1. During resting state
– voltage-gated sodium channels and voltage-gated potassium
RESTING POTENTIAL
channels are closed.
The sodium-potassium pump generates and maintains the
concentration gradients of Na+ and K+ shown in diagram above. – Maintain polarised
2. When the stimulus is applied,
The [Na+] gradient results in very little net diffusion of Na+ in a
– some voltage-gated sodium channels open
resting neuron because very few sodium channels are open.
– to allow Na+ to diffuse into the cell
In contrast, the many open potassium channels allow a significant
– causes depolarisation
net outflow of K+. Because the membrane is only weakly permeable
to chloride and other anions, this outflow of K+ results in a net – the influx of Na+ will cause further depolarisation.
negative charge inside the cell.

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 – if the depolarisation reaches the threshold level,
i. More voltage-gated sodium channels will open
ii. And triggers an action potential.
3. During the rising phase of action potential,
– More and more voltage-gated sodium channels open
– But voltage-gated potassium channels are still closed
– The influx of Na+ makes the inside of the membrane
becomes positive.
• And the outer membrane becomes negative

4. During the falling phase of action potential. Then, the potential

difference drop back down
• The voltage-gated sodium channels close and
• voltage-gated potassium channels open.
– To allow K+ outflow
• The inside of the membrane negative again.
• This is called as repolarisation of the membrane potential.

5. During undershoot/hyperpolarisation
• The membrane potential return to the resting potential.
• The permeability to K+ is higher than at rest because
– voltage-gated potassium channels are still open.
• But then the voltage-gated potassium channels eventually
close.
• And the membrane returns to resting potential.

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The transmission of impulse 2. All-or-nothing event
• Is an electrical phenomenon that occurs through the dendrite, • The action potential will occur only if the depolarisation of the
dendron & the axon. membrane reach the threshold level.
• Involves 2 important phases: • Below the threshold level, the stimulation is not sufficient to
depolarise the membrane & thus triggering the action
– the resting stage
potential.
– the action potential
• If an action potential is achieved, a stronger intensity of a
• The characteristics of an impulse: stimulus won’t increase the size of it.
1) stimulation
2) all-or-nothing event
3) refractory period
4) speed of conduction
The characteristics of an impulse / action potentials:
1. Stimulation
• There are 2 kinds of stimulation that affect the nerves:
i. common stimulation
ii. situational stimulation
• common stimulation
i. involves the stimulation of the receptor organs
ii. e.g light, sound, taste, smell
• situational stimulation
i. all the stimulation that are capable of depolarising the
3. Refractory period
axons.
• Impulse ‘travels’ one-way along the axon from the excitable
ii. e.g mechanical, chemical, heat, pressure, electrical
region to the resting region next to it.
stimulations

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• The previously active region undergoes a recovery phase which 4. Speed of conduction
is known as the refractory period. Depends on:
• Two phases are involved in this very short period of about 5- i. The presence of myelin sheath
10ms
ii. The diameter of axon
i. absolute refractory
ii. relative refractory period

Absolute refractory period

• the previously active region undergoes a recovery phase
• during which the axon cannot respond to a depolarisation
even if the stimulus intensity is increased.
• during this period the axon membrane goes through
hyperpolarisation; i. The presence of myelin sheath
• the membrane’s permeability to K+ ions increases • act as an electrical insulator
dramatically. • depolarisation only occurs at the nodes of Ranvier where
• these ions diffuse out very highly making the charge no myelin sheath is present.
within the neuron becomes too negative. • local circuits are set up at these points & current flows
Relative refractory period across the axon membrane generating the next action
potential.
• a phase following the absolute refractory period where a
high-intensity stimulus may produce a depolarisation. • in effect, the action potential ‘jumps’ from node to node &
passes along the myelinated axon faster.
• the axon membrane reaching its normal permeability state,
• this type of conduction is called saltatory.
• allowing the Na+ ions into the cell;
• the conduction velocities are increased up to 50x as
• the charge within the cell slowly becomes less negative;
compared to in the unmyelinated axon.
• nearing its resting state.

