A2 animal and plant behaviours, nerves (topic 6)

Question 1

taxis def

Answer 1

directional response to a stimulus eg moving toward +ve or away from -ve

Question 2

kinesis def

Answer 2

non-directional response to a stimulus, changing speed an organism moves or the rate it changes direction

Question 3

what are plant growth factors

Answer 3

plant responses to external stimuli (hormone like substances) eg IAA

Question 4

what does IAA do in the shoot

Answer 4

causes plant cell elongation

synthesised in shoot tip, asymmetric illumination detected by shoot tip causing IAA to move to the darker side
diffuses down the stem

Question 5

what does IAA do in the root

Answer 5

inhibits growth

gravity moves it to the lower side of the root tip, and it diffuses along (increased conc on lower side)
IAA inhibits cell elongation here, so other side elongates more, grows downwards

positive gravitropism = to support plant in soil, access to water, minerals

Question 6

nervous system is good because

Answer 6

it allows humans to react to surroundings and co-ordinate behaviour
the withdrawal reflex makes survival more likely => so we can reproduce and pass on alleles

Question 7

reflex arc

Answer 7

stimulus detected by receptor => impulse travels along sensory neuron to spinal cord => intermediate neuron passes impulse across spinal cord => along motor neuron to effectors => contracts => response, move away from stimulus

this is immediate, rapid, short lived, localised response

Question 8

receptors => 2 stages to sensing a stimulus

Answer 8

sensory reception (detecting change in environment)
sensory perception (brain making sense of the info from the receptors)

Question 9

how receptors work

Answer 9

(stimuli involves a change in energy)
receptors called transducers detect this and translates that message into nerve impulses that travel down sensory neurons to CNS.
the nerve impulses they create are called generator potential

Question 10

Pacinian corpuscle

Answer 10

transfers mechanical energy to a generator potential
responds to pressure
single sensory neuron at the centre of layers of tissue (lamellae) separated by a gel
sensory neuron ending has a stretch-mediated sodium channel
when pressure applied, shape deforms and these channels open, Na+ diffuses through into neurone, potential of the membrane changes and becomes depolarised => creates generator potential

Question 11

rod cells (vision, density, pigment, sensitivity, acuity)

Answer 11

• monochromatic vision, can’t distinguish wavelengths of light
• 120 million per eye so high density
• contain pigment rhodopsin
• very sensitive to light, stimulated in low light conditions
• low visual acuity, 3 rod cells shares a synapse with a bipolar neurone, so multiple rods need to be stimulated to create a generator potential

Question 12

cone cells (vision, density, pigment, sensitivity, acuity)

Answer 12

• colour vision
• 6 million per eye, lower density than rod
• contains pigment iodopsin
• not sensitive to light, require bright light to work (3 types each sensitive to a primary colour)
• good visual acuity, each cone cell has its own synapse via a bipolar neurone

Question 13

distribution of rod and cone cells

Answer 13

cone cells around fovea as that receives highest intensity of light
rod cells at peripheries of the retina at lower light intensity

Question 14

control of heart rate: myogenic, SAN, AVN, Purkyne, bundle of His

Answer 14

myogenic => contractions are initiated within the muscle itself, from a group of cells called sinoatrial node (SAN)

SAN has a basic rhythm of simulation that determines the beat of the heart, referred to as the pacemaker
how it works => a wave of electrical excitation spreads out across both atria so they contract, and there’s a layer of non-conductive tissue preventing the wave crossing to the ventricles
=> wave enters 2nd group of cells called atrioventricular node (AVN) between the atria
=> AVN after a short delay, conveys wave of electrical excitation between ventricles, along Purkyne tissue which collectively make up the bundle of His
=> bundle of His conducts wave through AV septum to base of ventricles
=> wave released from Purkyne tissue causing ventricles to contract from bottom of the heart upwards

Question 15

modifying resting heart rate

Answer 15

medulla oblongata in the brain controls changes to heart rate, it has 2 centres:
- one that increases heart rate => linked to SAN by the sympathetic nervous system
- one that decreases heart rate => linked to SAN by the parasympathetic nervous system

which one is used is determined by nerve impulses received from 2 types of receptor which respond to chemical or pressure change stimuli in the blood

