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A2 Biology > Topic 6: Organisms respond to changes in their internal and external environments > Flashcards

Topic 6: Organisms respond to changes in their internal and external environments Flashcards

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1
Q

3.6.1.1 Survival and response

Define a stimulus.

A
  • a detectable change in the environment, detected by receptors.
  • Organisms can increase chance of survival by responding to a stimuli i.e. taxis and kinesis
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2
Q

3.6.1.1 Survival and response

Define taxes.

A
  • movement of an organism in response to a stimuli.
  • towards stimulus = + taxes
  • away stimulus = - taxes.
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3
Q

3.6.1.1 Survival and response

Define kinesis.

with an example.

A
  • change in speed of movement or rate of turning.
  • i.e woodlouse must be in damp conditions to prevent excess water loss, rate of turning increases in dry conditions.
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4
Q

3.6.1.1 Survival and response

What are the advantges of taxes and kinesis?

A
  • Maintain a mobile organism in a favourable environment.
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5
Q

3.6.1.1 Survival and response

What are plant growth factors and where are they produced?

A
  • Chemicals that regulate plant growth response to directional stimuli that are produced in plant growing regions.
  • diffuse from cell to cell.
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6
Q

3.6.1.1 Survival and response

What do plants respond to?

A
  1. Light : shoots grow towards light (+PT), roots grow away from light (-PT).
  2. Gravity : Roots are (+ gravitropic)
  3. Water : Plants grow towards water (+ hydroptropic)
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7
Q

3.6.1.1 Survival and response

What is a type of growth factor?

A
  • IAA, type of auxin.
  • Move around via diffusion or active transport.
  • IAA makes cell walls become soft and stretchy OR short and hard.
  • shoots = cell elongation
  • roots = cell inhibitation.
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8
Q

3.6.1.1 Survival and response

Explain why shoots show positive phototropism.

A
  1. Shoots produce IAA which is transported down (diffusion) to the shaded side of the shoot tip.
  2. High concentration of IAA in shaded side of shoot.
  3. IAA causes cells on shaded part to elongate more + faster due to higher turgor pressure
  4. Shoot bends towards light = + PT
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9
Q

3.6.1.1 Survival and response

Describe how roots show negative phototropism.

A
  1. High concentration of IAA inhibits cell elongation.
  2. Cells elongate more on the shaded side.
  3. Roots bend away from light = - PT
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10
Q

3.6.1.1 Survival and response

Describe how roots respond to gravitropism.

A
  • Cells in the tip of the root produce IAA.
  • Transported along root on all sides.
  • IAA increases on the lower side of the root due to gravity.
  • IAA inhibits cell elongation, cells on this side elongate less.
  • Root bends downwards = + gravitropism.
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11
Q

3.6.1.1 Survival and response

Describe how shoots respond to gravitropism.

A
  • Cells in the tip of the shoot produce IAA.
  • Transported along shoot on all side.
  • IAA increases on the lower side of the shoot due to gravity.
  • IAA promotes cell elongation, cells on this side elongate more.
  • Shoots grow upwards = - gravitropism.
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12
Q

3.6.1.1 Survival and response

What is a reflex arc?

A
  • A rapid, involuntary, short-lived response to a stimulus
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13
Q

3.6.1.1 Survival and response

Outline what happens in a 3-neurone simple reflex arc.

A

Receptor detects stimuli -> sensory neurone-> coordinator -> motor neurone -> effector -> response.

Sam = stimuli
Raced = receptor
Susie = sensory neurone
Cause =Coordinator
Mike = Motor neurone
Eats = effector
Rats = response

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14
Q

3.6.1.1 Survival and response

What neurones are involved in the reflex arc?

A

Motor, sensory and relay neurones

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15
Q

3.6.1.1 Survival and response

What is the role of a sensory neurone?

A
  • To transmit nerve impulses from sensory receptors to the central nervous system
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16
Q

3.6.1.1 Survival and response

What is the role of a relay neurone?

A
  • To transmit impulses between other neurones
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17
Q

3.6.1.1 Survival and response

What is the role of a motor neurone?

A
  • To transmit nerve impulses from the central nervous system to an effector.
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18
Q

3.6.1.1 Survival and response

RP 10 Outline the method for the movement of an animal using either a choice chamber or maze.

Required practical 10: Investigation into the effect of an environmental variable on the movement of an animal using either a choice chamber or maze

A

Choice chamber:
1. Secure nylon fabric between lid and base to create surface for inverterbrates to move over.
2. Secure the lid.
3. Use teaspoon to add 12 invertebrates into central hole lid of each choice chamber.
4. Leave them for 5 mins to adjust.
5. Remove lid and count n.o of invertebrates in each chamber.

TOP TIP: take a picture before the invertebrates move.

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19
Q

3.6.1.1 Survival and response

What is the aim of RP 10?

Required practical 10: Investigation into the effect of an environmental variable on the movement of an animal using either a choice chamber or maze

A
  • Investigstion into the response of invertebrates (woodlouse) to light/dark and humid/dry conditions in a choice chamber.
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20
Q

3.6.1.1 Survival and response

What is the hypothesis of RP10 ?

Required practical 10: Investigation into the effect of an environmental variable on the movement of an animal using either a choice chamber or maze

A

Most invertebrates will move into the chamber which is dark and humid.

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21
Q

3.6.1.1 Survival and response

Outline why the following are needed in the experiment:
1. silica beads
2. filter paper and water
3. black paper and cellotape.

Required practical 10: Investigation into the effect of an environmental variable on the movement of an animal using either a choice chamber or maze

A
  1. creates a dry chamber } absorbs mositure in air.
  2. Creates a damp/humid chamber.
  3. Creates a dark chamber.
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22
Q

3.6.1.1 Survival and response

Outline a conclusion for this practical.

Required practical 10: Investigation into the effect of an environmental variable on the movement of an animal using either a choice chamber or maze.

