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A level biology > responding to changes in environment > Flashcards

responding to changes in environment Flashcards

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1
Q

explain why plants show positive phototropism

A
  • IAA diffuses to shaded side of shoot tip.
  • as IAA diffuses down shaded side, it causes active transport of H+ ions into the cell wall
  • disruption to H-bonds between cellulose molecules and action of expansions make cell more permeable to water
  • cells on shaded side elongate faster due to higher turgor pressure
  • shoot bends toward light
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2
Q

explain why roots show positive gravitropism

A
  • gravity causes IAA to accumulate on lower side of root
  • IAA inhibits elongation of root cells
  • cells on upper side of root elongate faster, so the root top bends downwards
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3
Q

define taxis and kinesis

A

taxis: directional movement in response to external stimulus

kinesis: non- directional response to presence and intensity of external stimulus

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4
Q

state the advantage of taxis and kinesis

A

maintain mobile organism in optimum order environment e.g. to prevent dessication.

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5
Q

many organisms respond to temperature and humidity via kinesis rather than taxis. why?

A

less directional stimuli; often no clear gradient from one extreme to the other

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6
Q

how could a student recognise kinesis in an organisms movement?

A
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7
Q

outline what happens in a simple reflex arc

A

receptor detects stimulus —> sensory neuron —> relay neurone in CNS coordinates response —> motor neurone —> response by effector

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8
Q

give the advantage of a simple reflex

A

rapid response to potentially dangerous stimuli since only 3 neurones involved

instinctive

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9
Q

what features are common to all sensory receptors?

A

act as energy transducers which establish a generator potential

respond to specific stimuli

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10
Q

what features are common to all sensory receptors?

A

act as energy transducers which establish a generator potential

respond to specific stimuli

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11
Q

describe the basic structure of a Pacinian corpuscle

A
  • single nerve fibre surrounded by layers of connective tissue which are separated by viscous gel and contained by a capsule
  • stretch-mediated Na+ channels on plasma membrane
  • capillary runs along base layer of tissue
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12
Q

what stimulus does a Pacinian corpuscle respond to and how

A

pressure deforms membrane, causing stretch-mediated Na+ ion channels to open.

if the influx of Na+ raises membrane to threshold potential, a generator potential is produced.

action potential moves along sensory neuron.

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13
Q

name the two types of receptor cell found in the retina

A

cone cells

rod cells

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14
Q

where are rod and cone cells located in the retina?

A

Rod: evenly distributed around periphery but not central fovea

cone: mainly central fovea no photoreceptors at blind spot

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15
Q

compare and contrast rod and cone cells

A

pigment
ROD - rhodopsin

CONE- iodopsin

visual acuity
ROD - many rod cells synapse with one bipolar neuron (low resolution)

CONE - one cone cell synapses with one bipolar neuron (high resolution)

colour sensitivity
ROD- monochromatic: all wavelengths of light detected

CONE - tricolour: red, blue, green wavelengths absorbed by different types of iodopsin

light sensitivity
ROD- very senstitive: spacial summation of subthreashold impulses

CONE- less sensitive: not involved in night vision

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16
Q

outline the pathway of light from a photoreceptor to the brain

A

photoreceptor —> bipolar neurone —> ganglion cell of optic nerve —> brain

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17
Q

define myogenic

A

contraction of the heart is initiated within the muscle itself rather than by nerve impulses

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18
Q

state the name and location of the two nodes involved in heart contraction

A

Sinoatrial node (SAN): within the wall of the right atrium

Atrioventricular node (AVN): near lower end of right atrium in the wall that separates the two atria.

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19
Q

describe how heartbeats are initiated and coordinated

A
  • SAN initiates a wave of depolarisation across both atria
  • layer of fibrous, non-conducting tissue delays impulse (prevents it directly going to ventricles) while ventricles fill and valves close.
  • impulses travel to AVN, down septum via bundle of His, which carries impulses to the Purkinje fibres.
  • Purkinje fibres carry impulse from bottom of heart up both ventricles simultaneously, ventricles contract.
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20
Q

state the formula for cardiac output

A

cardiac output = stroke volume x heart rate

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21
Q

what is the autonomic nervous system?