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THE SALTATORY CONDUCTION ALONG THE MYELINATED AXON • An action potential generates local currents that tend to
depolarise the membrane immediately adjacent to the
action potential
– because the depolarised area has a different charge
from the inactive area next to it;
– thus a local circuit is produced.
• When depolarisation caused by the local currents reaches
threshold,
– A new action potential is produced adjacent to the
original one
• The current flow from one activated region to the
inactivated area enables depolarisation to occur,
– thus produces the action potential.
• The continuous occurrence of depolarisation from one area
to the one next to it,
– ensures the transmission of impulse even in a great
distance.
• Action potential propagation occurs in one direction.
ii. The axon diameter
– Because the recently depolarised area of the membrane
• the bigger the diameter, the higher the velocity of the
is in absolute refractory period and cannot generate an
propagated action potential.
action potential.
• the resistance is reduced when the diameter of the axon is
big
• The action potential is produced locally in axon;
– the membrane is depolarised at a specific area in the
axon.
• The action potential ‘flows’ along the axon because it is
self-propagated.

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THE PROPAGATION OF IMPULSE ALONG THE AXON The structure of synapse and the mechanism of synaptic
transmission across synapses.

• Junction between two adjacent neurons or between a neuron

and the effector.
• Junction between the axon terminal end of a presynaptic
neuron & a dendrite or a cell body of the postsynaptic neuron.

• Transfers information between neurons.

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Structure of Synapse • Synaptic knob
– at the end of axon
– contains mitochondria & numerous synaptic vesicles
– synaptic vesicles contain neurotransmitter
molecules
– Function of mitochondria in synaptic knob is to provide
ATP for:
– Synthesis of neurotransmitter
– Release the neurotransmitter into the synaptic cleft
– Uptake of neurotransmitter
• Neurotransmitter:
– a small chemical
– Helps to transmit impulse across a synapse
– 2 main types:
– Acetylcholine
– Noradrenaline / norepinephrine
Mechanism of impulse transmission across synapses
• Action potential arrive at the synaptic knob
– depolarises the presynaptic membrane.
• The permeability of the membrane to Ca2+ ions is increased, and
they easily enter the knob. // The depolarisation opens voltage-
gated channels, triggering an influx of Ca2+
• The entrance of Ca2+ ions
– causes the synaptic vesicles to fuse with the presynaptic
membrane and rupture;

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 – releasing neurotransmitter into the synaptic cleft via
exocytosis
• The vesicles then return to the cytoplasm
– where they are refilled with neurotransmitter substance.
• The neurotransmitter substance
– diffuses across the synaptic cleft and
– bind to ligand-gated ion channels on the postsynaptic
membrane;
 causing the opening of the protein channels.
 Allowing Na+ and K+ to diffuse through
• This leads to a depolarisation of the postsynaptic membrane.
• The depolarisation response is known as
– an excitatory postsynaptic potential (EPSP)
– If EPSP exceeds a threshold level, action potential will be
produced at the postsynaptic neuron.
• After changing the permeability of the postsynaptic membrane,
– the neurotransmitter substance is then hydrolysed by a
specific enzyme
 acetylcholine is hydrolysed by acetylcholinesterase
 noradrenalin is hydrolysed by monoaminoxidase
• The neurotransmitter is degraded by an enzyme & products can
be reabsorbed by the synaptic knob.
• E.g.

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Mechanism of action of drugs on the nervous system – As a result, dopamine will stay in the synaptic cleft
• Definition: – Continuously binds to the receptors on the post synaptic
– Any chemical substance that alters the physiological state of membrane
a living organisms – Causes depolarisation occurs continuously at the
• Also known as psychoactive substance postsynaptic neuron

• Could lead to addiction if abused: give harmful effect to mental & – This continuous impulse transmission causes feelings of
physical activities intense pleasure & increased level of energy

• Interferes with impulse transmission at the synapse
– by interacting with the neurotransmitters / enzymes /
transporter proteins / receptors
MECHANISM OF ACTION OF COCAINE AT SYNAPSE
– Neurons will respond by reducing the number of dopamine
receptors
– This creates a less-sensitive nerve pathway
– With so few receptors, more drug is needed to have the
pleasurable effects
– Eventually, the drug is needed to maintain even normal
level of pleasure. Without it, depression occurs

• Cocaine interferes with impulse transmission by blocking the

reabsorption of neurotransmitters (dopamine)
• Neurotransmitters should be removed from the receptors (by
the action of hydrolysing enzymes or transporter proteins) &
reabsorbed into the presynaptic membrane
• After depolarisation of postsynaptic membrane,
– Dopamine will bind to transporter that shuttles it back into
the presynaptic terminal
• When cocaine is present:
– Cocaine will block the reuptake of dopamine
– By binding competitively with the transporter

