The Human Nervous System

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Organisation of the 
Nerve Cells Reflex Arc
Nervous System

Humans, like all living organisms, can respond to their environment. Humans have two complimentary
control systems to do this: the nervous system and the endocrine (hormonal) system. The human nervous
system controls everything from breathing and producing digestive enzymes, to memory and intelligence.

Nerve Cells   [back to top]

The nervous system composed of nerve cells, or neurones:

Motor Neurone:

 Efferent Neuron – Moving toward a central organ or point

 Relays messages from the brain or spinal cord to the muscles and organs

Sensory Neurone:
  Afferent Neuron – Moving away from a central organ or point

 Relays messages from receptors to the brain or spinal cord

Interneuron (relay neurone):

 Relays message from sensory neurone to motor neurone

 Make up the brain and spinal cord

  Sensory neuron Interneuron Motor Neuron

Length of Long dendrites and short Short dendrites and short or Short dendrites and long
Fibers axon long anxon axons
Cell body and dendrite are Dendrites and the cell body
outside of the spinal cord; Entirely within the spinal are located in the spinal
Location
the cell body is located in a cord or CNS cord; the axon is outside of
dorsal root ganglion the spinal cord
Interconnect the sensory
Conduct impulse to the Conduct impulse to an
Function neuron with appropriate
spinal cord effector (muscle or gland)
motor neuron

A neurone has a cell body with extensions leading off it.

Numerous dendrons and dendrites provide a large
surface area for connecting with other neurones, and carry
nerve impulses towards the cell body. A single long axon
carries the nerve impulse away from the cell body. The
axon is only 10µm in diameter but can be up to 4m in
length in a large animal (a piece of spaghetti the same
shape would be 400m long)! Most neurones have many
companion cells called Schwann cells, which wrap their
cell membrane around the axon many times in a spiral to
form a thick insulating lipid layer called the myelin sheath. Nerve impulse can be passed from the axon
of one neurone to the dendron of another at a synapse. A nerve is a discrete bundle of several thousand
neurone axons.

 There are several differences between axons and dendrites:

Axons Dendrites

 Take information away from the cell body  Bring information to the cell body

 Smooth Surface  Rough Surface (dendritic spines)

 Generally only 1 axon per cell  Usually many dendrites per cell

 No ribosomes  Have ribosomes

 Can have myelin  No myelin insulation

 Branch further from the cell body  Branch near the cell body

 
 Neurons are similar to other cells in the body because:

1. Neurons are surrounded by a cell membrane.

2. Neurons have a nucleus that contains genes.
3. Neurons contain cytoplasm, mitochondria and other organelles.
4. Neurons carry out basic cellular processes such as protein
synthesis and energy production.

Neurons differ from other cells in the body because:

1. Neurons have specialised extensions called dendrites and axons.

Dendrites bring information to the cell body and axons take
information away from the cell body.
2. Neurons communicate with each other through an
electrochemical process.
3. Neurons contain some specialized structures (for example,
synapses) and chemicals (for example, neurotransmitters).

Check Point  Humans have three types of neurones:

 Sensory neurones have long axons and transmit nerve impulses from sensory receptors all
over the body to the central nervous system.
 Motor neurones also have long axons and transmit nerve impulses from the central nervous
system to effectors (muscles and glands) all over the body.
 Interneurones (also called connector neurones or relay neurones) are usually much smaller
cells, with many interconnections.

The Reflex Arc   [back to top]

The three types of neurones are arranged in circuits and networks, the simplest of which is the reflex arc.
In a simple reflex arc, such as the knee jerk, a stimulus is detected by a receptor cell, which synapses
with a sensory neurone. The sensory neurone carries the impulse from site of the stimulus to the central
nervous system (the brain or spinal cord), where it synapses with an interneurone. The interneurone
synapses with a motor neurone, which carries the nerve impulse out to an effector, such as a muscle,
which responds by contracting.

