Nervous Control

A neurone (nerve cell) is a specialised cell adapted to carrying nerve impulses (wave of depolarisation) quickly from one part of the body to another. They are adapted to serve this function in several different ways:

• Large amounts of rough ER in the cell body (for production of proteins, incl. some types of neurotransmitters)
• Presense of dendrons, extensions of the cell membrane and cytoplasm which further divide into dendrites (carry nerve impulses to the cell body)
• Cell body elongates into the axon, a long fibre which carries impulses away from the cell

In some neurones, other cells are associated with the axon, which further enhance its ability to transmit nerve impulses. They are called Schwann cells and they wrap around the axon, proving protection and electrical insulation. They wrap around the axon many times, building up multiple layers of their membranes which are rich in a lipid known as myelin. These Schwann cells make up the myelin sheath around some neurones. There are gaps every 1-3mm between Schwann cellls where there is no myelin sheath. These gaps are called nodes of Ranvier. Neurones with a muelin sheath are described as myelinated and they are able to transmit nerve impulses faster than unmyelinated neurones.

Myelin sheath: thick insulating layer around axon. Has high electrictal conductivity. 

Nerve cells can be classified according to their function. There are 3 main types of neurone:

• Intermediate or relay neurones which transmit impulses BETWEEN neurones (found in the CNS)
• Sensory neurones which transport impulses FROM a receptor (eg skin,eyes) to an intermediate or motor neurone
• Motor neurones which transmit impulses FROM an intermediate or sensory neurone to an effector (eg muscles or glands)

A nerve impulse may be defined as 'a self-propagating wave of electrical disturbance that travels along the surface of the axon membrane. It is not, however, an electrical current, but a temp reversal of the electrical potential difference across the axon membrane. This reversal is between 2 states, called the RESTING POTENTIAL and the ACTION POTENTIAL.

All cells have a difference in electrical charge across the plasma membrane. This is called the potential difference measured in milivolts (MV)

If a voltmeter is placed across the plasma membrane of an inactive axon, the electrical potential difference (ie difference in charge between the inside and outside) is generally -65 to -70 millivolts (mV). This is known as the RESTING POTENTIAL.

The resting potential is negative as the inside of the axon is MORE negative than the tissue fluid outside it. The resting potential is maintained through a balance between sodium ions and potassium ions inside and outside the axon. 

This balance is maintained through strict controls on the movement of these ions. Controls are:

• The phospholipid bilyar is impermeable to charged particles, so the sodium and potassium ions cannot diffuse across it.
• Specific, intrinsic proteins embedded through the phospholipid bilayer can act as channels to allow these ions to pass into or out of the axon. Some are 'gated' channels, which open and close when needed, allowing or restricting movements of ions as the occasion demands. There are different 'gates' (ie channels) for potassium and sodium ions. There are also some channels which remain open at all times. These are known as 'leak' channels. Ions move through these gates by facilated diffusion. 
• Some proteins actively transport potassium ions into the axon and sodium ions out of the axon. (potassium ions leak out and in). These are known as sodium potassium pumps. Each pump doubles up as an ATPase enzyme to allow ATP to be hydrolysed, thus proving the energy for active transport. - 3 sodium out for every 2 potassium into axon.

Through these different controls the resting potential is maintained. The inside of the axon is negatively charged (due to presence of anions such as glucose, proteins etc) compared to the outside and the axon is said to be polarised. 

Why are sodium and potassium ions unable to diffuse through the phospholipid bilayer: Because they are charged particles/hydrophilic so cannot easily pass through the hydrophobic phospholipid bilayer. 

Inside the axon is -ve because the -ve conc. inside stays the same and +ve lead out and negative stay. 

2 types of ion channels in neurone membrane:

voltage gated channels: open and close in response to changes in voltage (closed when neurone at rest)

leak channels - permanently open (for potassium ions mainly)

Similarities and differences between facilitated diffusion and active transport:

S: Both take place through membrane proteins and both involve movement of charged particles/polar particles. 

