Starter Questions
1. Following a stimulus, explain how the
opening of sodium ion channels affects
the potential difference across a neurone
cell membrane.
2. Describe and explain the movement of
sodium ions if the potential difference
across a neurone cell membrane reaches
the threshold level.
3. Describe the structure of a militated
neurone.
Answers
1. Sodium ions diffuse into the neurone down the
sodium ion electrochemical gradient. This makes
the inside of the neurone less negative and so
decreases the potential difference across the
membrane.
2. More sodium ions diffuse into the neurone
because more sodium ion channels open.
3. A myelinated neurone has a myelin sheath. The
myelin sheath is made of a type of cell called a
schwann cell. Between the schwann cells are tiny
patches of bare membrane called the nodes of
ranvier. Sodium ion channels are concentrated at
the nodes of ranvier.
• http://www.youtube.com/watch?v=LT3VKAr4r
oo
• Synapses are gaps between neurones
• Information is sent between neurones by
chemical transmission
• Neurotransmitters pass across the
synaptic cleft
• A new action potential will be triggered in
the post synaptic neurone
The synapse
• Where two neurones meet, there is a gap, usually
about 20nm wide. This is the synaptic cleft
• The end of the neurone immediately before the
synaptic cleft, ends in a presynaptic bulb.
• After the synaptic cleft is the postsynaptic bulb,
i.e. the start of the next neurone
• Together they make up the synapse
Structure of the synapse
Neurotransmitters
• There are more than 40 different
neurotransmitter substances.
• Noradrenalin and acetylecholine (ACh) are
found throughout the nervous system
• Dopamine and glutamate are found only in
the brain.
• Synapses releasing achetylcholine and known
as cholinergic synapses
Presynaptic
Neurone
Mitochondrion
Synaptic
Membrane of
Knob
postsynaptic
Synaptic
neurone
Cleft
Smooth
Incoming
ActionEndoplasmic
Potential
Reticulum
Calcium ion
channel
Synaptic vesicle
containing
neurotransmitter
Sodium ion
channels
Postsynaptic Neurone
Incoming
Action Potential
Neurotransmitter
New action
Potential
• The incoming action potential causes
depolarisation in the synaptic knob
• This causes calcium channels to open
• Calcium ions (Ca2+) flood into the synaptic
knob
Incoming
Action Potential
Ca2+
Ca2+
Ca2+
Ca2+
• The influx of calcium ions causes synaptic
vesicles to fuse with the presynaptic
membrane
• This releases neurotransmitter in to the cleft
 So calcium ions cause the release of
neurotransmitter
Incoming
Action Potential
Ca2+
Ca2+
Ca2+
Ca2+
• Neurotransmitter (acetylcholine) is released
into the synaptic cleft.
• Acetylcholine binds to the receptor site on the
sodium ion channels.
• Sodium ion channels open
Ca2+
Ca2+
Ca2+
Ca2+
Neurotransmitter (acetlycholine) is released into the synaptic cleft.
Acetlycholine binds to the receptor site on the sodium ion channels.
• The sodium channels on the postsynaptic
membrane are normally closed.
• When the neurotransmitter binds there is a
conformational change opening the channel.
• This allows sodium ions to flood in and causes
depolarisation.
Na
+
Neurotransmitter binds
and opens the channel.
Empty Synaptic
Vesicles
Sodium ions diffuse into
the postsynaptic neurone
Depolarised
• Neurotransmitter (acetylcholine) is released into the
synaptic cleft.
• Acetylcholine binds to the receptor site on the sodium
ion channels.
• Sodium ion channels open
• Sodium ions diffuse in (down steep concentration
gradient)
• Postsynaptic neurone depolarises
• Depolarisation inside the postsynaptic
neurone must be above a threshold value
• If the threshold is reached a new action
potential is sent along the axon of the post
synaptic neurone
Incoming
Action Potential
Neurotransmitter
New action
Potential
• When do the calcium channels open and close?
• Why are the calcium ions important?
• What is the name of the neurotransmitter?
• Explain how the neurotransmitter causes a new
action potential to be generated.
•
•
•
•
Step 1 Calcium channels open
Step 2 Neurotransmitter release
Step 3 Sodium Channels
Step 4 New action potential
• Step 5 Acetylcholinesterase
• Step 6 Remaking acetylcholine
• A hydrolytic enzyme
• Breaks up acetylcholine (the
neurotransmitter) into acetyl (ethanoic acid)
and choline.
• Acetylcholinesterase is an enzyme that
hydrolyses acetylcholine in to separate acetyl
(ethanoic acid) and choline.
• Sodium ion channels close.
• The two bits diffuse back across the cleft into
the presynaptic neurone.
• This allows the neurotransmitter to be
recycled.
Acetylcholine binds and
opens Sodium channels
Acetylcholinesterase breaks up
acetylcholine. Sodium channels close
Depolarised
• If the neurotransmitter is not broken down
this could allow it to continuously generate
new action potentials
• Breaking down acetylcholine prevents this
• Name the hydrolytic enzyme and the products
of the reaction.
• Why must the neurotransmitter be broken
down?