Reflex arc can also be represented by a simple flow diagram:

Organisation Of The Human Nervous System  

[back to top]

The human nervous system is far more complex than a simple reflex arc, although the same stages still
apply. The organisation of the human nervous system is shown in this diagram:
It is easy to forget that much of the human nervous system is concerned with routine, involuntary jobs,
such as homeostasis, digestion, posture, breathing, etc. This is the job of the autonomic nervous system,
and its motor functions are split into two divisions, with anatomically distinct neurones. Most body organs
are innervated by two separate sets of motor neurones; one from the sympathetic system and one from
the parasympathetic system. These neurones have opposite (or antagonistic) effects. In general the
sympathetic system stimulates the “fight or flight” responses to threatening situations, while the
parasympathetic system relaxes the body. The details are listed in this table:

Organ Sympathetic System Parasympathetic System

Eye Dilates pupil
Constricts pupil

Tear glands No effect

Stimulates tear secretion

Salivary glands Inhibits saliva production

Stimulates saliva production

Lungs Dilates bronchi

Constricts bronchi

Heart Speeds up heart rate Slows down heart rate

Stimulates peristalsis
Gut Inhibits peristalsis

Stimulates bile production

Liver Stimulates glucose production

Stimulates urination
Bladder Inhibits urination
 Check Point  The Human Nervous system compromises  of:
 The CNS and peripheral nervous system

 Peripheral nervous system includes the autonomic and somatic nervous system

 The sympathetic and parasympathetic have antagonistic effects

 
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Last updated 17/04/2004

 
 Nerve Impulses
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Resting
How impulses Propagation of Speed of
Membrane Action Potentials
start (receptors) Impulses Impulses
Potential

Neurones send messages electrochemically; this means that chemicals (ions) cause an electrical
impulse. Neurones and muscle cells are electrically excitable cells, which means that they can transmit
electrical nerve impulses. These impulses are due to events in the cell membrane, so to understand the
nerve impulse we need to revise some properties of cell membranes.

The Resting Membrane Potential  [back to top]

When a neurone is not sending a signal, it is at ‘rest’. The membrane is responsible for the different
events that occur in a neurone. All animal cell membranes contain a protein pump called the sodium-
potassium pump (Na+K+ATPase). This uses the energy from ATP splitting to simultaneously pump 3
sodium ions out of the cell and 2 potassium ions in. 

The Sodium-Potassium Pump (Na+K+ATPase)

(Provided by:  Doc Kaiser's Microbiology Website)

Three sodium ions from inside the cell first bind to

the transport protein. Then a phosphate group is
transferred from ATP to the transport protein causing
it to change shape and release the sodium ions
outside the cell. Two potassium ions from outside the
cell then bind to the transport protein and as the
phospate is removed, the protein assumes its
original shape and releases the potassium ions
inside the cell.

If the pump was to continue unchecked there would be no sodium or  potassium ions left to pump, but
there are also sodium and potassium ion channels in the membrane. These channels are normally
 closed, but even when closed, they “leak”, allowing sodium ions to leak in and potassium ions to leak out,
down their respective concentration gradients.

Concentration of ions inside and outside the neurone at rest:

Concentration
Concentration inside Why don’t the ions move down their concentration
Ion outside cell/mmol
cell/mmol dm-3 gradient?
dm-3

K+ 150.0 2.5 K+ ions do not move out of the neurone down their
concentration gradient due to a build up of positive charges
outside the membrane. This repels the movement of any more
Na+ 15.0 145.0 K+ ions out of the cell.

The chloride ions do not move into the cytoplasm as the

Cl- 9.0 101.0 negatively charged protein molecules that cannot cross the
surface membrane repel them.

The combination of the Na+K+ATPase pump and the leak channels cause a stable imbalance of Na + and
K+ ions across the membrane. This imbalance of ions causes a potential difference (or voltage) between
the inside of the neurone and its surroundings, called the resting membrane potential. The membrane
potential is always negative inside the cell, and varies in size from –20 to –200 mV (milivolt) in different
cells and species (in humans it is –70mV). The Na+K+ATPase is thought to have evolved as an
osmoregulator to keep the internal water potential high and so stop water entering animal cells and
bursting them. Plant cells don’t need this as they have strong cells walls to prevent bursting.