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10.2 Mechanism of Muscle Contraction
Objective:
a) Describe the structure of neuromuscular junction.
b) Explain impulse transmission at the neuromuscular junction.
c) Describe the structure of sarcomere.
d) Explain the mechanism of muscle contraction based on Sliding
filament theory.
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Structure
• The junction of a motor neuron with a muscle fibre.
• Neurotransmitter: acetylcholine
• The plasma membrane of the muscle known as the sarcolemma
• The sarcolemma lies directly under the terminal portion of the
motor neuron
– known as the motor end plate
• Sarcolemma has many inward extensions that form T tubules.
• the cytoplasm of is referred to as sarcoplasm
• The endoplasmic reticulum is referred as sarcoplasmic reticulum.
Impulse transmission at the neuromuscular junction.
1. Impulse arrives at the synaptic terminal of the motor neuron,
2. Causes Ca2+ ions enter the synaptic terminal
3. Triggers synaptic vesicles to fuse with presynaptic membrane
4. & releases of acetylcholine (ACh) into synaptic cleft
5. Ach molecule binds to receptor of gated ligand ion channel on the
postsynaptic membrane
6. Ligand-gated ion channels open
7. Na+ enter the postsynaptic membrane, causing depolarisation
8. This triggers an action potential in the muscle cell.
9. The action potential that occur along sarcolemma will spread
through T tubules,
– And cause the sarcoplasmic reticulum to release Ca2+
– The presence of Ca2+ in the sarcoplasm will cause muscle
contraction.
10. When the excitation of the sarcomeres stops, Ca2+ are pumped
back into the sarcoplasmic reticulum.
11. Sarcomeres relaxes.

The role of thin filaments and Ca2+ in muscle contraction

1. At rest, tropomyosin blocks the attachment of myosin head to
actin
2. Action potential causes the sarcoplasmic reticulum to release
Ca2+ into the sarcoplasm
3. The Ca2+ binds to the troponin complex
4. Troponin complex changes its conformation
5. Now the myosin-binding sites on actin are exposed
6. Myosin heads attach to the actin filament  forming cross-
bridges

The importance of Ca2+ in muscle contraction

1. Ca2+ that binds to troponin help to expose the myosin-binding
site
– And allow myosin to bind to actin filament.
2. Ca2+ also stimulates the myosin ATPase activity
Structure of sarcomere
– Myosin molecule has a head containing ATPase
– The ATPase hydrolyses the ATP & change the myosin head
to a high energy configuration/ is in energised state

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The Sliding – Filament Theory
 Proposed by Huxley and Hanson in 1954.
 They suggested that the muscle contracts when the thin filament
(actin) and the thick filament (myosin) slide past each other.
 During contraction the actin filament move inwards towards the
centre of the sarcomere, making it (the sarcomere) looks shorter
without changing the length of the A band.
The event of muscle contraction based on the sliding filament
theory.
1. Firstly, the myosin head is bound to ATP and is in its low-energy
configuration
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2. Then ATP is hydrolysed to ADP and inorganic phosphate (ADP+Pi)
by ATPase and change myosin head from low to high energy
configuration.
3. The myosin head binds to myosin-binding site on actin molecule
forming a cross-bridge with the thin filament.
4. The formation of the cross-bridge will release ADP and inorganic
phosphate (ADP+Pi) from myosin head. Myosin head then returns
to its low-energy configuration. Myosin head bends pulling the
actin/ thin filament towards the centre of the sarcomere
5. Binding of a new molecule ATP will release the myosin head from
actin, breaking the cross-bridge. And a new cycle begins.
THE MECHANISM OF MUSCLE CONTRACTION
10.3 Hormones in mammals
Objective:
a) State the types of hormone.
b) State the types of mechanism of hormone action.
c) Explain the mechanism of hormone action:
i. Gene activation: steroid hormone
ii. Second messenger (cAMP): non-steroid hormone (adrenalin
and glucagon)

Hormone
 Definition:
• a specific chemical secreted by cells in one part of the body
that is transported in the bloodstream to other parts of the
body where it affects particular target cells