D: Passive - down a conc. gradient and active transport involves movement against a conc. gradient. active transport requires ATP facilitated diffusion doesn't. ; Channel proteins (Gated and leak) ; carrier (sodium potassium pump)

• Sodium ions are actively transported OUT of the axon via the sodium potassium pump
• Potassium ions are actively transported INTO the axon via the sodium potassium pump 
• 3 sodium ions move OUT of the axon to every 2 potassium ions that move IN so there is a greater movement of sodium ions compared to potassium ions
• The active transport of ions also creates a CONCENTRATION GRADIENT between the outside and the inside of the axon. There are more potassium ions inside the axon compared to the outside, and more sodium ions outside compared to inside. In the resting state, voltage gated channels for sodium ions and potassium ions are closed, but there are more leak potassium channels than those for sodium ions. This means the membrane as a whole is MORE PERMEABLE to potassium ions compared to sodium ions. Sodium ions therefore diffuse only very slowly back into the axon, while potassium ions DIFFUSE RAPIDLY out of the axon. The resting potential is therefore mainly determined by the loss of potassium ions.

There are therefore 2 gradients that have a role in establishing and maintaining the resting potential: the chemical (concentration) gradient and the electrical potential gradient. These 2 gradients working together form an electrochemical gradient. 

Key points:

• The sodium potassium pumpactively transports more sodium ions OUT of the axon than potassium ions in
• The membrane is MORE PERMEABLE TO POTASSIUM IONS than to sodium ions
• POTASSIUM ions therefore DIFFUSE back OUT FASTER than sodium ions diffuse back in

.... causing the inside of the membrane to be more negative than the outside at rest.

Depolarisation and repolarisation

An action potential is a membrane potential temporarily reverses in response to a stimulus then returns to resting.

When a stimulus is received by a receptor or nerve ending, its energy causes a temporary reversal of the charges across the axon membrane. The usual resting potential of -65mV inside the axon BECOMES MORE POSITIVE. In this state the axon is known as being DEPOLARISED. If the axon is depolarised enough it can result in the generation of an ACTION POTENTIAL. 

(Look pg 7 for graph & back for drawing)

• 1) The axon is in its resting state, with a resting potential of approx. -65mV
• 2) Gated sodium ion channels in the membrane of the axon open. Sodium ions diffuse into the axon, causing DEPOLARISATION. If sufficiently large this depolarisation causes more sodium channels to open (voltage gated channels), making the membrane much more permeable to sodium ions. This causes sodium ions to diffuse rapidly into the axon. This then activates and opens even more voltage gated sodium channels, leading to a greater influx of sodium ions into the axon (positive feedback), until the inside of the membrane becomes charged to +40mV. This is the action potential.
• 3) When the inside of the axon becomes charged to +40mV, all of the gated sodium ion channels close, meaning the acon is against almonst impermeable to sodium ions.
• 4) At +40mV, as the sodium ion channels close, voltage gated potassium ion channels open (ie the axon's permeability to potassium ions increases) and potassium ions diffuse rapidly out of the axon, beginning to return the potential difference across the membrane back to -65mV (repolarisation)

• 5) So many potassium ions diffuse out of the axon that they cause a more negative potential difference than normal, dropping the axon interior down to about -90mV. This is known as hyperpolarisation and causes the refractory period.
• 6) The voltage gated potassium ion channels close and the sodium potassium pump restores the concentration gradients for sodium ions and potassium ions. This returns the resting potential of the axon to -65mV. The resting permeability of the axon is restored. The whole process lasts 2-3 milliseconds. 

The events outlined above will only be set into motion of the initial stimulus is larger than a specific threshold value. If the initial stimulus is not large enough, then the voltage gated sodium channels will not open and the axon membrane will not become fully depolarised, ie no action potential will be generated. If the stimulus is large enough, then the impulse will be generated at a constant size and speed. Increasing the intial stimuluse will not produce a larger or faster action potential. This is known as the all or nothing principle. It will however, increase the frequency of action potentials.

Action potentials are propagated (spread) along a neurone from the point of initiation without loss of size or speed. The region of the axon which is currently depolarised is known as the active zone of the axon. In the active zone, the axon is positively charged on the inside and negative charged on the outside. This causes small local electrical currents which flow between the active zone and the negatively charged resting zones on either side. In front of the active zone these local currents act as a stimulus and cause depolarisation of the adjacent region of the axon (by opening voltage gated sodium channels), propagating the action potential. This passage of the action potential is relatively slow (1ms-1)

In a myelinated neurone, the Schwann cells which make up the myelin sheath are pressed tightly against the axon membrane, providing electrical insulation and preventing ion movement across the membrane. (myelinated sheath prevents ions leaking out). 