Check Point   The Resting Membrane Potential is always negative (-70mV)

 K+ pass easily into the cell

 Cl- and Na+ have a more difficult time crossing

  Negatively charged protein molecules inside the neurone cannot pass the membrane

 The Na+K+ATPase pump uses energy to move 3Na+ out for every 2K+ into neuron

 The imbalance in voltage causes a potential difference across the cell membrane - called the
resting potential

The Action Potential  [back to top]

The resting potential tells us about what happens when a neurone is at rest. An action potential occurs
when a neurone sends information down an axon. This involves an explosion of electrical activity, where
the nerve and muscle cells resting membrane potential changes.

In nerve and muscle cells the membranes are electrically excitable, which means they can change their
membrane potential, and this is the basis of the nerve impulse. The sodium and potassium channels in
these cells are voltage-gated, which means that they can open and close depending on the voltage
across the membrane.

The normal membrane potential inside the axon of nerve cells is –70mV, and since this potential can
change in nerve cells it is called the resting potential. When a stimulus is applied a brief reversal of the
membrane potential, lasting about a millisecond, occurs. This brief reversal is called the action potential:

An action potential has 2 main phases called depolarisation and repolarisation:

At rest, the inside of the neuron is slightly negative due to a higher

concentration of positively charged sodium ions outside the
neuron. 

When stimulated past threshold (about –30mV in humans),

sodium channels open and sodium rushes into the axon, causing
a region of positive charge within the axon. This is called
depolarisation 
 The region of positive charge causes nearby voltage gated
sodium channels to close. Just after the sodium channels close,
the potassium channels open wide, and potassium exits the axon,
so the charge across the membrane is brought back to its resting
potential. This is called repolarisation. 

This process continues as a chain-reaction along the axon.  The

influx of sodium depolarises the axon, and the outflow of
potassium repolarises the axon. 

The sodium/potassium pump restores the resting concentrations

of sodium and potassium ions 

 
 

 
(provided by: Markham)
 

 
 
Check Point    Action Potential has two main phases:
 Depolarisation. A stimulus can cause the membrane
potential to change a little. The voltage-gated ion channels can
detect this change, and when the potential reaches –30mV the
sodium channels open for 0.5ms. The causes sodium ions to rush
in, making the inside of the cell more positive. This phase is
referred to as a depolarisation since the normal voltage polarity
(negative inside) is reversed (becomes positive inside).

Repolarisation. At a certain point, the depolarisation of the

membrane causes the sodium channels to close. As a result the
potassium channels open for 0.5ms, causing potassium ions to
rush out, making the inside more negative again. Since this
restores the original polarity, it is called repolarisation. As the
polarity becomes restored, there is a slight ‘overshoot’ in the
movement of potassium ions (called hyperpolarisation). The
resting membrane potential is restored by the Na+K+ATPase
pump.

‘All or Nothing’ Law

The action potential only
occurs if the stimulus causes
enough sodium ions enter the
cell to change the membrane
potential to a certain
threshold level. At the
threshold, sodium gates open
in the membrane and allow a
sudden flood of sodium ions to
enter the cell. If the
depolarisation is not great
enough to reach the threshold,
then an action potential (and
hence an impulse) will not be
produced. This is called the
all or nothing law. This
means that the ion channels
are either open or closed;
there is no half-way position.
This means that the action
potential always reaches
+40mV as it moves along an
axon, and it is never
attenuated (reduced) by long
axons. Action potentials are
always the same size,
however the frequency of the
impulse carrying the
information can determine the
intensity of the stimulus, i.e.
strong stimulus = high
frequency.

How do Nerve Impulses Start?  [back to top]

We and other animals have several types of receptors of mechanical stimuli. Each initiates nerve
impulses in sensory neurons when it is physically deformed by an outside force such as:
 touch

 pressure

 stretching

 sound waves

 motion

Mechanoreceptors enable us to
 detect touch

 monitor the position of our muscles, bones, and joints - the sense of proprioception

 detect sounds and the motion of the body.

E.g. Touch
Light touch is detected by receptors in the skin. These are often found close to a hair follicle so even if the
skin is not touched directly, movement of the hair is detected.

In the mouse, light movement of hair triggers a generator potential in mechanically-gated sodium
channels in a neuron located next to the hair follicle. This potential opens voltage-gated sodium
channels and if it reaches threshold, triggers an action potential in the neuron.