• What happens to the remnants of the
neurotransmitter?
• ATP released by mitochondria is used to recombine
acetyl (ethanoic acid) and choline thus recycling the
acetylcholine.
• This is stored in synaptic vesicles for future use.
• More acetylcholine can be made at the SER.
• Sodium ion channels close in the absence of
acetylcholine at their receptor sites.
• The synapse is now ready to be used again.
The Whole Process
Incoming
Action Potential
Ca2+
Ca2+
Ca2+
Ca2+
A neuromuscular junction is
a specialised cholinergic
between a motor neurone
and a muscle cell.
Neuromuscular junctions
use the neurotransmitter
acetylcholine (Ach), which
binds to cholinergic
receptors called nicotinic
cholinergic receptors.
Very similar to Cholinergic synapses
with a few differences
• Postsynaptic membrane has lots of folds that
form clefts. These clefts store the enzyme that
breaks down Ach (acetylcholinesterase)
• Postsynaptic membrane has more receptors
than other synapses
• Motor neurone fires an action potential, it
always triggers a response in a muscle cell.
This isn't always the case for a synapse
between two neurones.
• Excitable neurotransmitters depolarise the
postsynaptic membrane. E.g.Acetylcholine.
• Inhibitory neurotransmitters e.g. GABA is an
inhibitory neurotransmitter, when it binds to
its receptors it causes potassium ion channels
to open on the postsynaptic membrane,
hyperpolarising the neurone.
• Low frequency action potentials often release
insufficient amounts of neurotransmitter to
exceed the threshold in the postsynaptic
neurone
• Summation allows action potentials to be
generated
• This enables a build up of neurotransmitter in
the synapse
• A number of different presynaptic neurones
share the same synaptic cleft
• Together they can release enough
neurotransmitter to create an action potential
• Multiple neurones
Threshold reached action potential can be sent
• A single presynaptic neurone releases
neurotransmitter many times over a short
period
• If the total amount of neurotransmitter
exceeds the threshold value an action
potential is sent
• 1 neurone
Low frequency action potentials
High frequency action potentials
• What is summation?
• What is the main difference between temporal
summation and spatial summation?
• Explain how temporal summation allows the
postsynaptic membrane to reach the threshold value.
• Suggest an advantage of responding to high-level
stimuli but not low-level ones.
• There are chloride ion channels on the
postsynaptic membrane
• If these are made to open chloride ions (Cl-)
flood into the postsynaptic neurone
• This hyperpolarises the neurone
• This make it harder to achieve a action
potential
Neurotransmitter that
opens calcium channels
Chloride ion (Cl-)channel on the postsynaptic membrane
Chloride ions diffuse into
the postsynaptic neurone
Hyperpolarised
• Inhibitory and excitatory neurones will work
antagonistically at the same synapse
• Summation will occur
1. (a) (i)
A
Three marks for three of:
Negatively charged proteins / large anions inside axon;
Membrane more permeable to potassium ions than to
sodium ions;
Potassium ions diffuse* out faster than sodium ions diffuse in;
Sodium / potassium pump;
Sodium ions pumped* out faster than potassium ions pumped
in / 3 for 2;
* mechanism is necessary for mark
[3 max]
B Sodium ion gates open / membrane more permeable to
sodium ions / sodium ions rush in;
[1]
(ii) Two marks for two of:
Membrane impermeable to sodium ions / sodium ion channels closed;
Sodium ions cannot enter axon;
Membrane becomes more negative than resting potential; [2 max]
(b) (i) Two marks for two of:
Unique shape of receptor protein / binding site;
reject ‘active site’
Due to (tertiary) structure of protein molecule;
Concept of complementary shape / ref. to neurotransmitter ‘fitting’;
[2 max]
(ii) Cause vesicles to move to presynaptic membrane /
fuse with membrane;
[1]
(c) (i)
Two marks for two of:
Impulses / action potentials from neurones A and B together /spatial summation;
Cause sufficient depolarisation / open sufficient sodium ion channels;
For threshold to be reached;
[2 max]
(ii) Two marks for two of:
Impulses from A and B independent / no summation;
Threshold not reached;
Insufficient sodium ion channels opened;
[2 max]
(iii) Inhibitory;
More IPSPs than EPSPs / reduces membrane potential / makes more
negative (allow hyperpolarisation) / cancels effect of action potential
from A;
[2 max]
2.(a) Initially membrane impermeable to Na+;
Sodium channels open;
allowing Na+ into axon;
reverses potential difference across
membrane/ charge on either
side/depolarised;
membrane becomes more permeable to K+
ions/K+ leave the axon;
[max. 4]
(b) (i) All action potentials are the same size;
threshold value for action potential to occur
[2]
(ii)
frequency of action potentials
[1]
(c) several (sub-threshold) impulses add to
produce an action potential
[1]
Drugs at Synapses
• Drugs can affect the synaptic transmission.
They can do this by various ways. E.g. Some
drugs are the same shape of
neurotransmitters so they mimic their action
at receptors (Agonists)
Example: Nicotine mimics acetylcholine so
binds to nicotinic cholinergic receptors in the
brain.