A

The woodlice prefer dark/damp environments } greater number of woodlice to be in side of chamber with damp paper. In unfavourable environements they move quickly + change directions often, stop moving once they reach dark/damp area.

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23
Q

3.6.1.2 Receptors

What features are common to all sensory receptors and what is used as an example of a receptor to illustrate that?

A
  • Respond to specific stimuli
  • stimulation of a receptors lead to the establishment of a generator potential.
  • Pacinian corpuscle.
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24
Q

3.6.1.2 Receptors

Describe the basic structure of a pacinian corpuscle.

A
  • Has a single sensory neurone wrapped with connective tissue (lamellae) sepearated by gel.
  • stretched-mediated Na+ channels on plasma membrane.
  • capillary runs along base layer of tissue.
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25
Q

3.6.1.2 Receptors

What stimulus does a pacinian corpuscle respond to? How?

A
  • Stimuli = pressure
  • Pressure deforms membrane, causing stretched mediated Na+ ion channels to open.
  • If influx of Na+ ions raises membrane to threshold potential, generator potetial is produced.
  • Action potential moves along the sensory neurone.
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26
Q

3.6.1.2 Receptors

Name two types of photoreceptor cell located in the retina.

A
  • Cone cells
  • Rod cells
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27
Q

3.6.1.2 Receptors

Where are the cone and rod cells located?

A

CONE
mainly in the central fovea where it can receive high light intensity.
ROD
evenly distrubted around the periphery NOT in fovea.

BLIND SPOT
No photoreceptors located here (no cone or rod cells).
No light is detected here.

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28
Q

3.6.1.2 Receptors

Compare and contrast cone and rod cells.

A

CONE
pigment: Iodopsin = red, green, blue
visual acuity / reason: High = each cone cell synapses with 1 bipolar neurone = no retinal convergence.
colour sensitivity: Tricolour = red, green, blue wavelengths are absorbed by different types of iodopsin.
density in fovea: High
density out of fovea: Low
light intensity: High
light sensitivity: less sensitive = not involved in night vision.

ROD
pigment: Rhodopson = black, white
visual acuity / reason: low = many rod cells synapse with 1 bipolar neurone.
colour sensitivity: Monochromatic = black, white, all wavelengths of light detected.
density in fovea: Low
density out of fovea: High
light intensity: Low
light sensitivity: Very sensitive = spatial summuation of subthreshold impulses.

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29
Q

3.6.1.3 Control of heart rate

Define myogenic.

A
  • Contraction of heart is initiated within the muscle itself rather than by nerve impulses.
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30
Q

3.6.1.2 Receptors

Outline a pathway of light from a photoreceptor to the brain.

A
  • Photoreceptor -> bipolar neurone -> ganglion cell of optic nerve -> brain.
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31
Q

3.6.1.3 Control of heart rate

State the name and location of the two nodes which are involved in heart contraction.

A
  1. Sinoatrial node (SAN): within the wall of the right atrium
  2. Atriventricular node (AVN): near lower end of right atrium in the wall that seperates the 2 atria.
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32
Q

3.6.1.3 Control of heart rate

Outline the role of SAN.

A
  • acts as a pacemaker by transmitting waves of electrical activity along the walls of the atria at regular intervals.
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33
Q

3.6.1.3 Control of heart rate

Describe how heartbeats are intiated and coordinated.

A
  • SAN initates waves of depolarisation (WOD).
  • WOD spreads across atria and atrial systole.
  • Layer of fibrous, non-conducting tissue delays impulses while ventricles fill and valves close. Creates a delay to ensure the atria are empty before the ventricles begin to contract.
  • AVN carries WOD down septum via Bundle of His, which branches into purkinje fibres along ventricles.
  • Causes ventricles to contract from apex upwards.
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34
Q

3.6.1.3 Control of heart rate

What is the role of the Bundle of His?

A
  • a collection of conducting tissue that transmits the electrical activity to the apex (bottom) of the heart and around the ventricle walls along fibres called the Purkyne fibres.
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35
Q

3.6.1.3 Control of heart rate

What is the role of AVN?

A
  • Waves of electrical activity cannot pass from the atria to the ventricles due to a collection of non-conducting tissue.
  • Delay is created to ensure atria is empty before ventricles contract.
  • Electrical activity pass through the AVN to the bundle of His.
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36
Q

3.6.1.3 Control of heart rate

Outline the role and location of chemoreceptors.

A

ROLE
* sensitive in changes in CO2 concentration.
* If CO2 is high, heart rate increases.

LOCATION
* found in aortic body = wall of aorta
* found in carotid body = wall of the carotid artery in the neck.

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37
Q

3.6.1.3 Control of heart rate

Outline the role and location of baroreceptors.

A

ROLE
* sensitive to changes in blood pressure.
* If blood pressure increases, heart rate decreases.

LOCATION
* found in walls of various arteries but mainly in carotid sinus (in wall of carotid artery.)

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38
Q

3.6.1.3 Control of heart rate

What is the autonomic nervous system?

A
  • System that controls involuntary actions of muscles and glands
  • Consists of: sympathetic and parasympathetic
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39
Q

3.6.1.3 Control of heart rate

State the difference between sympathetic and parasympathetic.

A

SYMPATHETIC:
* involved in flight or fight response = stimulates effectors to speed up activity.

PARASYMPATHETIC:
* involved in normal resting conditions = inhibits effectors to slow down activity.

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40
Q

3.6.1.3 Control of heart rate

Name the receptors and their location and how they are involved in changing heart rate.

A

CHEMORECEPTORS
* detect changes in pH e.g. increase concentration in CO2
* Carotid and aortic body.

BARORECEPTORS
* detect changes in blood pressure.
* Carotid body.

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41
Q

3.6.1.3 Control of heart rate

How does the body respond to an increase in blood pressure?

A

BARORECEPTORS
* baroreceptors send more impulses from the medulla oblongata to the SAN via parasympathetic nervous system
* acetylcholine is released (neurotransmitter)
* heart rate slows down = blood pressure decreases.