Touch receptors are not distributed evenly over the body. The fingertips and tongue may have as many
as 100 per cm2; the back of the hand fewer than 10 per cm2. This can be demonstrated with the two-
point threshold test. With a pair of dividers like those used in mechanical drawing, determine (in a
blindfolded subject) the minimum separation of the points that produces two separate touch sensations.
The ability to discriminate the two points is far better on the fingertips than on, say, the small of the back.

The density of touch receptors is also reflected in the amount of somatosensory cortex in the brain
assigned to that region of the body.

Proprioception
 Proprioception is our "body sense".

 It enables us to unconsciously monitor the position of our body.

 It depends on receptors in the muscles, tendons, and joints.

 If you have ever tried to walk after one of your legs has "gone to sleep", you will have some
appreciation of how difficult coordinated muscular activity would be without proprioception.
The Pacinian Corpuscle
  Pacinian corpuscles are pressure receptors.
They are located in the skin and also in various
internal organs. Each is connected to a sensory
neuron. Pacinian corpuscles are fast-
conducting, bulb-shaped receptors located deep
in the dermis. They consist of the ending of a
single neurone surrounded by lamellae. They are
the largest of the skin's receptors and are
believed to provide instant information about how
and where we move. They are also sensitive to
vibration. Pacinian corpuscles are also located in
joints and tendons and in tissue that lines organs
and blood vessels.

 Pressure on the skin changed the shape of the

Pacinian corpuscle. This changes the shape of
the pressure sensitive sodium channels in the
membrane, making them open. Sodium ions diffuse in through the channels leading to depolarisation
called a generator potential. The greater the pressure the more sodium channels open and the larger
the generator potential. If a threshold value is reached, an action potential occurs and nerve impulses
travel along the sensory neurone. The frequency of the impulse is related to the intensity of the stimulus.

Adaptation
When pressure is first applied to the corpuscle, it initiates a volley of impulses in its sensory neuron.
However, with continuous pressure, the frequency of action potentials decreases quickly and soon
stops. This is the phenomenon of adaptation.

Adaptation occurs in most sense receptors. It is useful because it prevents the nervous system from
being bombarded with information about insignificant matters like the touch and pressure of our clothing.

Stimuli represent changes in the environment. If there is no change, the sense receptors soon adapt. But
note that if we quickly remove the pressure from an adapted Pacinian corpuscle, a fresh volley of
impulses will be generated.

The speed of adaptation varies among different kinds of receptors. Receptors involved in proprioception -
such as spindle fibres - adapt slowly if at all.
Check Point   The Pacinian Corpuscle
Deforming the corpuscle creates a generator potential in the sensory neuron arising within it. This is a
graded response: the greater the deformation, the greater the generator potential. If the generator
potential reaches threshold, a volley of action potentials (also called nerve impulses) are triggered at the
first node of Ranvier of the sensory neuron.

Overall:
In living cells nerve impulses are started by receptor cells. These all contain special sodium channels that
are not voltage-gated, but instead are gated by the appropriate stimulus (directly or indirectly). For
example:  

 Chemical-gated sodium
channels in tongue taste
receptor cells open when a
certain chemical in food binds to
them hemical-gated sodium
channels in tongue taste
receptor cells open when a
certain chemical in food binds to
them
 Mechanically-gated ion channels
in the hair cells of the inner ear
open when they are distorted by
sound vibrations
 
In each case the correct stimulus causes
the sodium channel to open
i
Causes sodium ions to flow into the cell
i
Causes a depolarisation of the membrane
potential
i
 Affects the voltage-gated sodium channels
nearby and starts an action potential
Check
(providingPoint   An point
the threshold action occurs
is reached)  due to an increase in membrane permeability
to Na+
 An action potential is initiated by receptor cells that cause sodium channels to open
  An action potential can only occur if the depolarisation of the membrane reaches the threshold
point.  This is the all or nothing law.

How are Nerve Impulses Propagated?  [back to top]

Once an action potential has started it is moved (propagated) along an axon automatically. The local
reversal of the membrane potential is detected by the surrounding voltage-gated ion channels, which
open when the potential changes enough.
The ion channels have
two other features that
help the nerve impulse
work effectively:
 For an action
potential to
begin, then the
depolarisation of
the neurone
must reach the
threshold value,
i.e. the all or
nothing law.
 After an ion
channel has
opened, it
needs a “rest
period” before it
can open again.
This is called
 the refractory period, and lasts about 2 ms. This means that, although the action potential
affects all other ion channels nearby, the upstream ion channels cannot open again since they
are in their refractory period, so only the downstream channels open, causing the action potential
to move one-way along the axon.