A

system that controls involuntary actions of glands and muscles
2 subdivisions: sympathetic and parasympathetic

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22
Q

state the difference between sympathetic and parasympathetic nervous system

A

sympathetic involved in ‘fight or flight’ response. stimulates effectors to speed up activity

parasympathetic involved in ‘rest and digest’ response - normal resting conditions. inhibits effectors to slow down activity

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23
Q

name the receptors involved in changing heart rate and state their location

A

**baroreceptors: **detect changes in blood pressure, Carotid artery

chemoreceptors: detect changes in PH, e.g. due to an increase of CO2 conc), Carotid artery and aortic body

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24
Q

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

A
  • Baroreceptors send more impulses to cardio-inhibitory centre in the medulla Oblongata
  • more impulses to SAN via parasympathetic nervous system.
  • stimulates release of acetylcholine, which decreases heart rate
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25
Q

how does the body respond to decrease in blood pressure?

A
  • Baroreceptors send more impulses to cardioacceleratory centre in medulla oblongata
  • more impulses to SAN via sympathetic nervous system
  • stimulates release of noradrenaline, which increases heart rate and strength of contraction
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26
Q

how does the body respond to an increase in CO2 concentration?

A
  • Chemoreceptors detect PH decrease and send more impulses to cardioacceleratory centre of medulla oblongata
  • more impulses to SAN via sympathetic nervous system
  • heart rate increases, so rate of blood flow to lungs increases, so rate of gas exchange increases and ventilation rate increases.
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27
Q

describe the general structure of a motor neurone

A

cell body- contains organelles and high proportion of RER

dendrons - branch into dentrites which carry impulses toward cell body

axon- long, unbranched fibre carries nerve impulses away from cell body

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28
Q

describe the additional features of a myelinated motor neuron

A

**Schwann cells: **wrap around axon many times

**myelin sheath: **made from myelin-rich membranes of Schwann cells.

nodes of ranvier: very short gaps between neighbouring Schwann cells where there is no myelin sheath.

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29
Q

name 3 processes Schwann cells are involved in

A

electrical insulation

phagocytosis

nerve regeneration

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30
Q

how does an axon potential pass along an unmyelinated neuron?

A
  • stimulus leads to an influx of Na+ ions. first section of membrane depolarises
  • local electrical current cause sodium voltage-gated channels further along the membrane to open
  • the section behind begins to repolarise
  • sequential wave of depolarisation
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31
Q

explain why myelinated axons conduct impulses faster than unmyelinated axons

A

saltatory conduction: impulse ‘jumps’ from one node of ranvier to another. Depolarisation cannot occur where myelin sheath acts as electrical insulator.

so impulse doesn’t travel along entire axon length.

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32
Q

what is resting potential?

A

the voltage across neuron membrane when not stimulated: -70 mV

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33
Q

how is resting potential established?

A
  • membrane is more permeable to K+ than Na+
  • sodium-potassium pump actively transports 3Na+ out of cell and 2K+ into cell
  • establishes electrochemical gradient: cell contents more negative than extracellular environment
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34
Q

name the stages in generating an action potential

A
  1. depolarisation
  2. Repolarisation
  3. Hyperpolarisation
  4. return to resting potential
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35
Q

what happens during an action potential?

A
  • a stimulus excites the neurone
  • This causes voltage-gated Na+ ion channels to open on the axon
  • Na+ moves in my f.diff
  • this causes the inside of the neurone to become less negatively charged
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36
Q

what happens during depolarisation?

A

a stimulus causes the facilitated diffusion of Na+ ions into cell down electrochemical gradient.

potential difference across the membrane becomes more positive

if the membrane reaches the threshold potential (-50mV), voltage gated Na+ ion channels open.

significant influx of Na+ ions reverses potential difference to +40mV.

37
Q

what happens during repolaristation?

A

voltage gated Na+ ion channels close and voltage -gated K+ ion channels open.

