6B - Nervous coordination

AQA A Level Biology

membrane potential of an axon at rest

-70mV

process of a cell becoming polarised

potassium ions diffuse out of axon membrane through leaky potassium ion channels, Na/K pump actively transports 3 sodium ions out of the axon for every 2 potassium ions that it pumps in, build up of positive ions outside the axon causes the inside of the axon to be relatively negative

nerve impulse

a wave of depolarisation that travels down a neurone

state of transport proteins in axon membrane at rest

voltage-gated sodium ion and potassium ion channels are closed, leak potassium ion channels are open

process of depolarisation of neurone

a stimulus causes the voltage-gated sodium ion channels to open which allows sodium ions to diffuse across the membrane into the axon down the electrochemical gradient, voltage-gated potassium ion channels remain closed, this reduces the potential difference outside the axon so it becomes depolarised

process of repolarisation of a neurone

when peak voltage (+30mV) is reached after an action potential has been generated, the voltage-gated sodium ion channels close and voltage-gated potassium ion channels open, potassium ions diffuse out of the axon which repolarises the axon, the influx of ions diffusing out of the axon causes hyperpolarisation to occur

maximum membrane potential reached during depolarisation

+30mV

threshold potential of a neurone

around -50mV

refractory period

the axon is unresponsive because it is in a period of recovery after generating an action potential, all voltage-gated sodium ion channels close

adaptations of the synaptic knob

many mitochondria to synthesise ATP needed for neurotransmitter release, many ribosomes and rough endoplasmic reticula to synthesise protein channels, lots of Golgi apparatus to produce vesicles to transport neurotransmitters

hyperpolarisation

a short period when the potential difference across this section of axon membrane briefly becomes more negative than the normal resting potential

the all or nothing principle

An impulse is only transmitted if the initial stimulus is sufficient to increase the membrane potential above a threshold potential

importance of the refractory period

ensures that action potentials are discrete events (they don’t merge into one another), new action potentials are generated further down the axon than the original action potential so the impulse can only travel in one direction, ensures there is a minimum time between action potentials occuring at one place on the neurone

absolute refractory period

no action potential can be produced

relative refractory period

an action potential will only be produced with a very strong stimulus

why action potentials only travel in one direction

1. depolarisation of one area of the membrane causes adjacent voltage-gated sodium ion channels to open

2. sodium ions to diffuse into the axon and reach the threshold

3. next section of the membrane depolarises

4. after depolarisation the membrane becomes hyperpolarised

5. during this period the membrane cannot be re-excited because sodium ion channels in the previous area of the axon won’t open

factors that affect the speed of an action potential

a myelin sheath, diameter of the axon, temperature

effect of myelin sheath on speed of action potential

myelin increases the speed because it allows saltatory conduction to occur so the whole membrane of the axon doesn’t need to be depolarised

effect of axon diameter on speed of action potential

thicker axons have faster action potentials because there is a greater surface area for the diffusion of ions to occur across and they have larger cytoplasms which reduces their electrical resistance

effect of temperature on speed of action potential

higher temperatures cause faster action potentials because particles have more kinetic energy available for the facilitated diffusion of potassium and sodium ions during an action potential

excitatory synapse

a synapse that increases the probability of an action potential being generated, when neurotransmitters bind to receptors on the postsynaptic membrane it is depolarised

inhibitory synapse

a synapse that decreases the probability of an action potential being generated, when neurotransmitters bind to receptors on the postsynaptic membrane the membrane is hyper polarised

spatial summation

multiple presynaptic neurones form a junction with a postsynaptic neurone and each neurone releases neurotransmitters so their effects add together to reach the threshold at the postsynaptic neurone

temporal summation

multiple nerve impulses arrive at the same synaptic knob within a short period of time, so more neurotransmitters are released which bind to receptors on the postsynaptic neurone and reach the threshold to generate an action potential

cholinergic synapse

an excitatory synapse that uses the neurotransmitter acetylcholine

cholinergic synaptic transmission process

1. an action potential arrives at the presynaptic knob and depolarises the membrane

2. this stimulates voltage-gated calcium ion channels to open

3. calcium ions diffuse down an electrochemical gradient into the presynaptic knob

4. this stimulates presynaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine molecules into the synaptic cleft

5. acetylcholine diffuses across the synaptic cleft and temporarily binds to ligand-gated sodium ion channels in the postsynaptic membrane

6. this causes a conformational change in the receptor proteins, which open allowing sodium ions to diffuse down an electrochemical gradient

7. the sodium ions cause the postsynaptic membrane to depolarise

8. acetylcholinesterase in postsynaptic clefts hydrolyses acetylcholine into acetate and choline to prevent sodium ion channels staying permanently open and depolarising the postsynaptic membrane

9. choline is reabsorbed into the presynaptic membrane and reacts with acetylcholine coenzyme A to reform acetylcholine

importance of inhibitory synapses

prevent random impulses from being sent, to allow specific pathways to be stimulated

cholinergic synapses

excitatory and inhibitory

neuromuscular junction

excitatory synapse

3 types of muscle fibres

cardiac, smooth, skeletal

features of cardiac muscle fibres

found in the heart, involuntary, striated

features of smooth muscle fibres

found in organs, involuntary, not striated

features of skeletal muscle fibres

attached to bones, voluntary

antagonistic pair

pair of muscles in which one contracts and one relaxes

antagonist

muscle in an antagonistic pair that is relaxing

agonist

muscle in an antagonistic pair that is contracting

sarcomere

functional unit of contraction

sarcolemma

plasma membrane in a sarcomere

tendon

length of strong connective tissue that connects muscle to bone

isometric contraction

muscles maintaining posture by antagonistic pairs both contracting at joints to keep the joint at a certain angle

muscle fibre

a highly specialised cell-like unit which contains an organised arrangement of contractile proteins in the cytoplasm, multinucleate because it’s formed from multiple stem cells

transverse system tubules

deep tube-like projections that fold in from the outer surface of the sarcolemma

myofibril

a bundle of actin and myosin filaments which slide past each other during muscle contraction