The refractory period is necessary as it allows the proteins of voltage sensitive ion channels to restore to
their original polarity.

 The absolute refractory period  = during the action potential, a second stimulus will not cause a
new action potential.
 Exception:  There is an interval in which a second action potential can be produced but only if the
stimulus is considerably greater than the threshold = relative refractory period
 The refractory period can limit the number o faction potentials in a given time.

 Average = about 100 action potentials per second.

Check Point   Nerve Impulses travel in one direction

 This is due to the refractory period i.e. Na+ channels are open or recovering.

 The refractory period allows the voltage sensitive ion channels to restore their original polarity

o Absolute refractory period - Na+ channels are open or recovering

o Relative refractory period - Occurs when the membrane is hyperpolarised (-80mV),
where the K+ channels are open. Action potentials are more difficult to generate during
this period relative to resting potential (-70mV)

 
How Fast are Nerve Impulses?  [back to top]
Action potentials can travel along axons at speeds of 0.1-100 m/s. This means that nerve impulses can
get from one part of a body to another in a few milliseconds, which allows for fast responses to stimuli.
(Impulses are much slower than electrical currents in wires, which travel at close to the speed of light,
3x108 m/s.) The speed is affected by 3 factors:

 Temperature - The higher the temperature, the faster the speed. So homoeothermic (warm-
blooded) animals have faster responses than poikilothermic (cold-blooded) ones.
 Axon diameter - The larger the diameter, the faster the speed. So marine invertebrates, who live
at temperatures close to 0°C, have developed thick axons to speed up their responses. This
explains why squid have their giant axons.
 Myelin sheath - Only vertebrates have a myelin sheath surrounding their neurones. The voltage-
gated ion channels are found only at the nodes of Ranvier, and between the nodes the myelin
sheath acts as a good electrical insulator. The action potential can therefore jump large distances
from node to node (1mm), a process that is called saltatory propagation. This increases the
speed of propagation dramatically, so while nerve impulses in unmyelinated neurones have a
maximum speed of around 1 m/s, in myelinated neurones they travel at 100 m/s.

 
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Last updated 17/04/2004
  

Synapses  
[Back to Nervous System] 

Why have Drugs and

Types of
Synapses Summation gaps in Neurotransmitters the Nervous
synapses
nerves? System

 
  

Information from one neuron flows to another neuron across a synapse. The synapse is a small gap
separating neurons. The synapse consists of:

 a presynaptic ending that contains neurotransmitters, mitochondria and other cell organelles,

 a postsynaptic ending that contains receptor sites for neurotransmitters and,

 a synaptic cleft or space between the presynaptic and postsynaptic endings. It is about 20nm
wide.
An action potential cannot cross the synaptic cleft between neurones. Instead the nerve impulse is
carried by chemicals called neurotransmitters. These chemicals are made by the cell that is sending the
impulse (the pre-synaptic neurone) and stored in synaptic vesicles at the end of the axon. The cell that
is receiving the nerve impulse (the post-synaptic neurone) has chemical-gated ion channels in its
membrane, called neuroreceptors. These have specific binding sites for the neurotransmitters. 

Check Point  Synapse is a small gap separating neurones

 Synapses consist of:

o presynaptic ending (where neurotransmitters are made)

o post synaptic ending (has neuroreceptors in the membrane)
o synaptic cleft
 Action potentials cannot cross the synaptic cleft

 Nerve impulse is carried by neurotransmitters

1. At the end of the pre-synaptic neurone there are voltage-gated calcium channels. When an action
potential reaches the synapse these channels open, causing calcium ions to flow into the cell.

2. These calcium ions cause the synaptic vesicles to fuse with the cell membrane, releasing their
contents (the neurotransmitter chemicals) by exocytosis.
3. The neurotransmitters diffuse across the synaptic cleft.

4. The neurotransmitter binds to the neuroreceptors in the post-synaptic membrane, causing the
channels to open. In the example shown these are sodium channels, so sodium ions flow in.