Depolarisation can therefore only occur at the nodes of Ranvier, the gaps between Schwann cells. This means that, in effect, the impulse jumps from node to node, thereby skipping sections of the axon covered in myelin. This type of conduction is known as SALTATORY CONDUCTION and greatly INCREASES the speed of an impulse as it travels along the axon, reaching speeds of up to 120 ms-1 

After an action potential has occurred there is a short period of time where that area of the axon membrane is recovering from its own depolarisation. This is known as the refractory period.

There are 2 stages to this:

1st, lasting about 1ms, is known as the absolute refractory period and during this time that area of the membrane cannot respond to ANY stimulus or conduct an impulse. This corresponds to the repolarisation phase, where the gated sodium ion channels have closed and are temporarily inactivated. 

2nd, For the next few milliseconds the zone can only respond to high intensity stimuli, this is known as the relative refractory period. This is due to the hyperpolarisation of the axon membrane. 

The refractory period is important for 3 reasons:

• It ensures that action potentials travel in only 1 direction
• It produces discrete, separate action potentials
• It limits the number of action potentials an axon can carry in a given time

Myelination and saltatory conduction - myelinated neurones conduct action potentials much faster than unmyelinated ones due to saltatory conduction.

Axon diameter - the larger the diameter of the axon, the faster the action potential can pass because large axons have less resistance to flow and can maintain a more stable potential difference.

Temperature - this affects the rate of diffusion of ions across the axon membrane. It also affects the proteins involved in the transport of ions across the membrane and the enzymes involved in the generation of ATP from respiration that power the sodium potassium pump. The greater the temp the faster the conduction of action potentials, up to an optimum (eg 40 deg)

A synapse is a junction between the axon of one neurone and a dendrite of another. (junction between 2 neurones). Action potentials cannot pass from 1 neurone to another. The electrical nerve impulse must be turned into a chemical message. The groups of chemicals involved in communication between neurones at synpases are called neurotransmitters.

A synapse provides a connection between neurones that allows sensory information to flow between them. It is the function of a synpase to allow sensory impulses to travel in only 1 direction, divide impulses between multiple neurones, or merge impulses onto a single neurone. 

Individual neurones do not touch; they are separated from each other by a 20-30 nanometer gap called the synpatic cleft. The neurone which releases the transmitter is called the presynaptic neurone. The end of the axon swells to form the synpatic knon (or bouton). The knob contains many mitochondria.

Once manufactured, the transmitter is stored in synaptic vesicles, which, when stimulated, will fuse to the presynaptic membrane and release the neurotransmitter into the cleft. Once there, it will diffuse across to the postsynaptic neurone which has specific receptor molecules to bind to the transmitter. 

There are more than 40 neurotransmitters although the most common in vertebrates is acetylcholine (ACh). ACh is made of two parts: acetic acid & choline. Synapses which use ACh as a transmitter are known as cholinergic synapses and are found in the central nervous system and at neuromuscular junctions. 

Neuromuscular junction: Synapses between neurones and uscles.

• 1) Arrival of an action potential at the synaptic knob opens calcium ion channels in the membrane which allows calcium ions (Ca2+) to diffuse in.
• 2) Influx of calcium ions causes synpatic vesicles to fuse with the presynaptic membrane and release ACh by exocytosis into the synpatic cleft. 
• 3) ACh diffuses across synpatic cleft and binds to receptors on the sodium ion channels on the membrane of the postsynaptic neurone.
• 4) This causes the sodium ion channels to open and sodium ions diffuse rapidly into the post synpatic cell, causing depolarisation. If threshold is reached an action potential will be initiated. 
• 5) To prevent the initiation of more action potentials in the postsynpatic membrane, by the continued presence of ACh, an enzyme, acetylcholinesterase, hydrolyses ACh
• 6) These products diffuse back across the cleft and can be reabsorbed into the presynaptic neurone. They are recombined back into ACh and repackaged into vesicles. 

When this occurs at a neuromuscular junction, the postsynaptic neurone is replaced by a muscle. When neurotransmitters cross the synpatic cleft and bind to receptors the muscle contracts.

Why the presynaptic knob contains many mitochondria: Energy from ATP is neeed to generate the neurotransmitter, so exocytosis that are released into the synaptic cleft. Also needed to regenerate ACh. 

Products from the hydrolysis of ACh by acteylcholinesterasse: ethanoic acid (acetic acid) & choline.