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Mechanism of hormone action
1. Gene Activation
• Steroid hormones are secreted by an endocrine gland and
transported to a target cell.
• When the hormone reached the target cell:
– it will diffuse through the cell surface membrane of the target
cell easily because they are small and lipid soluble.
• The hormone enters the cytoplasm & then into the nucleus.
• The hormone binds to a specific receptor protein either in the
cytoplasm or in the nucleus
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• The hormone-receptor complex formed & passes through the
nuclear pore & then enters the nucleus (if the receptors were in
the cytoplasm)
• The steroid hormone-receptor complex then binds to the DNA/
specific genes.
• This activates (or represses) specific genes.
• Transcription of the gene occurs to produce mRNA. Then, mRNA
leaves the nucleus.
• The ribosomal subunits (ribosomes) get attached to the mRNA &
translation occurs in the cytoplasm.
• Polypeptide chains are synthesised to form the specific proteins or
enzymes
• The proteins/enzymes cause specific response recognised as the
hormone’s action.
• Eg: If the steroid hormone is estrogen, it stimulates the repair &
thickening of the endometrium.
2. Second messenger (cAMP)
• A non-steroid hormone/water-soluble hormone cannot diffuse
through the cell surface membrane because it is not soluble in the
lipid bilayer of the membrane
• It binds to a protein receptor (G protein-linked receptor) in the
cell surface membrane of the target cell & form hormone-
receptor complex.
• The hormone acts as the first messenger.
• G protein is activated
• The G protein activates adenylyl cyclase
• ATP is converted to cAMP which acts as a second messenger
• Cyclic AMP (cAMP) activates protein kinase A, an enzyme that Differences between gene activation and the cyclic AMP activation.
phosphorylate (add a phosphate group to) certain specific 1. The permeability of plasma membrane towards the hormone
proteins.
2. The location (the binding of the hormone to the protein receptor)
• This triggers a series of enzymatic reactions (cascade reactions)
3. The gene need to be activated or not.
which change the metabolic activity of the cell.
4. The involvement of transcription and translation
• Eg 1: If the hormone is adrenalin (epinephrine), the cAMP that is
formed in the muscle activates the enzymes responsible in 5. The production of specific protein is involved or not
converting glycogen to glucose which finally alter the cell’s 6. The involvement of G protein, adenylyl cyclase and cAMP
metabolism activity
• Eg 2: If the hormone is glucagon, the cAMP that is formed in the
10.4 Photoperiodism
liver activates the enzymes responsible in converting glycogen to
glucose which finally alter the cell’s metabolism activity Objective:
a) Explain the role of phytochrome in the regulation of flowering.

Role of phytochrome in the regulation of flowering

Phytochrome
• A plant pigment (photoreceptor) that can detect the presence or
absence of light
• Involves in regulating many processes that are linked to day length
(photoperiod)
– Eg : flowering, germination
• Phytochromes exist in 2 forms:
– Pr or P 660

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 • blue phytochrome which absorbs red light with a peak at
about 660nm
– Pfr or P 730
• blue- greenish phytochrome which absorbs far-red light at
about 730nm
• Normal sunlight contains more red light than far-red light
– So, absorption of red light by Pr converts Pr into the form Pfr
(active form).
– Absorption of far-red light by Pfr converts Pfr into Pr

• At night or in the dark, Pfr reverts spontaneously but slowly to

more stable but inactive Pr form
– Pfr activates production of specific proteins or enzymes for
physiological responses such as: control of flowering & seed
germination.
PHOTOPERIODISM PHENOMENON
• PHOTOPERIOD is the relative lengths (the number of hours) of
daylight & darkness in each 24-hour cycle
• PHOTOPERIODISM in a plant
– is the response of a plant to changes in photoperiod
• Flowering plants can be classified according to the photoperiod in
which they flower:
• Short-day plants (eg: Soya bean, Strawberry)
– these plants flower only when the length of daylight they have
been exposed to is shorter than a certain critical length
– plants that only flower if the period of darkness is longer than a
certain critical length

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• Long-day plants (eg: barley, oat, spinach)
– these plants flower only when the daylight they have been
exposed to is longer than a certain critical length
– or the period of darkness is shorter than a certain critical length
• Day-neutral plants (eg: tomato, cucumber)
– these plants are not dependent on the length of daylight or
darkness.
• During the day,
– the red light predominates in larger quantity.
– under this condition, Pr absorbs the red light and changes
rapidly to Pfr form.
• Pfr
– promotes flowering in long-day plants &
– inhibits flowering in short-day plants
• In long-day plants,
– high level of Pfr stimulates the conversion of inactive hormone
precursor into florigen
– florigen induces flowering in long-day plants.
• In short-day plants,
– low level of Pfr stimulates conversion of inactive hormone
precursor to florigen.

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