5. This causes a depolarisation of the post-synaptic cell membrane, which may initiate an action
potential, if the threshold is reached.

6. The neurotransmitter is broken down by a specific enzyme in the synaptic cleft; for example the
enzyme acetylcholinesterase breaks down the neurotransmitter acetylcholine. The breakdown
products are absorbed by the pre-synaptic neurone by endocytosis and used to re-synthesise more
neurotransmitter, using energy from the mitochondria. This stops the synapse being permanently on.

Check Point  How the impulse is transmitted across the synaptic cleft
action potential reaches the presynaptic terminal
i
  
i
 
i
 
i



i


i



i

 

i




Different Types of Synapses  [back to top]  

The human nervous system uses a number of different neurotransmitter and neuroreceptors, and they
don’t all work in the same way. We can group synapses into 5 types:

1. Excitatory Ion Channel Synapses.

These synapses have neuroreceptors that are sodium channels. When the channels open, positive
ions flow in, causing a local depolarisation and making an action potential more likely. This was the
kind of synapse described above. Typical neurotransmitters are acetylcholine, glutamate or aspartate.
2. Inhibitory Ion Channel Synapses.
These synapses have neuroreceptors that are chloride channels. When the channels open, negative
ions flow in causing a local hyperpolarisation and making an action potential less likely. So with these
synapses an impulse in one neurone can inhibit an impulse in the next. Typical neurotransmitters are
glycine or GABA.
3. Non Channel Synapses.
These synapses have neuroreceptors that are not channels at all, but instead are membrane-bound
enzymes. When activated by the neurotransmitter, they catalyse the production of a “messenger
chemical” inside the cell, which in turn can affect many aspects of the cell’s metabolism. In particular
they can alter the number and sensitivity of the ion channel receptors in the same cell. These
synapses are involved in slow and long-lasting responses like learning and memory. Typical
neurotransmitters are adrenaline, noradrenaline (NB adrenaline is called epinephrine in America),
dopamine, serotonin, endorphin, angiotensin, and acetylcholine.
4. Neuromuscular Junctions.
These are the synapses formed between motor neurones and muscle cells. They always use the
neurotransmitter acetylcholine, and are always excitatory. We shall look at these when we do muscles.
Motor neurones also form specialised synapses with secretory cells.
5. Electrical Synapses.
In these synapses the membranes of the two cells actually touch, and they share proteins. This allows
the action potential to pass directly from one membrane to the next. They are very fast, but are quite
rare, found only in the heart and the eye.
 
Check Point  Different types of synapses
Excitatory ion channel synapses -  neuroreceptors are Na+ channels.  When Na+ channels open,
local depolarisaition occurs, if threshold is reached then action potential is initated

inhibitory ion channels - neuroreceptors are Cl- channels.  When Cl- channels open, hyperpolarisation
occurs, making action potential less likely

Non channel synapses - neuroreceptors are membrane-bound enzymes.  When activated, they
catalyse the 'messenger chemical', which in turn can affect the sensitivity of the ion channel receptors in
the cell

Neuromuscular junctions - synapses formed between motor neurones and muscle cells.  Always use
the neurotransmitter acetylchline, and are always excitatory

Electrical synapses - the membranes of the two cells actually touch and they chare proteins.  The
action potential can pass directly from one membrane to the next
 

Summation  [back to top]  

When one postsynaptic neuron is excited/inhibited by more than one presynaptic neuron. Thus several
neurons converge and release their neurotransmitters towards one neuron.

One neurone can have thousands of synapses on its body and dendrons. So it has many inputs, but only
one output. The output through the axon is called the Grand Postsynaptic Potential (GPP) and is the
sum of all the excitatory and inhibitory potentials from all that cell’s synapses. If there are more excitatory
potentials than inhibitory ones then there will be a GPP, and the neurone will “fire”, but if there are more
inhibitory potentials than excitatory ones then there will not be a GPP and the neurone will not fire.
This summation is the basis of the processing power in the nervous system. Neurones (especially
interneurones) are a bit like logic gates in a computer, where the output depends on the state of one or
more inputs. By connecting enough logic gates together you can make a computer, and by connecting
enough neurones together to can make a nervous system, including a human brain.

