6B Flashcards
The Resting Membrane Potential
In a neurones resting state (when its not being stimulated) the outside of the neurone is more positively charged compared to the inside. This means the membrane is polarised - Theres a different in charge (Potential Difference/Voltage) across it. Its resting potential is around 70 mV.
Movement of Sodium and Potassium Ions
- The Resting Potential is created and maintained by Sodium-Potassium pumps and Potassium ion channels in the neurones membrane
- Sodium-Potassium pumps use Active Transport to move 3 sodium ions out of the neurone for every 2 Potassium ions in.
- Potassium ion channels allow facilitated diffusion of Potassium ions out of the neurone, down their conc. grad.
- The Sodium-Potassium pumps move sodium ions out of the neurone, but the membrane isn’t permeable to sodium ions, so they can’t diffuse back in. This creates a sodium ion Electrochemical Gradient.
- When the cells at rest, most potassium ion channels are open. This means that the membrane is permeable to potassium ions, so some diffuse back out through Potassium ion channels
Action Potentials - What happens to cause one?
When a neurone is stimulated, Sodium ion channels, in the cell membrane, open. If the stimulus is big enough, it will trigger a rapid change in Potential Difference. This causes the cell membrane to become Depolarised.
The Sequence of events for an Action Potential - Stimulus
This excites the Neurone cell membrane, causing Sodium ion channels to open. The membrane becomes more permeable to Sodium, so Sodium ions diffuse into the neurone down the Sodium-Electrochemical gradient. This makes the inside of the neurone less negative.
The Sequence of events for an Action Potential - Repolarisation
At a potential difference of around +30mV occurs, the Sodium ion channels close and the Potassium ion channels open. The membrane is more permeable to Potassium so Potassium ions diffuse out of the neurone down the Potassium ion Concentration Gradient. This starts to get the membrane back to its Resting Potential
The Sequence of events for an Action Potential - Depolarisation
If the Potential Difference reaches the Threshold (Around - 55mV) more Sodium ion channels open. More Sodium ions diffuse into the neurone
The Sequence of events for an Action Potential - Hyperpolarisation
Potassium ion channels are slow to close so there’s a slight ‘overshoot’ where too many Potassium ions diffuse out of the neurone. The Potential Difference becomes more negative than the Resting Potential
The Sequence of events for an Action Potential - Resting Potential
The ion channels are reset by the Sodium-Potassium pump pumping 3 Sodium ions out for every 2 Potassium ions in the neurone.
What is the Refractory period?
After an Action Potential, the neurone cell membrane can’t be excited again straight away. This is because the Ion channels are recovering, so they can’t be made to open - The Sodium ion channels are closed during Repolarisation and Potassium ion channels are closed during Hyperpolarisation. The Refractory period can act as a time delay to prevent Action Potentials overlapping. It also means theres a limit to the frequency at which the nerve impulses can be transmitted, and ensures the Action Potentials are unidirectional.
Order of which An Action Potential is made
- Stimulus
- Threshold
- Depolarisation
- Repolarisation
- Hyperpolarisation
- