A2 Biology Unit 5

Front 1

What is taxis?

Back 1

Directional movement in response to a stimulus

Front 2

What is kinesis

Back 2

Non-directional movement in response to a stimulus.
Increase in number of turns to escape poor environment.

Front 3

What and how is passed on in nervous communication?

Back 3

Electrical impulses along neurones.

Front 4

Describe pathway of nervous communication

Back 4

Stimulus > Receptors > Sensory Neurone > Relay Neurone in central nervous system > Motor Neurone > Effectors > Response

Front 5

Why do we have reflexes?

Back 5

To prevent harm to the body.

Front 6

What is a reflex?

Back 6

A rapid involuntary response to a stimulus.

Front 7

Nervous system vs hormonal system
What carried to where?
Speed of response?
Spread of effect?
Lasting of effect?

Back 7

Nervous- electrical impulses carried by neurones, fast, localised and short lived.

Hormonal- hormones carried in blood, slow, widespread and long lasting.

Front 8

2 types of cell that act as effectors?

Back 8

Muscle cells
Cells in glands

Front 9

What is role of receptor?

Back 9

To detect stimuli.

Front 10

Explain why nervous control is localised and short lived

Back 10

Neurotransmitters are secreted directly onto cells.

Front 11

What is a chemical mediator?

Back 11

Chemical messenger that acts locally.
Secreted from cells all over body.
Target cells are right next to where chemical mediators are produced.
Only have small distance so quick response.

Front 12

What is histamine and how does it work?

Back 12

Chemical mediator. Increases permeability of capillaries nearby to allow more immune system cells to move to infected area.

Front 13

What is prostaglandin and how does it work?

Back 13

Chemical mediator. Involved in inflammation, fever, blood pressure regulation and clotting.

Front 14

Why do chemical mediators only provide a local response?

Back 14

Secreted from

Front 15

Why do chemical mediators produce a faster response than hormones?

Back 15

Short distance to travel so quicker response.

Front 16

What triggers release of histamine?

Back 16

Injury or infection.

Front 17

What are two types of chemical mediator?
How do they work?

Back 17

Prostaglandins and histamine.
Prostaglandins involved in inflammation, fever, BP regulation and clotting.
Histamine increases permeability of cells to WBCS so more immune system cells can arrive.

Front 18

1cm to __mm to __µm to __nm

Back 18

1cm = 10mm = 10,000µm = 10,000,000nm

Front 19

Magnification=

Back 19

Image size/Actual size

Front 20

Rod cells
Location
Black and white/colour
How many rods to neurones
Sensitivity to light
Visual acuity? Why?

Back 20

Peripheral area of retina
Black and white
Many rods to one neurone
High sensitivity to light
Low visual acuity- many rods to one neurone so light from two objects cannot be told apart.

Front 21

Cone cells
Location
Black and white/colour
How many cones to neurones
Sensitivity to light
Visual acuity? Why?

Back 21

Fovea
Colour
1 rod to neurone
Low light sensitivity
Good visual acuity- 1 cone to 1 neurone so can tell close light sources apart

Front 22

How is generator potential produced?

Back 22

Stimulus detected, cell membrane becomes more permeable, more ions enter. PD changes and gen potential produced.

Front 23

What type of stimulus does Pacinian corpuscle respond to?

Back 23

Mechanical. Pressure.

Front 24

Structure of Pacinian Corpuscle?

Back 24

End of a sensory neurone. Wrapped in connective tissue called lamellae.

Front 25

Explain how stimulus triggers AP in Pacinian Corpuscle?

Back 25

Stimulated and lamallae are deformed and press on nerve ending. This causes stretch mediated sodium channels to stretch and open Na+ ions diffuse into cell and cause generator potential. If reaches threshold- AP will fire

Front 26

Rods/cones which give better visual acuity? Why?

Back 26

Cones have 1 cone to 1 neurone.
Can tell different light sources as 2 different points

Front 27

4 differences between Rods and Cones?