So why bother? Why have gaps in the nerves?  [back to top]  

1. They make sure that the flow of impulses is in one direction only. This is because the vesicles
containing the transmitter are only in the presynaptic membrane and the receptor molecules are
only on the postsynaptic membrane.
2. They allow integration, e.g. an impulse travelling down a neurone may reach a synapse which
has several post synaptic neurones, all going to different locations. The impulse can thus be
dispersed. This can also work in reverse, where several impulses can converge at a synapse.
3. They allow ‘summation’ to occur. Synapses require the release of sufficient transmitter into the
cleft in order for enough of the transmitter to bind to the postsynaptic receptors and the impulse to
be generated in the postsynaptic neurone. In spatial summation, several presynaptic neurones
converge at a synapse with a single post synaptic neurone. In temporal summation there is
only one presynaptic and one postsynaptic neurone but the frequency of impulses reaching the
synapse is important. Both types of summation allow for ‘grading’ of nervous response – if the
stimulation affects too few presynaptic neurones or the frequency of stimulation is too low, the
impulse is not transmitted across the cleft.
4. They allow the ‘filtering out’ of continual unnecessary or unimportant background stimuli. If a
neurone is constantly stimulated (e.g. clothes touching the skin) the synapse will not be able to
renew its supply of transmitter fast enough to continue passing the impulse across the cleft. This
‘fatigue’ places un upper limit on the frequency of depolarisation.

Neurotransmitters  [back to top]  

You only need to know about two main neurotransmitters:

Acetylcholine (Ach) Noradrenaline

 Widely used at synapses in the peripheral nervous This is another transmitter substance which may be
system. Released at the terminals of: in some synapses instead of acetylcholine, e.g.
some human brain synapses and sympathetic
 All motor neurones activating skeletal nervous system synapses.
 muscle Synapses result in an appreciable delay, up to one
  Many neurones of the autonomic millisec. Therefore slows down the transmission in

nervous system especially those in the nervous system.

parasympathetic branch
Synapses are highly susceptible to drugs and
 Some synapses in the central nervous
fatigue e.g.
system

 Curare (poison used by S. American

Acetylcholine is removed from the synapse by
Indians) and atropine stops Acetylcholine
enzymatic breakdown into inactive fragments. The
from depolarising the post-synaptic
enzyme used is acetylcholinesterase.
membrane, i.e. become paralysed.

Nerve gases used in warfare (e.g. sarin) and the
organophosphate insecticides (e.g. parathion)
achieve their effects by inhibiting
acetylcholinesterase thus allowing ACh to remain
active. In the presence of such inhibitors ACh
keeps stimulating the postsynaptic membranes and
the nervous system soon goes wild, causing
contraction of the muscles in uncontrollable
spasms and eventually death. Atropine is used as
an antidote because it blocks ACh receptors.
 Strychnine and some nerve gases inhibit
or destroy acetylcholinesterase formation.
Prolongs and enhances any stimulus, i.e.
leads to convulsions, contraction of
muscles upon the slightest stimulus.
 Cocaine, morphine, alcohol, ether and
chloroform anaesthetise nerve fibres.
 Mescaline and LSD produce their
hallucinatory effect by interfering with nor-
adrenaline.

Synapses where acetylcholine is the Synapses where noradrenaline is the

neurotransmitter = cholinergic synapses neurotransmitter = adrenergic synapses

Check Point  Neurotransmitters

Acetylcholine - released by all motor neurones, activating skeletal muscles
                      - involved in the parasympathetic nervous system (relaxing responses)
                      - cholinergic synapses

Noradrenaline - involved in the sympathetic nervous system ('fight or flight' responses)

                       - adrenergic synapses
Drugs and the Nervous System [back to top]  

(additional information, however, helpful to your understanding)

Almost all drugs taken by humans (medicinal and recreational) affect the nervous system. From our
understanding of the human nervous system we can understand how many common drugs work. Drugs
can affect the nervous system in various ways, shown in this table:

Drug action Effect

Mimic a neurotransmitter
Switch on a synapse
Stimulate the release of a
Switch on a synapse
neurotransmitter
Switch on a synapse
Open a neuroreceptor channel
Switch off a synapse
Block a neuroreceptor channel
Switch on a synapse
Inhibit the breakdown enzyme
Stop action potentials
Inhibit the Na+K+ATPase pump
Stop action potentials
Block the Na+ or K+ channels