Feature of synapses

Synapses act as junctions, joining one neurone to another. Through this they allow:

• A single impulse from one neurone to be transmitted to several others at a synapse, allowing an umber of simultaneous responses
• Multiple impulses my be combined at one synapse to form a single response

1) Unidirectionality - synapses can only pass impulses in one direction, the transmitter is only released by the presynaptic knob and receptors are found only on the postsynaptic knob. In this way synapses act like valves.

2) Summation - low frequency impulses often don't release enough neurotransmitter to generate an action potential in the postsynaptic neurone. The effect of different impulses can be combined by a process called SUMMATION to build up enough transmitter to generate an action potential. There are two types of summation:

• Spatial summation - in which a number of differnt presynaptic neurones together release enough transmitter AT THE SAME TIME to cause enough depolarisation to exceed the threshold of the postsynaptic neurone and trigger an action potential. e.g. rod cells in the eye
• Temporal summation - in which a single presynaptic neurone releases small amounts of neurotransmitter many times in a short period (due to several impulses arriving in quick succession), which may add up to cause enough depolarisation to exceed thershold and trigger a new action potential in the post synaptic neurone (eg cone cells in the eye)

1) Unidirectionality - synapses can only pass impulses in one direction, the transmitter is only released by the presynaptic knob and receptors are found only on the postsynaptic knob. In this way synapses act like valves.

2) Summation - low frequency impulses often don't release enough neurotransmitter to generate an action potential in the postsynaptic neurone. The effect of different impulses can be combined by a process called SUMMATION to build up enough transmitter to generate an action potential. There are two types of summation:

• Spatial summation - in which a number of differnt presynaptic neurones together release enough transmitter AT THE SAME TIME to cause enough depolarisation to exceed the threshold of the postsynaptic neurone and trigger an action potential. e.g. rod cells in the eye
• Temporal summation - in which a single presynaptic neurone releases small amounts of neurotransmitter many times in a short period (due to several impulses arriving in quick succession), which may add up to cause enough depolarisation to exceed thershold and trigger a new action potential in the post synaptic neurone (eg cone cells in the eye)

3) Inhibition - On the postsynaptic membranes of some neurones there are chloride ion channels which can be opened when activated by a certain neurotransmitter. This causes chloride ions to flood into the postsynaptic knob and make it more negative than it normally is at rest (hyperpolarisation). This in turn makes it less likely that the membrane can depolarise and so a new action potential cannot be generated. For this reason they are known as INHIBITORY SYNAPSES. Synapses and neurotransmitters that cause depolarisation of the postsynaptic membrane are called EXCITATORY. Many neurones have both inhibitory and excitatory synapses.

Synapses link neurones which report to and from the CNS about the world around us, and allow us to react to it. Many recreational and medicinal drugs act on our synapses, altering our perceptions or reactions to our environment, whether internal or external. There are many different types of neurortransmitter and they can be roughly categorised by their effect on the nervous system. 

Some drugs STIMULATE the nervous system by creating, or making it easier to create action potentials in postsynaptic neurones. A drug could do this by:

• Mimicking the neurotransmitter, e.g. having a similar shape
• Causing the release of excess neurotransmitter
• Reducing the activity of the enzyme that breaks it down

This causes an INCREASE in the number of impulses sent along that neurone. (E.g. incl. caffeine, nicotine, amphetamines & cocaine)

Some drugs INHIBIT the nervous system by causing fewer action potentials in the post synaptic neurone. A drug could do this by:

• Inhibiting the release of the neurotransmitter
• Blocking the sodium channels that the transmitter opens on the post synpatic neurone (or blocking the receptors)

This causes a reduction in the number of impulses sent along that neurone. (E.g. incl. alcohol, cannabis, ketamine & barbituurates)

The effect of a particular drug depends on the type of neurotransmitter and synapse. For example, if a drug INHIBITS the release of an EXCITATORY transmitter, then the postsynpatic neurone will be LESS likely to fire action potentials; however, if a drug inhibits the release of an INHIBITORY transmitter the postsynpatic neurone will be MORE likely to fire action potentials.

What kind of effect would nicotine (excitatory) have on the nervous system: Nicotine will bind to ACh receptors in the post synaptic membrane, open sodium ion channels and allowing sodium ions to diffuse into postsynpatic neurone and triggering action potentials. More impulses will be generated in nervous system = excitatory effect. 

