Topic 6B: Nervous Coordination Flashcards
Maintaining the resting potential
1) The sodium/potassium pump actively transports sodium ions out of the neurone and potassium ions into the neurone.
2) Potassium ions then diffuse through potassium ion channels back out of the cell, but sodium ions are unable to diffuse back into the neurone.
3) Therefore, there are more positively charged ions outside the cell, meaning it is more positively charged than inside.
Action potential
1) A stimulus excites the cell causing sodium ion channels to open, allowing sodium ions to diffuse into the neurone, making the inside of the neurone less negative.
2) Depolarisation: If the potential difference exceeds the threshold, more sodium ion channels open, and more sodium ions diffuse through.
3) Repolarisation: At 30mV, the sodium ion channels close and the potassium ion channels open, allowing potassium ions to diffuse out of the neurone.
4) Hyperpolarisation: Potassium ion channels are slow to close, meaning too many potassium ions diffuse out of the cell.
5) Resting potential: Ion channels are reset and the sodium/potassium pump returns the membrane to its resting potential.
The refractory period
Act as a time delay between one action potential and the next so that:
Action potentials do not overlap.
Action potentials only move in one direction.
All or nothing principle
If the threshold isn’t exceeded - an action potential won’t occur.
Waves of depolarisation
1) During an action potential some sodium ions entering the neurone diffuse sideways, causing sodium ion channels in the next region of the neurone to open.
2) Sodium ions are now able to diffuse into this part of the neurone, creating a wave of depolarisation.
Factors affecting the speed of conduction
Myelination
Axon diameter
Temperature
How does myelination affect speed of conduction
Schwann cells act as insulators meaning depolarisation can only occur at Nodes of Ranvier. Therefore, the impulse jumps from one node to the next instead of travelling through the whole neurone.
How does axon diameter affect the speed of conduction
Axons with a larger diameter have less resistance to the flow of ions meaning the speed of conduction is faster.
How does temperature affect the speed of conduction
As temperature increases, the speed of conduction increases as the ions diffuse faster. However, after 40 degrees, proteins denature so the speed decreases.
What is a synapse
A junction between two neurones
How is an impulse carried over a synapse
1) An action potential arrives in the presynaptic neurone, causing voltage gated calcium ion channels to open, allowing calcium ions to diffuse into the synaptic knob.
2) These ions cause vesicles to fuse with the presynaptic membrane, where they release acetylcholine into the synaptic cleft by exocytosis.
3) Acetylcholine diffuses across the synaptic cleft and binds to cholinergic receptors on the postsynaptic membrane, causing sodium ion channels in the postsynaptic neurone to open.
4) Sodium ions diffuse into the postsynaptic neurone, causing depolarisation to occur. If the threshold is exceeded, an action potential is generated.
5) Acetylcholine is then removes from the synaptic cleft and broken down by acetylcholinesterase. Products are also reabsorbed to make more acetylcholine.
Excitatory and inhibitory neurotransmitters
Excitatory neurotransmitter:
Depolarise the postsynaptic membrane, making it fire an action potential.
Inhibitory neurotransmitter:
Hyperpolarise the postsynaptic membrane, preventing an action potential from firing.
Summation at synapses
Spatial summation:
A number of presynaptic neurones release their neurotransmitters onto the same postsynaptic neurone at the same time.
Temporal summation:
A number of Nervous impulses arrive in quick succession from the same presynaptic neurone.
Neuromuscular junctions
They are the same as cholinergic synapses, however:
The postsynaptic membrane has clefts which store acetylcholinesterase.
It has more receptors.
Acetylcholine is always excitatory.
Drugs at synapses
Agonists have the same shape as the neurotransmitter so more receptors are activated.
Antagonists block receptors so they cannot be activated by neurotransmitters so less receptors are activated.
Some inhibit the enzyme that breaks down the neurotransmitter meaning more neurotransmitters are present.
Some stimulate the release of neurotransmitters so more receptors are activated.
Some inhibit the release of neurotransmitters so less receptors are activated.
Types of muscle
Smooth muscle: Contracts without conscious control. Found in the walls of internal organs.
Cardiac muscle: Contracts without conscious control. Found in the heart.
Skeletal muscle: The muscle used to move with conscious control.
The structure of skeletal muscles
1) Made up of large bundles of muscle fibres which have a cell membrane called the sarcolemma.
2) This sarcolemma folds inwards to form T tubules, which help spread electrical impulses throughout the muscle fibres.
3) Sarcoplasmic reticulum run through the sarcoplasm and store/release calcium ions needed for contractions to occur.
4) They also have lots of mitochondria to produce lots of ATP needed for contractions and have lots of myofibrils.
Structure of myofibrils
Made up of myosin (a protein which makes up thick myofilaments) and actin (a protein which makes up thin myofilaments.
A band = a band where myosin is present.
I band = a band where only actin is present.
Z line = marks the end of a sarcomere.
M line = the middle of the sarcomere.
H zone = a band where only myosin is present.
Sarcomere = a short unit which myofibrils are made up of.
The sliding filament theory
1) Myosin and actin filaments slide over one another, causing the sarcomere to contract.
2) If many sarcomeres contract at once, the actual myofibrils and muscle fibres contract.
3) As the muscle relaxes, the sarcomeres return to their original length. (The actin/myosin do not actually contract themselves)
Muscles in a rested state
1) In unstimulated muscles, the actin-myosin binding site is blocked by tropomyosin.
2) This means the myofilaments are unable to slide past each other because the myosin heads are unable to bind to the actin filament.
The process of a muscle contraction
1) An action potential stimulates the muscle cell causing the sarcolemma to depolarise.
2) The depolarisation then spreads down the T tubules to the sarcoplasmic reticulum causing stored calcium ions to be released.
3) The calcium ions bind to a protein attached to tropomyosin causing it to change shape and move away from the binding site.
4) This allowed the myosin head to bind to the exposed site forming an actin-myosin cross bridge.
5) Calcium ions also activate ATP hydrolase which hydrolyses ATP into ADP + Pi. This provides the energy needed for the myosin head to bend, pulling the actin filament along.
6) Another ATP molecule provides the energy needed to break down the actin-myosin cross bridge, allowing the myosin head to detach from the actin filament.
7) The myosin head then returns to its starting position and reattaches to a different binding site further along the actin filament.
8) This cycle repeats rapidly, pulling the actin filament along, which shortens the sarcomere causing the muscle to contract.
ATP-phosphocreatine
ATP is made by phosphorylating ADP by adding a phosphate group from phosphocreatine. Phosphocreatine runs out quickly providing short bursts of vigorous exercise.
Slow twitch muscle fibres
Contract slowly and have a high resistance to fatigue.
Energy is released slowly through aerobic respiration.
Lots of mitochondria and blood vessels to supply the muscles with oxygen.
Fast twitch muscle fibres
Contract quickly but with a low resistance to fatigue.
Energy is released quickly through anaerobic respiration using glycogen.
Have few mitochondria and blood vessels, but lots of phosphocreatine stores do energy can be generated quickly.