Drugs that stimulate a nervous system are called agonists, and those that inhibit a system are called
antagonists. By designing drugs to affect specific neurotransmitters or neuroreceptors, drugs can be
targeted at different parts of the nervous system. The following paragraph describe the action of some
common drugs. You do not need to know any of this, but you should be able to understand how they
work.. By designing drugs to affect specific neurotransmitters or neuroreceptors, drugs can be targeted at
different parts of the nervous system. The following paragraph describe the action of some common
drugs. You do not need to know any of this, but you should be able to understand how they work.

1. Drugs acting on the central nervous system

In the reticular activating system (RAS) in the brain stem noradrenaline receptors are excitatory and
cause wakefulness, while GABA receptors are inhibitory and cause drowsiness. Caffeine (in coffee,
cocoa and cola), theophylline (in tea), amphetamines, ecstasy (MDMA) and cocaine all promote the
release of noradrenaline in RAS, so are stimulants. Antidepressant drugs, such as the tricyclics, inhibit
the breakdown and absorption of noradrenaline, so extending its effect. Alcohol, benzodiazepines (e.g.
mogadon, valium, librium), barbiturates, and marijuana all activate GABA receptors, causing more
inhibition of RAS and so are tranquillisers, sedatives and depressants. The narcotics or opioid group of
 drugs, which include morphine, codeine, opium, methadone and diamorphine (heroin), all block opiate
receptors, blocking transmission of pain signals in the brain and spinal chord. The brain’s natural
endorphins appear to have a similar action.

The brain neurotransmitter dopamine has a number of roles, including muscle control, pain inhibition
and general stimulation. Some psychosis disorders such as schizophrenia and manic depression are
caused by an excess of dopamine, and antipsychotic drugs are used to block the dopamine receptors
and so reduce its effects. Parkinson’s disease (shaking of head and limbs) is caused by too little
dopamine compared to acetylcholine production in the midbrain. The balance can be restored with
levodopa, which mimics dopamine, or with anticholinergic drugs (such as procyclidine), which block
the muscarinic acetylcholine receptors.

Tetrodotoxin (from the Japanese puffer fish) blocks voltage-gated sodium channels, while
tetraethylamonium blocks the voltage-gated potassium channel. Both are powerful nerve poisons.
General anaesthetics temporarily inhibit the sodium channels. Strychnine blocks glycine receptors in
the brain, causing muscle convulsions and death.

2. Drugs acting on the somatic nervous system

Curare and abungarotoxin (both snake venoms) block the nicotinic acetylcholine receptors in the
somatic nervous system, and so relax skeletal muscle. Myasthenia gravis (a weakening of the muscles
in the face and throat caused by inactive nicotinic acetylcholine receptors) is treated by the drug
neostigmine, which inhibits acetylcholinesterase, so increasing the amount of acetylcholine at the
neuromuscular junction. Nerve gas and organophosphate insecticides (DDT) inhibit
acetylcholinesterase, so nicotinic acetylcholine receptors are always active, causing muscle spasms
and death. Damaged tissues release prostaglandins, which stimulate pain neurones (amongst other
things). The non-narcotic analgesics such as aspirin, paracetamol and ibuprofen block prostaglandin
production at source of pain, while paracetamol has a similar effect in the brain. Local anaesthetics
such as procaine block all sensory and motor synapses at the site of application.
3. Drugs acting on the autonomic nervous system
Sympathetic agonists like salbutamol and isoprenaline, activate the adrenergic receptors in the
sympathetic system, encouraging smooth muscle relaxation, and are used as bronchodilators in the
treatment of asthma. Sympathetic antagonists like the beta blockers block the noradrenaline receptors
in the sympathetic nervous system. They cause dilation of blood vessels in the treatment of high blood
pressure and migraines, and reduce heartbeat rate in the treatment of angina and abnormal heart
rhythms. Parasympathetic antagonists like atropine (from the deadly nightshade belladonna) inhibit the
muscarinic acetylcholine receptors in parasympathetic system, and are used as eye drops to relax the
ciliary muscles in the eye.
 
 [back to top]

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Last updated 17/04/2004