Atropine had a similar shape to ACh and binds to its receptors but doesn't allow the passage of sodium through the channels. Explain what effect atropine would have on the muscle at a neuromuscular junction: Atropine will bind to ACh receptors in the postsynaptic neurone membrane but will not cause the sodium ion channels to open. It will effectively block the receptor and prevent ACh from binding. Therefore depolarisation will not occur and action potentials will not be generated in the muscle cell membranes. This prevents muscles contracting = causing paralysis.

A stimulus is a detectable change in the environment that is capable of causing a response by  the nervous system. However, very few neurones are sensitive to stimuli directly and so special structures, called receptors, are needed to convert stimuli into nerve impulses. Receptors thus act as TRANSDUCERS, i.e. they transfer the energy associated with a stimulus into an ELECTRICAL change in a neurone. 

How receptors work 

Most (but not all) receptors work in the following way: A SPECIFIC STIMULUS causes the membrane potential in the receptor to change (i.e. depolarise), producing a GENERATOR POTENTIAL. The more intense the stimulus the larger the generator potential. If this causes the membrane potential to exceed a certain threshold value it will cause an ACTION POTENTIAL to be produced, and this can then be transmitted to a sensory neurone via synpatic transmission. 

Stimulus -> generator potential in receptor -> action potential in receptor -> action potential in sensory neurone 

A bigger generator potential (above threshold) causes more FREQUENT action potentials in the sensory neurone. Each receptor is sensitive to only 1 type of stimulus; all others fail to cause a generator potential. e.g. 

Photoreceptors respond to light (rods and cones in retina)

Mechanoreceptors respond to mechanical pressure (pressure receptors in skin)

Thermoreceptors respond to temperature (skin)

Chemoreceptors respond to chemicals (carotid and aortic bodies in heart - blood pH, H+ ion conc.)

Baroreceptors respond to blood pressure (carotid and aortic bodies)

Mechanoreceptor we look at is Pacinian corpuscle 

Pressure receptors; Only respond to specific stimulus; When stimulated they create a generator potential. Higher intensity of stimulus = larger generator potential.

These are really modified neurones in that they consist of concentric layers (lamellae) of connective tissue surrounding the unmyelinated end of a myelinated sensory neurone

There is a viscous gel between the layers. 

Pacinian corpuscles are found deep in the skin, around joints, in the genital areas and in some internal organs. They are known as mechanoreceptors as they are sensitive to changes in mechanical pressure i.e. when they are physically distorted they send off a nerve impulse. They allow you to detect FIRM pressure applied to the skinm textured surface etc. 

Pacinian corpuscles have stretch mediated Na+ protein channels, found in the membrane of the sensory nerve ending. These channels change shape when under pressure so that only then can Na+ ions pass through the membrane and initiate a generator potential. 

At REST, the corupuscle is ROUND and the Na+ channels are the wrong shape to let the ions pass through.

When UNDER PRESSURE, the membrane is stretched and as a result the Na+ channels open and Na+ diffuse into the neurone (Axon). This leads to a generator potential which, if large enough, leads in turn to an action potential (impulse). The greater the pressure the greater the generator potential.

Once the pressure has been registered no further action potentials are sent until the pressure is released. Then the corpuscle temporarily springs into an elongated shape, deforming the membrane once again, and setting off another burst of impulses. 

The gel-filled lamellae act to filter the stimuli; if the pressure is applied slowly, the gel flows away from the stimulus and the membrane is not deformed. A fast application of pressure gives a deformation of the membrane for a few milliseconds, before the gel flows and the membrane resumts its normal shape. Sudden removal of pressure has the same effect as the original application. 

(pg 18 for diagram)

The eye is an example of a SENSE ORGAN. Here, PHOTORECEPTORS are organised together (in the retina) and surrounded by structures that collect, filter and amplify information from the environment. This information is relayed along neurones, as IMPULSES, to the brain, which interprets the information.

Diagram of eye:

The retina contains 2 types of photoreceptors, rods & cones, which have the same basic structure but differ in shape and the pigment they contain. Cones are mainly located in the FOVEA, the region of the retina where light is focused. Rods do not appear at the fovea at all but are all around the periphery of the retina. Rods and cones make synapses with BIPOLAR NEURONES, which in turn synapse with SENSORY NEURONES. All the sensory neurons are bundled together and form the OPTIC NERVE, which transmits impulses from the retina to the brain. 