Question 16

control of heart rate by chemoreceptors - process and where found

Answer 16

found in wall of carotid arteries
sensitive to pH change in blood resulting from co2 conc change (acid pH etc)

• chemoreceptors detect change and increase frequency of nervous impulses to the centre in the medulla oblongata that increases heart rate
• centre increases impulse frequency via sympathetic NS to SAN. this increases rate of electrical wave production by SAN and therefore heart rate
• increased blood flow that this causes leads to more co2 being removed by the lungs so co2 conc returns to normal
• therefore blood pH rises and chemoreceptors reduce frequency of nerve impulses to medulla oblongata, which reduces frequency of impulses to SAN, therefore reduction in heart rate

Question 17

control of heart rate by pressure receptors and where found

Answer 17

found in walls of carotid arteries

• when BP too high, pressure receptors transmit more nervous impulses to the centre that decreases heart rate in medulla oblongata. centre sends impulses via parasympathetic NS to SAN, heart rate decreases
• when BP too low, pressure receptors transit more nervous impulses to centre that increases heart rate in the medulla oblongata. centre sends impulses via sympathetic NS to SAN, heart rate increases

Question 18

resting potential def and value

Answer 18

difference in electrical charge maintained across the membrane of a neurone’s axon when not stimulated

-70mV (negatively charged in relation to the outside)

Question 19

how is the axon polarised (NaK) (resting potential)

Answer 19

Na K pump => 3 Na+ actively transported out the axon, 2 K+ actively transported into the axon

• although both ions are positive, the fact more sodium moves more creates electrochemical gradient
• K diffuses back naturally through channel proteins
• only K+ gates are open and Na+ gates are closed

Question 20

action potential def, value, how it works

Answer 20

change that occurs in electrical charge across membrane of an axon when it’s stimulated and a nerve impulse passes

+40mV

=> when a stimulus of sufficient size is detected by a receptor, its energy causes a temp reversal of charges either side of this part of the axon membrane. if stimulus is beyond the threshold, -70mv charge becomes +40mV (this part of the axon is now depolarised)
=> this occurs because channels (Na and K) in the axon membrane change shape and open or close, depending on voltage across the membrane (called voltage-gated channels)

Question 21

on a graph, direction of nerve impulse is always…

Answer 21

away from hyperpolarisation

Question 22

passage of an action potential (general)

Answer 22

the depolarisation of one part of the axon acts as a stimulus for the depolarisation of the next region of the axon

when previous part of axon goes back to rest (repolarisation)

Question 23

passage of action potential along MYELINATED axon

Answer 23

myelin = electrical insulator
so action potential can only occur along nodes of Ranvier

=> action potential jumps from node to node (saltatory conduction)

Question 24

what 3 things affect speed of nerve impulse

Answer 24

myelin sheath => in myelinated, saltatory conduction occurs which is faster than generating an action potential at every point along the axon

diameter of axon => greater the diameter the faster the conduction (larger diameter means less leakage of ions so it’s easier to maintain membrane potentials)

temperature => increased temp, ions will diffuse more rapidly, more respiration so more ATP made for faster active transport (as long as enzymes don’t denature)

Question 25

refractory period def

Answer 25

neurone membrane can’t be excited as the sodium channels are in recovery

=> means that an action potential can only pass in one direction

Question 26

synaptic transmission process

Answer 26

• action potential arrives, presynaptic membrane depolarises which causes calcium ion channels to open so Ca2+ enters presynaptic neuron by facilitated diffusion
• this causes fusion of synaptic vesicles filled with acetylcholine with presynaptic membrane
• this neurotransmitter is then released into synaptic cleft where it diffuses to postsynaptic membrane. binds to receptors on post synaptic membrane stimulating Na+ ligand gated channels to open by changing shape. Na+ diffuses into cell
• after new action potential has been made, acetylcholinesterase hydrolyses AC into choline and ethanoic acid which diffuses back across synaptic cleft into presynaptic neuron to be reassembled and reused (this uses ATP). this prevents continuous generation of an action potential in the post synaptic neuron as Na+ gates close

Question 27

features of synapses (3)