Facilitated diffusion of K+ ions out of cell down their electrochemical gradient.

the potential difference across the membrane (the neurone) becomes more negative

38
Q

what happens during hyperpolarisation?

A

an ‘overshoot’ - when K+ ions diffuse out and the p.d becomes more negative than the resting potential.

39
Q

what happens during the refractory period in hyperpolarisation?

A

no stimulus is large enough to raise the membrane potential to threshold.

voltage-gated K+ channels close and the sodium-potassium pump re-establishes resting potential.

40
Q

explain the importance of the refractory period

A

no action potentials can be generated in hyperpolarised sections of membrane

this ensures:
- a unidirectional impulse
- discrete impulses
- limits frequency of impulse transmission.

41
Q

what is the ‘all or nothing’ principle?

A

any stimulus that causes the membrane to reach threshold potential will generate an action potential.

All action potentials have the same magnitude. (larger stimulus won’t result in larger action potential)

42
Q

name the factors that affect the speed of conductance

A
  • myelin sheath
  • axon diameter
  • temperature
43
Q

how does axon diameter affect the speed of conductance?

A

greater diameter = faster

less resistance to flow of ions (depolarisation and repolarisation)

less ‘leakage’ of ions (easier to maintain membrane potential)

44
Q

how does temperature affect the speed of conductance?

A

higher temp = faster

faster rate of diffusion (depolarisation and repolarisation)

faster rate of respiration (enzyme-controlled) = more ATP for active transport to re-establish resting potential

but temp too high- membrane proteins denature

45
Q

how can you detect the strength of a stimulus?

A

larger stimulus raises membrane to the threshold more quickly after hyperpolarisation due to greater frequency of impulses.

46
Q

what is the function of synapses?

A

electrical impulse cannot travel over junction between neurones

neurotransmitters send impulses between neurones/from neurones to effectors

new impulses can be initiated in several different neurones for multiple simultaneous responses

47
Q

describe the structure of a synapse

A

presynaptic neurone ends in synaptic knob: contains lots of mitochondria, ER and vesicles of neurotransmitter.

synaptic cleft: gap between neurones.

post synaptic neurone: has complementary receptors to
neurotransmitter.

48
Q

describe the sequence of events involved in transmission across a synapse

A

wave of depolarisation travels down presynaptic neurone, causing Ca+ channels to open and calcium ions entering.

This causes the synaptic vesicles to move towards the presynaptic membrane and release acetylcholine neurotransmitter (via exocytosis) which diffuses across synaptic cleft.

acetylcholine neurotransmitter attaches to receptors in postsynaptic membrane

sodium ions enter leading to depolarisation.

49
Q

explain why synaptic transmission is unidirectional

A

only presynaptic neurone contains vesicles of neurotransmitter and only postsynaptic membrane has complementary receptor.

therefore impulse always travels presynaptic —> postsynaptic

50
Q

define summation and name the two types

A

neurotransmitter from several sub-threshold impulses accumulates to generate action potential:

-temporal summation
-spacial summation

51
Q

what is the difference between temporal and spacial summation?

A

temporal: one presynaptic neuron releases neurotransmitter several times in quick succession

spacial: multiple presynaptic neurones release neurotransmitter

52
Q

what are Cholinergic synapses?

A

use acetylcholine as primary neurotransmitter.
Excitatory/ inhibitory.

located at:
- motor end plate (muscle contraction)
-preganglionic neurones (excitation)
- parasympathetic neurones (inhibition
e.g. of heart rate/ breathing rate)

53
Q

what happens to acetylcholine from the synaptic cleft?

A
  • hydrolysis into acetyl and choline by acetylcholinesterase (AChE)
  • acetyl and choline diffuse back into the presynaptic neurone
  • ATP is used to reform acetylcholine for storage in vesicles
54
Q

explain the importance of AChE

A

prevents overstimulation of skeletal muscle cells

enables acetyl and choline to be recycled

55
Q

what happens in an inhibitory synapse?

A

neurotransmitter binds to and opens Cl- channels on postsynaptic membrane and triggers K+ channels to open.