Back 27

Visual acuity
Rods at edge, cones at fovea.
Rods black and white, cones in colour.
Rods more light sensitive.
Many rods to one neurone. 1 cone to 1 neurone.

Front 28

Two proteins involved in establishing resting potential.

Back 28

Sodium potassium pumps.
Potassium ion channels.

Front 29

Ratio of AT of sodium potassium pumps?

Back 29

3 sodium out 2 potassium in

Front 30

What is diffused out of membrane when establishing resting potential?

Back 30

Potassium ions down conc. gradient

Front 31

Which side of membrane is more positive?

Back 31

Outside

Front 32

What 3 factors effect speed of AP conduction?
Explain how

Back 32

Myelination- allows charge to jump between Nodes very quickly.
Axon diameter- wider diameter, less resistance
Temperature- higher temp quicker diffusion, although too high and proteins denature

Front 33

Explain process of AP

Back 33

Stimulus causes sodium ions to open and sodium diffuse into the neurone making inside less negative.
Depolarisation- if reaches threshold then more sodium ion channels open +ve feedback.
Repolarisation- Na+ close and K+ open causing them to diffuse back out.
Hyper polarisation- K+ channels are too slow to close and there is an overshoot of ion movement
Resting potential- ion channels reset.

Front 34

What is refractory period?
Why important?

Back 34

After AP neurone can't trigger AP again because ion channels are recovering.
Acts as time delay and stops overlapping APs. Makes sure unidirectional

Front 35

What are waves of depolarisation?

Back 35

When AP happens some ions diffuse sideways. this causes nearby ion channels to open and causes a wave of depolarisation.

Front 36

Explain the all or nothing principle

Back 36

once threshold is reached an AP will always fire with same change in voltage, no matter stimulus size.

Front 37

What does bigger stimulus cause in terms of AP

Back 37

more frequent APs to be fired

Front 38

After AP why can't cell cause another AP?
What effects does this have?

Back 38

Refractory period.
Makes separate impulses and causes unidirectionality

Front 39

How is conduction along a myelinated neurone different to non myelinated neurone.

Back 39

Faster

Front 40

Give 3 factors that affect speed of AP conduction?

Back 40

Diameter of axon
Temperature
Myelination

Front 41

Draw a synapse

Back 41

Neurone- synaptic knob, pre/postsynaptic knob, synaptic cleft, recepors, vesicles with neurotransmitter in.

Front 42

Draw a cholinergic synapse

Back 42

Neurone- synaptic knob, pre/postsynaptic knob, synaptic cleft, recepors, vesicles with ACh in.

Front 43

Summarise how a nerve impulse is transmitted

Back 43

AP arrives and causes Ca2+ ions to open.
These diffuse into synaptic knob.
Influx of Ca2+ causes synaptic vesicles to fuse with presynaptic membrane and ACh is released into the cleft.
ACh diffuses across and is picked up by receptors.
The leftover ACh is either broken down by enzymes or resorbed by presynaptic membrane.

Front 44

What is a neuromuscular junction?
Special features

Back 44

It is a specialised cholinergic synapse between motor neurone and a muscle cell.
More receptors. Always triggers response in muscle cell.
Forms clefts which hold ACh

Front 45

What are two types of summation?

Back 45

Spatial and temporal

Front 46

Describe temporal summation

Back 46

Where 2 impulses arrive in quick succession from the same presynaptic neurone. This increases the likelihood of threshold being reached.

Front 47

Describe spatial summation

Back 47

where 2/more presynaptic neurones release their neurotransmitters to the same postsynaptic neurone. The small amount combines to reach threshold level.

Front 48

3 types of cell with receptors for neurotransmitters

Back 48

Neurone, muscle, gland

Front 49

Describe the movement of Ca2+ ions following the arrival of an action potential at a cholinergic synapse?

Back 49

AP stimulates voltage gated Ca2+ ion channels in the presynaptic neurone to open so Ca2+ ions diffuse into the synaptic knob.

Front 50

Explain how ACh leaves the presynaptic neurone and causes an AP in the postsynaptic neurone.