ROD CELLS (Used in low light intensity in pheripheral region)

These contain the pigment rhodopsin which is very sensitive to light. It breaks down when it absorbs light and this triggers a sequence of events that eventually lead to the generation of action potentials (impulses) in the sensory neurones of the optic nerve. The impulses are then transmitted to the brain (Rhodopsin can be regenerated using energy from ATP)

Cone cells (Used in high light intensity and involved in colour)

Cone cells are of 3 different types, each responding to different wavelengths of light. Depending on the proportion of each type stimulated, we perceive images in colour. They contain a slightly different pigment (iodopsin) which can only be broken down by high intensity light. This is why your colour vision is poor in the dark. Once stimulated, cone cells react in a similar way to rod cells.

Cornea - light gets bent in this area of eye

Iris - is the coloured bit of the eye, pupil size changes and this is controlled by iris diaphram muscles

Lens - fine focusing

Retina - containd rods and cones

Fovea - cone cells concentrated here

Optic nerve - sensory neurones leave the eye, no rods and cones here - blind spot. 

Rod cells allow to see in the dark. Used in low light intensity and are in the peripheral region. Sensitive to low levels of light. Not good at resolving objects close together.

Cone cells in fovea of retina, used when there's lots of light and allow you to see in colour. 3 diff types of cones are red,green,blue. Have good resolution but poor sensitive (only sensitive to high light intensity) 

The distribution of rods and cones and their connections to the neurones in the retina result in them having very different properties. (pg 20 for diagram)

Rod cell; contains the pigment rhodopsin that is only sensitive to ow light intensities and is unable to distinguish colour. Rod cell can't see fine detail due to retinal convergence. Several rod cells connected to 1 bipolar neurone (Spatial summation). ATP involved contain lots of mitochondria. 

Cone cell; contains the pigment iodopisn that is sensitive only to high light intensities and allows for the discrimination of colour. Cone cell allows you to see fine detail. 

Bipolar neurone; transmits impulses from the photoreceptor cells to ganglion cells. This is where depolarisation occurs if generator potential is big enough.

Ganglion cells are sensory neurones. 

1 neurone connected to 1 cone therefore less pigment broken down = smaller generator potential = less likely to get action potential therefore high light intensity to break down more pigment. 

Breaking pigment leads to generator potential

Photoreceptors connect to a sensory neurone (ganglion cell) in the optic nerve via a bipolar neurone. Rod ces are said to show retina convergence: many rod cells connect to the same bipolar neurone, but each cone cell connects to just 1 bipolar neurone (1:1 ratio)

ROD cells are sensitive to low light intensity, but stimulation of 1 rod is not always enough to initiate an action potential in the sensory neurone. If several rods are stimulated at the same time, however, owing to the fact that many synapse with each bipolar neurone, the effects of each stimulation can be 'added together' to produced an action potential in a sensory neurone. This is because more depolarisation of the postsynaptic cell occurs, allowing threshold to be reached. This is called spatial summation and gives the rod cells great sensitivity to low light intensity.

CONE cells show no convergence and are therefore not very sensitive, only being stimulated at high light intensity. However, they do allow high visual acuity and resolution. This is because each cone synapses with a separate bipolar neurone which in turn generates impulses in a separate neurone in the optic nerve, so that the brain can interpret these stimuli as distinct, and can identiy the precise area of the retina where light rays fall. The FOVEA contains a very HIGH DENSITY of cone cells, with most of the cones packed into this tiny area, and no rods. As a result when the light hits this area the image interpreted by the brain has high acuity. Rods on the other hand give poor acuity due to convergence - brain can't distinguish which of the several rod cells have been activated.

Shape: rod-shaped outer segment

Visual pigment: rhodopsin 

Relative number: higher number (approx. 125 x 10^6 / eye)

Distribution: more at pheriphery (none at fovea)

Connections: show retinal convergence (several rods to each bipolar neurones)

Sensitivity: high sensitivity (stimulated at low light intensity)

Visual acuity: poor - no detail

Colour perception: none

Overall function: vision in dim light

Shape: Cone shaped

Visual pigment: Iodopsin

Relative number: Fewer number (approx. 7 x 10^6 / eye)

Distribution: Concentrated at fovea (high density)

Connections: 1 cone cell synapses with 1 bipolar neurones

Sensitivity: Low sensitivity (need high light intensity)

Visual acuity: High - detail seen

Colour perception: Provided

Overall function: Vision in bright light. Colour vision. Allows detail to be seen.