Cl- moves in and K+ moves out via facilitated diffusion.

p.d. becomes more negative (hyperpolarisation)

56
Q

describe the structure of a neuromuscular junction

A

synaptic cleft between a presynaptic neuron and a skeletal muscle cell

57
Q

contrast a cholinergic synapse and a neuromuscular junction

A

response
cholinergic: Excitatory or inhibitory
nmj:always excitatory

neurones involved
cholinergic:motor, sensory or relay
nmj:only motor

postsynaptic cell
Cholinergic:another neuron
nmJ:skeletal muscle cell

AChE location
cholinergic: synaptic cleft
nmj: postsynaptic membrane

Action potential
cholinergic: new action potential produced
nmj: end of neural pathway

58
Q

how might drugs increase synaptic transmission?

A
  • inhibit AChE
  • Mimic shape of neurotransmitter
59
Q

how might drugs decrease synaptic transmission?

A
  • inhibit release of neurotransmitter
  • decrease permeability of postsynaptic membrane to
    ions
  • hyperpolarise postsynaptic membrane
60
Q

name the three types of muscle in the body and where they are located

A

cardiac: exclusively found in heart

smooth: walls of blood vessels and intestines

skeletal: attached to incompressible skeleton by tendons

61
Q

what does the phrase ‘antagonistic pair of muscles’ mean?

A

pairs of muscles pull in opposite directions to move bones around joints

as one contracts (agonist), the other relaxes (the antagonist)

62
Q

describe the gross structure of skeletal muscles

A

muscle cells are fused together to form bundles of parallel muscle fibres (myofibrils)

each bundle is surrounded by endomycium: loose connective tissue with many capillaries

63
Q

describe the microscopic structure of skeletal muscles

A

myofibrils: site of contraction

sarcoplasm: shared nuclei and cytoplasm with lots of mitochondria and ER.

sarcolemma: folds inwards towards sarcoplasm to form transverse (T) tubules.

T tubules are conductive and help carry electrical impulses throughout the sarcoplasm.

64
Q

describe the ultrastructure of a myofibril

A

Z-line: boundary between sarcomeres

I-band: only actin

A-band: both myosin and actin

H-zone: only myosin

65
Q

how does each band appear under an
optical microscope?

A

I band: light
A band: dark

66
Q

How is muscle contraction stimulated?

A

Neuromuscular junction - wave of depolarisation leading to Ca+ channels to open and Ca+ to move in

causes vesicles to move towards and fuse with presynaptic membrane.
exocytosis of acetylcholine, which diffuses across synaptic cleft.

Acetylcholine binds to receptors on Na+ channel proteins on skeletal muscle cell membrane.

influx of Na+ = depolarisation.

67
Q

explain the role of Ca+ ions in muscle contraction

A

AP moves through T-tubules in the sarcoplasm = Ca2+ channels in sarcoplasmic reticulum open.

Ca2+ binds to troponin, causing a change in the shape of the troponin molecule.

the troponin pulls on tropomyosin which releases it from the action myosin binding site.

the myosin head is now free to bind to the actin-myosin binding site (forming actin-myosin cross bridge.

68
Q

outline the sliding filament theory

A

Myosin head with ADP attached forms cross bridge with actin.

during the power stroke, the myosin head changes shape and loses the ADP, pulling actin over myosin.

ATP attaches to myosin head, causing it to detach from actin.

ATP is hydrolysed into ADP and pi so that the myosin head can return to original position.

myosin attaches to actin further along the filament.

69
Q

how does sliding filament action cause a myofibril to shorten?

A

Myosin heads flex in opposite directions, so actin filaments are pulled towards each other.

Distance between adjacent sarcomere z lines shortens

70
Q

state 4 pieces of evidence that prove the sliding filament theory

A

H-zone narrows

I-band narrows

Z-lines get closer (sarcomere shortens)

A-zone remains the same width (proves that myosin filaments don’t shorten)

71
Q

what happens during muscle relaxation?