Back 50

Influx of Ca2+ causes vesicles to fuse with presynaptic membrane the ACh diffuses across the membrane into the receptor on the postsynaptic neurone. If threshold is reached the influx in postsynaptic causes an AP on the postsynaptic membrane.

Front 51

What is a neuromuscular junction?

Back 51

A synapse between a motor neurone and a muscle.

Front 52

3 muscle types

Back 52

Smooth
Cardiac
Skeletal

Front 53

What is the A band?

Back 53

Anisotrophic- length of the myosin
A is dark. A.

Front 54

What is the I band?

Back 54

Isotrophic- the non myosin section of muscle.
I for light I.

Front 55

Whats M line?

Back 55

The middle line

Front 56

Whats Z line?

Back 56

Z line is the end lines?

Front 57

What is the H zone?

Back 57

the Myosin section with no actin crossed over.

Front 58

Describe the process of a muscle contraction.
1st stage.

Back 58

1) Arrival of AP- AP arrives from motor neurone which depolarises the sarcolemma. Depolarisation spreads down the T tubules to sarcoplasmic reticulum. This causes Ca2+ ion release. Ca2+ ions bind to troponin causing it to change shape. This pulls tropomyosin off the binding site.

Front 59

Describe the process of a muscle contraction.
2nd stage.

Back 59

Movement of the actin filament.
Ca2+ ions also activate the ATPase to break down ATP to provide the energy for power stroke.

Front 60

Describe the process of a muscle contraction.
3rd stage.

Back 60

Breaking of the cross bridge
ATP also provides the energy to break the cross bridge. The myosin head then detaches and reattaches to a new binding site.

Front 61

Describe the process of a muscle contraction.
4th stage.

Back 61

Return to resting state
When the muscle is unstimulated Ca2+ ions leave their binding sites on the troponin molecules and care moved by AT into the sarcoplasmic reticulum. The troponin molecules return to original places so the tropomyosin reblocks the binding site.

Front 62

3 ways that ATP can be produced

Back 62

Aerobic respiration
Anaerobic respiration
ATP phosphocreatine system

Front 63

How does Phosphocreatine produce ATP

Back 63

ADP+PCr-->ATP+Cr

Front 64

Explain slow twitch muscle fibres?
Explain their adaptions?

Back 64

Contract slowly and work for long time without tiring.
Energy released by aerobic respiration.
Adaptions: Lots of mitochondria, lots of blood vessels, rich source of myoglobin (stores oxygen).

Front 65

Explain fast twitch muscle fibres?
Explain their adaptions?

Back 65

Short bursts of power.
Energy released by anaerobic resiration using glycogen. PCr stores to generate ATP.

Front 66

Describe A band

Back 66

Dark, presence of thick myosin.

Front 67

Name 2 proteins found between actin filaments that help myofilaments slide past each other.

Back 67

Troponin and tropomyosin

Front 68

Explain how Ca2+ ions in sarcoplasm allow formation of cross bridges.

Back 68

Ca2+ bind to troponin causing it to change shape and pull tropomyosin away and expose binding site allowing myosin head to attach

Front 69

Describe role of ATP in muscle contraction.

Back 69

Broken down to provide energy to break cross bridges.
Provides energy for the power stroke.

Front 70

Describe how ATP is generated from PCr.

Back 70

ADP+PCr--->ATP+Cr

Front 71

Give 1 advantage and 1 disadvantage of ATP generation from PCr.

Back 71

Quick generation of ATP.
Used in short bursts.
Doesnt require oxygen or produce lactate.

Runs out v quickly

Front 72

Give 3 ways of generating ATP

Back 72

Anaerobic/aerobic respiration. Phosphocreatine-ATP system.

Front 73

Give 3 ways slow twitch muscle fibres are adapted

Back 73

Lots of mitochondria
Lots of blood vessels
Lots of myoglobin

Front 74

Give 1 way fast twitch muscle fibres are adapted

Back 74

Stores of phosphcreatine