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42
Q

3.6.1.3 Control of heart rate

How does the body respond to a decrease in blood pressure ?

A

BARORECEPTORS
* baroreceptors send more impulses from medulla oblongata to SAN via sympathetic nervous system
* noradrenaline is released (neurotransmitter)
* Heart rate increases = blood pressure increases.

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43
Q

3.6.1.3 Control of heart rate

How does the body respond to an increase in CO2 concentration (low O2) ?

A

CHEMORECEPTORS
* Chemoreceptors detect pH decrease and send more impulses from the medulla oblongata to the SAN via sympathetic nervous system
* Noradrenaline is released
* Heart rate rises and O2, rate of blood flow to lungs increases = CO2 level decrease.

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44
Q

3.6.1.3 Control of heart rate

How does the body respond to a decrease in CO2 concentration (high O2)?

A

CHEMORECEPTORS
* chemoreceptor sends more impulses from the medulla oblongata to the SAN via a parasympathetic nervous system
* Acetylcholine is released (neurotransmitter)
* Heart rate slows down and O2 levels decrease = CO2 levels increase.

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45
Q

3.6.1.3 Control of heart rate

Medulla obolongata:

A
  • when stimulated baro and chemoreceptors send a signal to a part of the brain called medulla oblongata.
  • Part of the medulla oblongata that modifies heart rate is cardiovascular centre

CARDIOVASCULAR CENTRE has two regions:
1. Cardio-inhibitory centre
2. Cardio-acceleratory centre

  • Nerve impulses sent from theses centres via the autonomic nervous system to SAN.
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46
Q

3.6.1.3 Control of heart rate

State the formula for cardiac output.

A
  • Cardiac output = stroke volume x heart rate
    CO = V x R
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47
Q

3.6.1.3 Control of heart rate

What is cardiac output?

A
  • term used to describe the volume of blood that is pumped by the heart (the left and right ventricle) per unit of time
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48
Q

3.6.1.3 Control of heart rate

What is stroke volume?

A
  • volume of blood pumped out of the left ventricle during one cardiac cycle.
  • cm3
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49
Q

3.6.1.3 Control of heart rate

What is heart rate?

A
  • number of times a heart beats per minute
    This can also be described as the number of cardiac cycles per minute
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50
Q

3.6.1.3 Control of heart rate

WORKED EXAMPLE It took a woman 1 second to complete a single cardiac cycle. Their stroke volume was measured at 73cm3. Calculate their cardiac output, give your answer in dm3.

A

Step 1: Find the heart rate

1 cardiac cycle (atrial systole, ventricular systole and diastole) takes 1 second

To find the number of cardiac cycles completed in a minute, multiply by 60

60 x 1 = 60 bpm

Step 2: Insert relevant figures into the equation

Cardiac output = heart rate x stroke volume

Cardiac output = 60 x 73 = 4,380 cm3

CO = 4.38 dm3

1dm3 = 1000cm3

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51
Q

3.6.2.1 Nerve impulses

Describe the structure of a myelinated motor neurone.

6 structures.

A
  1. CELL BODY: contains usual cell organelles (nucleus, mitrochondria) and large amounts of R.E.R Produces proteins and neurotransmitters.
  2. DENDRONS: extension of cell body which divides into dendrites. Carry nerve impulses towards cell body.
  3. AXON: single fibre carrying nerve impulses away from cell body. Can be myelinated.
  4. SCHWANN CELLS: surround axon for electrical insulation & protection. Wrap around axon many times so layers of their membrane build up around it.
  5. MYELIN SHEATH: made from myelin-rich membranes of schwann cells.
  6. NODES OF RANVIER: short gaps between schwann cells that are next to each other when there is no myelin sheath.
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52
Q

3.6.2.1 Nerve impulses

Name 3 processes schwann cells are involved in.

A
  1. electrical insulation.
  2. phagocytosis.
  3. nerve regeneration.
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53
Q

3.6.2.1 Nerve impulses

How is a resting potential established?

A
  1. Sodium-potassium pumps move Na+ ions outof the axon = electrochemical gradient is created = more Na+ ions outside and the membrane is not permeable to Na+ ions.
  2. Sodium-potassium pumps actively transports K+ ions in the axon.

3.BUT K+ ions move out of the axon via FD due to potassium ion channels being opened and Na+ ion channels are closed.

  1. Outside of membrane is positively charged due to the imbalance of positive charged ions.
  2. 3Na+ ions = pumped out of axon.
    2K+ ions = pumped in axon.

PROCESS REQUIRES ATP - active transport.

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54
Q

3.6.2.1 Nerve impulses

At what value is resting potential established?

A
  • -65mV.
55
Q

3.6.2.1 Nerve impulses

What is resting potential?

A
  • Potential difference (voltage) across neurone membrane when not stimulated (usually -70mV)
  • Outside membrane = + charged.
  • Inside membrane = - charged.
56
Q

3.6.2.1 Nerve impulses

What is the all or nothing principle?

A
  • Any stimulus that causes the membrane to reach the threshold potential (-55mV) will generate an action potential.
  • NO THRESHOLD (-55mV) REACHED = NO AP
  • Small stimulus = less frequent AP
  • Bigger stimulus = more frequent AP.
57
Q

3.6.2.1 Nerve impulses

Name the stages in generating an action potential.

A
  1. Stimulus
  2. Depolarisation
  3. Repolarisation
  4. Hyperpolarisation
  5. Resting potential.

Silly Donkeys R Hyper Rarely

58
Q

3.6.2.1 Nerve impulses

How is an action potential generated?

