A2 animal and plant behaviours, nerves (topic 6) Flashcards
taxis def
directional response to a stimulus eg moving toward +ve or away from -ve
kinesis def
non-directional response to a stimulus, changing speed an organism moves or the rate it changes direction
what are plant growth factors
plant responses to external stimuli (hormone like substances) eg IAA
what does IAA do in the shoot
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
what does IAA do in the root
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
nervous system is good because
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
reflex arc
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
receptors => 2 stages to sensing a stimulus
sensory reception (detecting change in environment)
sensory perception (brain making sense of the info from the receptors)
how receptors work
(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
Pacinian corpuscle
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
rod cells (vision, density, pigment, sensitivity, acuity)
- 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
cone cells (vision, density, pigment, sensitivity, acuity)
- 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
distribution of rod and cone cells
cone cells around fovea as that receives highest intensity of light
rod cells at peripheries of the retina at lower light intensity
control of heart rate: myogenic, SAN, AVN, Purkyne, bundle of His
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
modifying resting heart rate
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
control of heart rate by chemoreceptors - process and where found
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
control of heart rate by pressure receptors and where found
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
resting potential def and value
difference in electrical charge maintained across the membrane of a neurone’s axon when not stimulated
-70mV (negatively charged in relation to the outside)
how is the axon polarised (NaK) (resting potential)
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
action potential def, value, how it works
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)
on a graph, direction of nerve impulse is always…
away from hyperpolarisation
passage of an action potential (general)
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)
passage of action potential along MYELINATED axon
myelin = electrical insulator
so action potential can only occur along nodes of Ranvier
=> action potential jumps from node to node (saltatory conduction)
what 3 things affect speed of nerve impulse
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)
refractory period def
neurone membrane can’t be excited as the sodium channels are in recovery
=> means that an action potential can only pass in one direction
synaptic transmission process
- 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
features of synapses (3)
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
antagonistic muscle pairs
pull in opposite directions, as one contracts the other relaxes
myofibril def
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)
sarcolemma def
the cell membrane of muscle fibre cells
2 types of muscle fibres
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.
adaptations of slow twitch fibres
adapted to aerobic exercise
- large store of myoglobin
- rich supply of blood vessels to deliver o2 and glucose
- numerous mitochondria for ATP
adaptations of fast twitch fibres
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
comparing neuromuscular junctions and cholinergic synapses
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
sliding filament mechanism
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)
muscle contraction stage 1 : muscle stimulation
- 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
muscle contraction stage 2: tropomyosin, myosin, actin, Ca2+
- 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
muscle contraction stage 3: relaxation
- 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
energy supply during muscle contraction
- 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.