A

Ca2+ is actively transported back into ER

Tropomyosin once again blocks actin binding site

72
Q

explain the role of phosphocreatine in muscle contraction

A

it phosphorylates ADP directly to ATP when oxygen for aerobic respiration is limited (e.g. during vigorous exercise)

73
Q

where are slow and fast twitch muscle fibres found in the body?

A

slow - sites of sustained contraction, e.g. calf muscles.

fast - sites of short-term, rapid, powerful contractions, e.g. biceps

74
Q

explain the role of slow twitch and fast twitch muscle fibres

A

slow twitch- long-duration contraction; well adapted to aerobic respiration to prevent lactate buildup.

fast twitch- powerful, short-term contraction; well adapted to anaerobic respiration.

75
Q

explain the structure and properties of slow twitch muscle fibres

A

glycogen store: many terminal ends can be hydrolysed to release glucose for respiration

contain lots of myoglobin: higher affinity for oxygen than haemoglobin at lower partial pressures.

many mitochondria: aerobic respiration produces more ATP

surrounded by many blood vessels: high supply of oxygen and glucose.

76
Q

explain the structure and properties of fast- twitch muscle fibres

A

large store of photocreatine

more myosin filaments that are thicker

high conc of enzymes involved in anaerobic respiration

fewer blood vessels, mitochondria and myoglobin

77
Q

contrast slow-twitch and fast-twitch muscle fibres

A

slow twitch is darker in colour as it has higher concentrations of myoglobin fast twitch is lighter in colour as it contains less myoglobin and contains lots of glycogen which can be broken down to release ATP (need a lot as anaerobic resp produces little ATP)

slow-twitch - contract slowly, slow to fatigue, used for endurance, e.g. long distance running.
fast-twitch - contract quickly, fatigue quickly, used for short bursts of speed and powder, e.g. sprinting.

slow twitch - energy is released slowly from aerobic respiration
fast twitch - energy is released quickly through anaerobic respiration

slow twitch - lots of mitochondria to provide ATP and lots of blood vessels to reduce diffusion pathway for O2 and CO2.
fast twitch - few mitochondria and blood vessels

78
Q

what is homeostasis?

A

internal environment is maintained within set limits around an optimum.

79
Q

why is it important that core temperature remains stable?

A

maintain stable rate of enzyme-controlled reactions and prevent damage to membranes

temperature too low- enzyme and substrate molecules have insufficient kinetic energy.

temperature too high - enzymes denature.

80
Q

why is it important that blood PH remains stable?

A

maintain stable rate of enzyme-controlled reactions.

Acidic PH - H+ ions interact with H-bonds and ionic bonds in tertiary structure of enzyme which leads to the shape of the actin site changing, so no ES complexes.

81
Q

why is it important that blood glucose concentration remains stable?

A

maintain constant blood water potential: prevents osmotic lysis/ crenation of cells

maintain constant concentration of respiratory substrate: organisms maintains constant level of activity regardless of environmental conditions.

82
Q

define negative and positive feedback

A

negative feedback- self-regulatory mechanisms return internal environment to optimum when there is a fluctuation.

positive feedback - a fluctuation triggers changes that result in an even greater deviation from the normal level.

83
Q

outline the general stages involved in negative feedback

A

receptors detect deviation —> coordinator —> corrective mechanism by effector —> receptors detect that conditions have returns to normal.

84
Q

suggest why separate negative feedback mechanisms control fluctuations in different directions

A

provides more control, especially in case of ‘over correction’ which could lead to a deviation in the opposite direction from the original one.

85
Q

suggest why coordinators analyse several inputs from several receptors before sending an impulse to effectors

A

receptors may send conflicting information

optimum response may require multiple types of effector

86
Q

name the factors that affect blood glucose concentration

A

amount of carbohydrate digested

rate of glycogenolysis

rate of gluconeogenesis

87
Q

define glycogenesis

A

liver converts glucose into the storage polymer glycogen.

88
Q

define glycogenolysis

A

liver hydrolyses glycogen into glucose which can diffuse into blood

89
Q

define Gluconeogenesis

A

liver converts glycerol and amino acids into glucose.

A level biology (7 decks)

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