A
  1. STIMULUS:
    * neurone membrane is exicted causing the Na+ ion channels to open.
    * The membrane is more permeable to Na+.
    * Na+ ions diffuse into neurone down the electrochemical gradient.
    * The membrane inside the neurone is less negative.
  2. DEPOLARISATION:
    * Potential difference reaches threshold (-55mV) more Na+ ion channels will open allowing a rapid influx of Na+ ions in the neurone.
    * Significant influx of Na+ ions reverses P.D to +40mV.
  3. REPOLARISATION:
    * P.D of +40mV causes Na+ voltage gated channels to be closed
    * K+ voltage gated channels to be opened.
    * membrane more permeable to K+ ions.
    * K+ ions diffuse out of neurone down K+ ion concentration gradient.
    * Membrane begin back to resting potential.
  4. HYPERPOLARISATION:
    * K+ ion channels too slow to close.
    * “overshoot” - too many K+ ions diffuse out of neurone.
    * PD become more negative than the RP (-70mV)
  5. RESTING POTENTIAL:
    * Ions channels reset
    * Na+-K+ pump returns membrane to RP.
    * membrane is maintained until stimulation excites the membrane again.
59
Q

3.6.2.1 Nerve impulses

Explain the importance of the resting / refractory period.

A
  • No AP can be generated in hyperpolarisation section in the membrane.
  • ion channels are recovering -> can’t be opened.
  • Ensures unidirectional impulses.
  • Ensures discrete impulses.
  • Limits frequency of impulses transmission.
60
Q

3.6.2.1 Nerve impulses

Explain the passage of an action potential along an unmyelinated axon.

A
  1. RESTING POTENTIAL
    * concentration of Na+ ions is higher outside than inside the membrane.
    * concentration of K+ ions is higher inside that outside the membrane.
    * Axon membrane is polarised = overall conc. of + ions is greater outside making it positive.
  2. STIMULUS:
    * causes sudden influx of Na+ ions hence a reversal of charge on axon membrane = AP = now depolarised
  3. LOCALISED ELECTRICAL CURRENT:
    * established by influx of Na+ ions = Na+ voltage gated channels open along axon = influx of Na+ ions = depolarisation.
    * Na+ voltage gated channels close, K+ voltage gated channels open.
    * K+ ions leave axon along ECG
  4. DEPOLARISATION MOVES ALONG MEMBRANE:
    * outward movement of K+ ions continue = membrane behind AP returns back to its orginal charged state = repolaristion.
  5. REPOLARISATION:
    * allows Na+ ions to be actively transported out , returns to the axon to resting potential waiting for a stimuli.
61
Q

3.6.2.1 Nerve impulses

Explain the passage of an action potential along a myelinated axon.

A
  • Fatty sheath of myelin around axon acts an electrical insulator = prevents AP from forming,
  • AP can only occur at the node of ranvier
  • Localised circuits arrise between adjacent nodes of ranvier = AP jump from node to node via saltortary conduction.
  • AP pass along myelinated neurone faster than along an unmyelinated neurone.
62
Q

3.6.2.1 Nerve impulses

What are the factors that affect the speed of conductance?

A
  1. Myelination.
  2. Saltatory conduction.
  3. Axon diameter.
  4. Temperature
63
Q

3.6.2.1 Nerve impulses

How does myelination affect the speed of conductance?

A

MYELINATED:
* myelin sheath = electrical insulator.
* Depolarisation occurs at the nodes of ranvier only
* impulses jump between the gaps in the myelin sheath (node to node) = saltatory conduction.
} more faster than generation of AP at each point of axon.

64
Q

3.6.2.1 Nerve impulses

State the name that is given to the type of condution used to pass action potentials along a myelinated axon.

A
  • Saltatory conduction.
65
Q

3.6.2.1 Nerve impulses

How does diameter of the axon affect the speed on conductance?

A

BIG DIAMETER:
* AP are conducted quicker along axons.
* Less resistance to flow of ions.
* Depolarisation reaches other parts of neurone quicker.

66
Q

3.6.2.1 Nerve impulses

Explain how temperature affects the speed of conductance.

A

INCREASE IN TEMPERATURE:
* Increases the speed of conductance.
* Ions diffuse faster only up to 40^c - denature above 40^c/
* affect rate of respiration.

67
Q

3.6.2.1 Nerve impulses

What is the appropiate units when calculating the maximum frequency of impulse conduction given the refactory period of a neurone?

A
  • Hz
68
Q

3.6.2.2 Synaptic transmission

What is the structure of a synapse?

A
  1. Transmits information not impulses from one neurone to another by neurotransmitters.
  2. Neurones sepearated by a gap called synaptic cleft.
  3. Neurone that releases neurotransmitters (acetylcholine) = presynaptic neurone
  4. Axon the neurone is swollen = synaptic knob = contains many mitrochondria and large amount of endoplasmic reticulum = required for the making of neurotransmitter (acetylcholine) .
  5. Synaptic vesicle: where neurotransmitters (acetylcholine) are stored.
  6. Once NT (acetylcholine) is released from vesicles diffuses across to the postsynaptic neurone = specific receptor proteins on its membrane to recieve it.
69
Q

3.6.2.2 Synaptic transmission

Explain how the presynaptic neurone is adapted for the manufacture of the neurotransmitter.

A
  • contains many mitrochondria and large amounts of endoplasmic reticulum.
70
Q

3.6.2.2 Synaptic transmission

Explain how the postsynaptic neurone is adapted to recieve the neurotransmitter.

A
  • contains specific receptor proteins / molecules on its membrane for the neurotransmitter.
71
Q

3.6.2.2 Synaptic transmission

If a neuron is stimulated in the middle of its axon, an action potential will pass both ways along it to the synapses at each end of the neurone. However, the action potential will only pass across the synapse at one end. Explain why.

A

only one end can produce neurotransmitter and so this end alone can create a new action potential in the neurone on the opposite side of the synapse. At the other end there is no neurotransmitter than can be released to pass across the synapse and so no new action potential can be set up.

72
Q

3.6.2.2 Synaptic transmission

Outline a sequence of steps involed in the transmission across a cholinergic synpase.