Answer 27

unidirectional => only pass info in one direction, receptors only on post synaptic neuron, neurotransmitters only made in presynaptic knob

summation => amplify effects of low frequency action potentials/make it more likely for a new action potential to be created.
spatial summation —> multiple presynaptic neurons release neurotransmitter
temporal summation —> a single presynaptic neuron releases neurotransmitter many times over a short period

inhibitory => neurotransmitter increases permeability of post synaptic neuron to K+ and Cl- ions. K+ moves out and Cl- moves in, increasing negativity (hyperpolarisation), and the membrane is moved further away from threshold value

Question 28

antagonistic muscle pairs

Answer 28

pull in opposite directions, as one contracts the other relaxes

Question 29

myofibril def

Answer 29

made from thick and thin protein filaments which overlap to give striations in appearance.
thick filaments made of myosin (has heads to attach to specific binding sites on the actin when the muscle contracts)
thin filaments made of actin (2 molecules twisted together)

Question 30

sarcolemma def

Answer 30

the cell membrane of muscle fibre cells

Question 31

2 types of muscle fibres

Answer 31

slow twitch => contract slowly and provide less powerful contractions, adapted for long exercise/endurance eg marathons. don’t fatigue quickly

fast twitch => contract intense and in short bursts. rapid release of energy in intense exercise eg sprinting.

Question 32

adaptations of slow twitch fibres

Answer 32

adapted to aerobic exercise

• large store of myoglobin
• rich supply of blood vessels to deliver o2 and glucose
• numerous mitochondria for ATP

Question 33

adaptations of fast twitch fibres

Answer 33

adapted to anaerobic respiration

• thick and numerous myosin
• high conc of glycogen
• high conc of enzymes needed for anaerobic respiration
• phosphocreatine so ATP can be rapidly generated

Question 34

comparing neuromuscular junctions and cholinergic synapses

Answer 34

NMJ => only excitatory, synapse can be both
NMJ => action potential ends here, synapse a new action potential can be generated
NMJ => acetylcholine binds to receptors on membrane of muscle fibres rather than post synaptic neuron

Question 35

sliding filament mechanism

Answer 35

I band becomes narrower

Z lines move closer together / sarcomere shortens

H zone becomes narrower

A band remains the same width (this proves the mechanism slides, otherwise A band width would change too)

Question 36

muscle contraction stage 1 : muscle stimulation

Answer 36

• action potential arrives at the end of a presynaptic neuron
• causes VG Ca2+ channels to open and Ca2+ moves into axon by diffusion
• synaptic vesicles bind to the presynaptic neuron and release neurotransmitters into cleft by exocytosis
• neurotransmitter diffuses across synaptic cleft and binds with receptor site on ligand gated Na+ channels
• Na+ channels open and Na+ diffuses into sarcoplasm causing a new action potential to be generated
• action potential travels deep into the muscle fibres (down t-tubules)
• wave of depolarisation causes VG Ca2+ channels on sarcoplasmic reticulum to open
• diffuses into sarcoplasm down conc gradient

Question 37

muscle contraction stage 2: tropomyosin, myosin, actin, Ca2+

Answer 37

• tropomyosin blocks binding sites on actin
• Ca2+ released from sarcoplasmic reticulum and changes shape of tropomyosin, exposing actin binding sites
• myosin heads bind to actin, releasing ADP
• myosin head changes conformation/angle and moves actin along (filaments slide past one another)
• ATP binds to myosin head, causing it to release the actin
• ATP hydrolysed into ADP by ATP hydrolyase. myosin head goes back to start position.
• myosin head reattaches to a binding site further along the filament.
• cycle repeats until Ca2+ or ATP runs out

Question 38

muscle contraction stage 3: relaxation

Answer 38

• VG calcium channels close
• Ca2+ is active transported through a pump back into sarcoplasmic reticulum. (against conc gradient)
• tropomyosin resumes position blocking actin binding sites

Question 39

energy supply during muscle contraction

Answer 39

• ATP regenerated from ADP during respiration of pyruvate in the mitochondria using oxygen
• in highly active muscles demand for ATP and o2 is greater than the rate blood vessels can supply o2, so they generate ATP anaerobically.
• if even anaerobic respiration can’t produce enough ATP, we use phosphocreatine. acts as a reserve of phosphate which can immediately combine with ADP to make ATP. phosphocreatine is later replenished using Pi from ATP when the muscle is relaxed.