H zone

a region in the myofibril of only thick myosin filaments

I band

a region in the myofibril of only thin actin filaments (lighter appearance)

A band

the region in the myofibril containing myosin, parts overlap with actin (darker appearance)

M line

attachment for myosin filaments

Z line

ends of the sarcomere where actin filaments are attached

effect of an agonistic drug

increases frequency of action potentials

ways agonistic drugs work

stimulate neurotransmitter release, inhibit neurotransmitter breakdown, mimic a neurotransmitter, provide chemicals to make a neurotransmitter

effect of an antagonistic drug

reduces frequency of action potentials

ways antagonistic drugs work

inhibit neurotransmitter release, block neurotransmitter receptors

2 types of drugs used to treat parkinsons

dopamine agonist and dopamine precursor

dopamine agonist

a drug that produces the same effect as dopamine by binding to the same receptors

dopamine precursor

a drug that can be used to synthesise dopamine in the neurones

transmission across a neuromuscular junction

1. an action potential arrives at the presynaptic membrane

2. calcium ions diffuse into the neurone

3. this stimulates vesicles containing acetylcholine to fuse with the presynaptic membrane

4. the acetylcholine is released and diffuses across the neuromuscular junction

5. acetylcholine binds to receptor proteins on the sarcolemma

6. ion channels in the sarcolemma are stimulated to open, allowing sodium ions to diffuse in

7. the sarcolemma becomes depolarised which generates an action potential that passes down the T-tubules towards the centre of the muscle fibre

8. the action potential causes voltage-gated calcium ion channels in the sarcoplasmic reticulum membrane to open

9. calcium ions diffuse out of the sarcoplasmic reticulum and into the sarcoplasm surrounding the myofibrils

10. calcium ions binds to troponin molecules which stimulates them to change shape

11. troponin and tropomyosin molecules change position on the actin filaments

12. the myosin-binding sites are exposed to the actin molecules

13. muscle contraction can now begin

features of a cholinergic synapse

uses acetylcholine as a neurotransmitter, found between neurones, can be excitatory or inhibitory, stimulated by an action potential on the presynaptic membrane

features of a neuromuscular junction

uses acetylcholine as a neurotransmitter, found between a motor neurone and a muscle, can only be excitatory, stimulated by an action potential on the presynaptic membrane

myosin

a fibrous protein molecule with a globular head that makes up thick filaments in a sarcomere

how myosin is arranged in thick filaments

fibrous part of the myosin anchors it into the filament, many myosin molecules lie next to each other with their globular heads pointing away from the M line

actin

a globular protein molecule that forms thin filaments in a sarcomere

how actin is arranged in thin filaments

many actin molecules link together to form 2 chains which twist together to form a filament, tropomyosin is twisted around the 2 actin chains and troponin is attached to the actin chains at regular intervals

the sliding filament model of muscle contraction

1. an action potential arrives at the neuromuscular junction which eventually leads to calcium ions being released from the sarcoplasmic reticulum and binding to troponin molecules

2. the troponin molecules change shape which causes troponin and tropomyosin to change position on the actin filaments

3. myosin binding sites are exposed on the actin molecules which the globular heads of the myosin molecules on the thick filament bind to

4. cross-bridges are formed between the 2 filaments

5. myosin heads spontaneously bend by rowing action, releasing ADP and Pi and pulling the actin filaments towards the centre of the sarcomere

6. the muscle contracts a very small distance

7. ATP binds to the myosin heads

8. the myosin heads change shape and release from the actin filaments

9. ATP hydrolase hydrolyses ATP into ADP and Pi so the myosin heads move back to their original positions

10. the myosin heads are able to bind to new binding sites on the actin filaments closer to the Z disc

11. the myosin heads move again, pulling the actin filaments even closer to the centre of the sarcomere

12. the sarcomere shortens again and pulls the Z discs closer together

13. this process repeats until the muscle is fully contracted as long as troponin and tropomyosin are not blocking the myosin-binding sites and the muscle has a supply of ATP

features of fast twitch muscle fibres

rapid contraction, few capillaries, ATP supplied mostly from anaerobic respiration, fewer, smaller mitochondria, large store of calcium ions in the sarcoplasmic reticulum, lots of glycogen and phosphocreatine, faster rate of ATP hydrolysis in myosin heads, fatigues rapidly due to greater lactate formation, small amount of myoglobin

features of slow twitch muscle fibres

long contraction, denser capillary network, ATP supplied mostly from aerobic respiration, many, large mitochondria, small store of calcium ions in the sarcoplasmic reticulum, little glycogen, slower rate of ATP hydrolysis in myosin heads, fatigues more slowly due to reduced lactate formation

causes of muscle fatigue

decreased availability of calcium ions which activate ATP hydrolase and cause troponin to move, production of lactate which lowers the pH of muscles and affects the contraction of fibres

how synapses ensure nerve impulses only travel in one direction

neurotransmitters only made in presynaptic neurone and receptors only located on post-synaptic membran

advantages of simple reflexes

rapid response, protect against damage to body tissues, do not have to be learnt, help escape from predators, enable homeostatic control

why ATP is a suitable energy source for cells

releases relatively small amounts of energy, releases energy instantaneously, phosphorylates other compounds which makes them more reactive, rapidly resynthesised, does not leave cells