A
  1. AP arrives at the end of the neurone, voltage-gated calcium ion channels open.
  2. Ca2+ ions diffuse into the synaptic knob causing vesicles to fuse with the presynaptic membrane
  3. Vesicles release neurotransmitter called acetylcholine into synaptic cleft.
  4. Binds to cholingeric receptors on postsynaptic membrane
  5. Na+ ion channels open in postsynaptic neurone results in Na+ ion entering, may generate an AP.
  6. Acetylchloinesterase (AChE) break down acetylcholine in synaptic cleft and products absorbed by presynaptic neurone to make more ACh.
73
Q

3.6.2.2 Synaptic transmission

Explain why the synaptic transmission is unidirectional.

A
  • Synapses can only pass information in one direction from pre to post synaptic neurone.
  • Only presynaptic neurones contain vesicles of NT
  • Only postsynaptic neurones contain specific receptors (proteins) on its membrane.
74
Q

3.6.2.2 Synaptic transmission

Define summation and name the two types.

A
  • low frequency action potentials lead to the release of insufficient conc of NT to trigger a new action potential in the postsynaptic neurone
  • Temporal summation
  • Spatial summation.
75
Q

3.6.2.2 Synaptic transmission

What is spatial summation?

A
  • A number of different presynaptic neurones release enough NT to exceed the threshold value of the postsynaptic neurone together.
  • Together they trigger a new AP.
76
Q

3.6.2.2 Synaptic transmission

What is temporal summation?

A
  • A single presynaptic neurone releases NT many times over a short period of time.
  • If conc of NT exceeds threshold value of the postsynaptic neurone, AP is generated.
77
Q

3.6.2.2 Synaptic transmission

Explain the importance of acetylcholinestrase.

A
  • prevents overstimulation of skeletal muscle cells.
  • Enables acetyl and choline to be recycled
78
Q

3.6.2.2 Synaptic transmission

What is an inhibitory synapse?

A
  • A synpase that makes it less likely that a new AP is generated on the postsynaptic neurone
79
Q

3.6.2.2 Synaptic transmission

How does an inhibitory synapse work?

A
  1. PRESYNAPTIC NEURONE: releases NT that binds to chloride ion protein channels on the postsynaptic neurone
  2. NT causes chloride ion protein channels to be open
  3. Chloride ions move into the postsynaptic neurone via FD.
  4. Binding of NT causes K+ protein channels to be opened.
  5. K+ ions move out of the postsynaptic neurone into the synapse
  6. Outside of postsynaptic neurone = more positive
    Inside of postsynaptic neurone = more negative.
    K+ ions moving out at the same time Cl- ions move in.
  7. Membrane potential increases to -80mV from -65mV at resting potential.
    } HYPERPOLARISATION = makes it less likely new AP will be generated as a large influx of Na+ ions needed to produce one
80
Q

3.6.2.2 Synaptic transmission

Describe the structure of the neuromuscular junction.

A
  • Synaptic cleft between the presynaptic neurone and the skeletal muscle cell.
81
Q

Outline a sequence of steps involved in the transmission across a neuromuscular junction.

A
  1. AP arrives at the end of neurone, voltage-gated Ca2+ ion channels open.
  2. Ca2+ ions diffuse into the synaptic knob = synaptic vesicles to fuse with presynaptic membrane.
  3. Vesicles release NT (acetylcholine) into synaptic cleft which binds to nicotinic cholinergic receptors on postsynaptic membrane.
  4. ACh = excitatory always triggers respone in muscle cells.
  5. Large n.o of Na+ ions diffuse into effector whilst small amount of K+ move into synaptic cleft.
  6. Acetylcholineestrase stored in clefts, breaks down ACh, products absorbed by presynaptic neurone to make more ACh.
82
Q

3.6.2.2 Synaptic transmission

Contrast a cholingeric synapse and a neuromuscular junction.

A

POSTSYNTAPTIC CELL
C = another neurone
NMJ = skeletal muscle cell

AChE location
C = synaptic cleft.
NMJ = Postsynaptic membrane

ACTION POTENTIAL
C = new AP produced.
NMJ = end of neural pathway.

RESPONSE
C = excitatory or inhibitory.
NMJ = always excitatory.

NEURONS INVOLVED
C = motor, sensory, and relay
NMJ = only motor.

83
Q

3.6.2.2 Synaptic transmission

What is an excitatory neurotransmitter?

A
  • They depolarise the postsynaptic membrane, making it fire an AP if threshold is reached.
  • i.e. ACh = excitatory NT at cholinergic synapses in the CNS and at NMJ
84
Q

3.6.2.2 Synaptic transmission

What is an inhibitatory neurotransmitter?

A
  • They hyperpolarise the postsynaptic membrane (makes the PD more negative), prevents it from firing an AP.
  • I.e. ACh = inhibitatory NT at cholinergic synpases in the heart.
85
Q

3.6.2.2 Synaptic transmission

How might drugs affect the synaptic transmission?

A
  1. Same shape.
  2. Block receptors.
  3. Inhibit enzyme.
  4. Stimulation of NT.
  5. Inhibit release of NT.
86
Q

3.6.2.2 Synaptic transmission

What is the effect of drugs being the same shape as neurotransmitters?

A
  • Mimic their action at receptors = drugs are called agonists
  • more receptors are activated.
  • i.e. nicotine mimics ACh so binds to nicotinic cholinergic receptors in brain.
87
Q

3.6.2.2 Synaptic transmission

What is the effect of drugs blocking the receptors?

A
  • Receptors can’t be activated by the NT.
  • Fewer receptors are activated.
  • These drugs are called antagonists
  • i.e Curare blocks the effects of ACh by blocking nicotinic cholernigic receptors at NMJ, so muscle cells cannot be stimulated. = muscle paralysed.
88
Q

3.6.2.2 Synaptic transmission

What is the effect of drugs inhibiting the enzyme that breaks down NT?

A
  • more NT left in the synaptic cleft left to bind to receptors hence are there for longer.
  • i.e. nerve gases stop ACh from being broken down in synaptic cleft = loss of muscle control.
89
Q

3.6.2.2 Synaptic transmission

What is the effect of drugs stimulating the release of NT in presynaptic neurone?

A
  • more receptors are activated.
  • i.e. amphetamines
90
Q

3.6.2.2 Synaptic transmission

What is the effect of some drugs inhibiting the release of NT from the presynaptic neurone?

A
  • fewer receptors are activated.
  • i.e. alcohol.
91
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Name the 3 types of muscles in the body and where they are located.

A
  1. cardiac: found only in the heart. Under involuntary (subconscious) control.
    * Contract rhymatically without fatigue.
  2. smooth muscle: found in the walls of the blood vessels and gut.
    Under involuntary (subconscious) control.
    * slow contraction without fatigue.
  3. skeletal muscle: attached to incomprehensible skeleton by tendons.
    * Under voluntary (conscious) control.
    * The quicker they contract the faster they fatigue
92
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

What does the phrase “antagonistic pair of muscles” mean?

A
  • pairs of muscles that act together to move bones around a joint.
  • pair pull in opposite directions : agonist contract muscle, antagonist relax muscle
93
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Describe the gross structure of skeletal muscle

A
  • muscle cells fused together to form bundles of parallel muslce fibres (myofibrils) = share nuceli and cytoplasm (sacroplasm)
  • Within sacroplasm large concentration of mitrochondira and ER.
  • Arrangement ensures no point of weakness between cells.
  • Each bundle surrounded by endomycium: loose connective tissue with many capillaries.
94
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Describe the microscopic structure of skeletal muscle.

HINT Myofibriils and its 2 proteins and the 3 S’s

A
  • Each muscle fibre made up of myofibrils.
  • Myofibrils (site of contraction) made up of 2 proteins:
  • Actin: thinner and consists of two strands twisted around one another.
  • Myosin: thicker and consists of long rod-shaped tail with bulbous heads that project to side.
  • Myosin + Actin = Sarcomere.
  • Sacroplasm: shared nuclei and cytoplasm with lots of mitrochondria and ER.
  • Sacrolemma: fold inwards towards sacroplasm to form T tubules.
    Many myofibrils = muscle fibres = surrounded by a membrane called sacrolemma.
95
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Outline the ultrastructure of myofibrils.

A
  • Z line= boundary between sarcomeres. Z-Z line is one sacromere.
  • I band = contains only actin. Decreases during muscle contraction. The band is light. There is no overlap of actin and myosin.
  • A band = contains actin and myosin except in H-zone.
    Thick filament = myosin
    Thin filament = actin.
  • H band = only contains myosin (no overlap of actin and myosin)
    Decreases during contraction of muscle.
  • M-line = marks the middle of the myosin filaments.
96
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Why is there high numbers of mitrochondria in the sarcoplasm?

A
  • ATP is essential for muscle contraction.
97
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

How does each band appear under the microscope?

A
  • I band = light
  • A band = dark
98
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

What theory describes how muscle contraction occurs?

A
  • Sliding filament theory.
99
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

How is muscle contraction stimulated?

A
  • Action potential reaches many NMJ causing voltage-gated Ca2+ channels to open.
  • Ca2+ ions diffuse into synaptic knob.
  • Ca2+ ions cause synaptic vesicles to fuse with presynaptic membrane.
  • Acetylcholine is released into the synaptic cleft.
  • Acetylcholine diffuses across the synaptic cleft and binds with the receptors on Na+ protein channels on muscle cell membrane.
  • Influx of Na+ = depolaristation.
100
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Explain the role of Ca2+ ions in muscle contraction.

A
  • Action potential moves into T tubules and into the sarcoplasm.
  • Tubules are in contact with ER of muscle (sarcoplasmic reticulum) which actively transports Ca2+ ions from cytoplasm of muscle = low conc. of Ca2+ ions in muscles.
  • Ca2+ ion protein channels open in sarcoplasmic reticulum and Ca2+ ions diffuse into muscle of cytoplasm down a conc. gradient.
  • Ca2+ ions attach to protein and causes tropomyosin that were blocking the binding sites on actin filament to move and uncover binding sites.
  • Allows actin-myosin bridges to form.
101
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Describe the sliding filament theory.

A
  1. Ca2+ ions enter & attaches with a protein. This causes the tropomyosin molecule that were blocking the binding sites on the actin filament to uncover the binding sites.
  2. ADP attaches to myosin head and can bind to actin filament to form actin-myosin bridges
  3. Myosin heads change shape = causes tension. Actin filament moves along and ADP is released.
  4. ATP attaches to myosin head, changes shape of myosin = detaches from actin.
  5. Ca2+ ions activate ATPase hydrolyses ATP -> ADP + Pi. This provides energy for myosin head to return to orignal position.
  6. Myosin head reattaches to binding site further along actin filament and cycle is repeated.
102
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Why is ATP an important molecule for muscle contraction?

A
  • Active muscles require high conc. of ATP to fully contract.
  • In times when aerboic respiration cannot create enough ATP, muscles respire anaerobically i.e. sprinters need high amount of ATP rapidly and they don’t need it for long, muscles respire anaerobically.
  • Chemical that assists anaerobic respiration is phosphocreatine = stored in muscles. Provides phosphates to regenerate ATP from ADP.
  • Phosphocreatine is “refilled” using inorganic phosphate from ATP when muscle is relaxed.
103
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

Outline evidence for sliding filament theory.

A
  • If SFT is correct then there will be more overlap of actin and myosin in a contracted muscle
  • When muscle contracts: sacromere changes:
    1. I band = more narrower.
    2. H band = more narrower.
    3. Z line = move close together / sacromere shortens.

A band remains the same width = proves myosin filament do not shorten.

104
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

State the structure, location and general properties of slow-twitch fibres.

A

SLOW-TWITCH FIBRES

S:
1. large store of myoglobin = high affinity for O2 than haemoglobin at lower partial pressures.
2. Many mitrochondria = aerobic respiration produces more ATP.
3. Surrounded by many blood vessels = high supply of O2 and glucose.
4. Glycogen store = many ends can be hydrolysed to release glucose for respiration.

L:
site of sustained contraction i.e. calf muscles.

GP:
1. Contract / respire aerobically for longer durations due to rich blood supply to prevent build up of lactic acid.
2. Contract for slower durations
3. Large store of myoglobin = high affinity for O2 at lower partial pressures.
4. Adapted for endurance work like marathons.

105
Q

3.6.3 Skeletal muscles stimulated to contract by nerves…

State the structure, location and general properties of fast-twitch fibres.

A

FAST-TWITCH FIBRES:

S:
1. Thicker and more myosin filaments.
2. Large store of phosphocreatine to help make ATP from ADP.
3. High concentration of enzymes involved in anaerobic respiration.
4. Extensive sarcoplasmic / endoplasmic reticulum for rapid uptake and release of Ca2+ ions.

L:
* Sites of short-term, rapid contractions = biceps.

GP:
1. Contracts faster = provides short burst of powerful contraction.
2. High concentration of glycogen
3. Short period of time
4. Adapted to intense exercise.

106
Q

3.6.4 Homeostasis is the maintenance of a stable

What is homeostasis?

A
  • The maintainence of internal environment within restricted limits in an organisms.
107
Q

3.6.4 Homeostasis is the maintenance of a stable

What does homeostasis ensure?

W

A
  • Cells of the body are in an environment that meets their requirements and allows them to function normally desptie external changes
108
Q

3.6.4 Homeostasis is the maintenance of a stable

State the importance of homesostasis.

A
  1. Enzymes that control biochemical reactions within cells and other proteins (i.e channel proteins) are sensitive to changes in pH and temperature. Any changes to these factors reduces rate of reaction of enzymes or may denature them.
  2. Changes to water potential of blood and tissue fluids may cause cells to shrink and expand water may leave or enter via osmosis. Both cases cells cannot operate normally.
    Maintentance of constant blood glucose concentration essential in ensuring constant water potential. Constant blood glucose concentration ensures reliable source of glucose = respiration in cells.
  3. Organisms with ability to maintain constant internal environment are more independent of changes in the external environment. May have a wider geographical range = greater chance of finding food, shelter.
109
Q

3.6.4 Homeostasis is the maintenance of a stable

Why is it important that core temperatures remains stable?

A
  • Maintain stable rate of enzyme-controlled reactions and prevent damage to membranes.
  • Temp. too low = Enzymes & substrate molecules have less kinetic energy.
  • Temp. too high = enzymes dentature
110
Q

3.6.4 Homeostasis is the maintenance of a stable

Why is it important that blood pH remains stable?

A
  • Maintain stable rate of enzyme-controlled reactions and optimum conditions for other proteins.
  • Acidic pH = H+ ions interact with H bonds and ionic bonds in tertiary structure of enzymes. Shape of active site changes so no enzyme-substrate complexes are formed
111
Q

3.6.4 Homeostasis is the maintenance of a stable

Why is it important that blood glucose concentration remains stable?

A
  • Maintain constant blood water potential ; prevents osmotic lysis = occurs when a cell bursts due to osmotic imbalance that causes excess water to diffuse into the cell.
  • Maintains constant concentration of respirtatory substrates = organism maintain constant level of activity regardless of enviromental conditions.
112
Q

3.6.4 Homeostasis is the maintenance of a stable

Define negative feedback.

A
  • When any deviation from the normal values are restored to their original level (optimum level) and prevents any overshoot.
  • involves nervous system and hormones too.
113
Q

3.6.4 Homeostasis is the maintenance of a stable

Define positive feedback.

A
  • Occurs when a deviation from an optimum causes changes that result in even greater deviation from the normal one.
  • EXAMPLE: in the neurones a stimulus causes an influx of Na+ ions. Influx increases permeability of neurone membrane to Na+ ions, more ions will enter = further increase in permeability. Small stimulus can bring a large and rapid response
114
Q

3.6.4 Homeostasis is the maintenance of a stable

Give an example of how negative feedback can occur when you’ve digested something.

A
  1. Blood glucose concentration increases beyond set limit due to ingestion of food and drink that contains carbohydrates, negative feedback will occur to bring the BGC back to the normal limit. (can be because of opposite way round)
115
Q

3.6.4 Homeostasis is the maintenance of a stable

Suggest why negative feedback mechanisms control fluctuations in different directions.

A
  • Provides more control, especially in cases of “overcorrection” = lead to deviation in opposite direction from the orignal one.
116
Q

3.6.4 Homeostasis is the maintenance of a stable

Why is the importance of having seperate negative feedback mechanisms that control departures in different directions from the original state?

A
  • Gives a greater degree of homeostatic control.
117
Q

3.6.4 Homeostasis is the maintenance of a stable

What are the factors that affect blood glucose concentration?

A
  1. Amount of carbs digested from the diet.
  2. Rate of glycogenolysis.
  3. Rate of gluconeogenisis.
118
Q

3.6.4 Homeostasis is the maintenance of a stable

Define glycogenesis.

(genesis means to make)

A
  • The process of excess glucose being converted to glycogen when blood glucose is higher than normal.
  • Occurs mainly in liver.
119
Q

3.6.4 Homeostasis is the maintenance of a stable

Define glycogenolysis.

(lysis means to breakdown)

A
  • Hydrolysis of glycogen back into glucose in the liver.
  • Occurs when blood glucose levels are lower than normal.
120
Q

3.6.4 Homeostasis is the maintenance of a stable

Define gluconeogenesis.

(amino acids to glucose.)

A
  • Process of creating glucose from non-carbohydrate stores in the liver.
  • Occurs if all glycogen has been hydrolysed into glucose and your body is still in need of glucose.
121
Q

3.6.4 Homeostasis is the maintenance of a stable

Outline the role of insulin when blood glucose levels increase.

A
  1. BGL have increased.
  2. Detected by beta cells (endocrine cells) in the islets of Langerhans (in the pancreas).
  3. Beta cells release insulin into bloodstream.
  4. Insulin decreases BGL in following ways:
    * attaches to the receptors on the surfaces on the target cells. This changes the tertiary structure of channel proteins = more glucose being absorbed via FD.
    * More protein carriers incorporated into CSM so more glucose is absorbed from the blood and into cells.
    * Activates enzymes in conversion of glucose to glycogen. = glycogenesis in the liver
122
Q

3.6.4 Homeostasis is the maintenance of a stable

Outline the role of glucagon when blood glucose levels decrease.

A
  1. BGL have decreased.
  2. Detected by alpha cells (endocrine cells) in Islets of Langerhans (in the pancreas).
  3. Alpha cells secrete glucagon into bloodstream.
  4. Glucagon increases BGL in the following ways:
    * Glucagon binds to the complementary receptors on the surfaces of the target cells (liver cells).
    * When glucagon binds it causes protein to be activated into adenylate cyclase and convert ATP to Cyclic AMP (cAMP) by removing 2 phosphate groups.
    * cAMP activates enzyme protein kinase that hydrolyses glycogen into glucose –> GLYCOGENOLYSIS
    * Activating enzymes involve the conversion of glycerol and amino acids into glucose.

Bullet points are the second messenger model.

123
Q

3.6.4 Homeostasis is the maintenance of a stable

What is the first messenger in the second messenger model?

A
  • Glucagon.
124
Q

3.6.4 Homeostasis is the maintenance of a stable

What is the second messenger in the second messenger model?

A
  • Cyclic AMP or cAMP.
125
Q

3.6.4 Homeostasis is the maintenance of a stable

Why is cAMP the second messenger?

A
  • cAMP activates the enzyme = protein kinase to hydrolyse glycogen into glucose.
126
Q

3.6.4 Homeostasis is the maintenance of a stable

Outline the role of adrenaline when blood glucose levels decrease.

A
  1. BGL have decreased.
  2. Adrenal glands secrete adrenaline.
  3. Adrenaline increases the BGL in the following ways:
    * Adrenaline attaches to the complementary receptors on the surfaces of the target cells. This causes a protein (G protein) to be activated and converts ATP into cAMP.
    * cAMP activates enzyme (protein kinase) that hydrolyses glycogen into glucose. (glycogenolysis)

Also second messenger model as process results in the formation of cAMP, which acts as second messenger.

127
Q

3.6.4 Homeostasis is the maintenance of a stable

Explain how type 1 diabetes are caused and how it can be treated.

A

CAUSE:
* body cannot produce insulin.
* starts in childhood and could be due to autoimmune disease where beta cells are attacked of Islets of Langerhans.

TREATMENT:
* Insulin injections.
* Insulin pump. } HYPOGLYCAEMIA must be monitored.
* Eating regularly and controlling simple carbohydrate intake prevents sudden rise in glucose.

128
Q

3.6.4 Homeostasis is the maintenance of a stable

Explain how type 2 diabetes are caused and how it can be treated.

A

CAUSE:
* Receptors on target cells lose their responsiveness to insulin.
* Glucose stays inside the blood increasing the concentration.
* develops later in life because of obesity, poor diet, kidney failure, visual impairment.

TREATMENT:
* Eating balanced diet = control intake of carbs.
* Exercise regularly.
* Glucose lowering medications can be taken if not under control.
* Insulin injections may be taken if not enough insulin is produced.

129
Q

3.6.4 Homeostasis is the maintenance of a stable

What is the concentration of glucose in urine?

A
  • very low.
  • between 0.0mM - 0.8mM
  • anything higher indicates possible prescence of diabetes.
130
Q

3.6.4 Homeostasis is the maintenance of a stable

Outline how colorimetry can be used to identify the glucose concentration in a sample.

A
  1. Take the stock of glucose solution and perform a serial dilution.
  2. Carry out benedicts test on diluted solutions. (place in water bath for 5 minuites)
  3. Use colorimeter to create calibration curve (absorbance reading on red-coloured light.)
  4. Carry out benedicts test on all three urines. (place in water bath for 5 minuites.)
  5. Use colorimeter and find an absorbance reading for each urine sample.
  6. Check glucose concentration for each urine sample using the calibration curve.

REMEMBER when placing the samples inside the cuvettes and then in the colorimeter to measure the absorbance to place a cuvette filled with distilled water first to reset colorimeter to 0.

High concentration of glucose = less blue = less red light is absorbed.
Low concentration of glucose = more blue = more red light is absorbed.

131
Q

3.6.4 Homeostasis is the maintenance of a stable

Define osmoregulation.

A
  • control of blood water potential via homeostatic mechanisms.
132
Q

3.6.4 Homeostasis is the maintenance of a stable

What is hypertonic in blood water potential? (give examples)
State the corrective mechanism.

A

HYPERTONIC:
* Blood with too low water potential = too much water will leave cells and move into blood via osmosis. Cells will shrivel. Not enough water = cannot dissolve solutes in cells.

EXAMPLES:
* too much sweating = hot day
* not drinking enough water.
* Lots of ions in diets = lots of salts.

CORRECTIVE MECHANISM:
* More water is reabsorbed by osmosis into blood from tubules of the nephrons.
* Urine is more concentrated.
* Less water is lost in urine.

133
Q

3.6.4 Homeostasis is the maintenance of a stable

What is hypotonic in blood water potential? (give examples.)
State the corrective mechanism.

A

HYPOTONIC:
* Blood with too high water potential.
* Too much water will move from the blood into the cells by osmosis. Cells will burst.

EXAMPLES:
* Drinking too much water.
* Not enough salt in diet.

CORRECTIVE MECHANISM:
* Less water is reabsorbed by osmosis into the blood from the tubules of the nephrons.
* Urine is more dilute
* more water is lost in urine.

A2 Biology (4 decks)

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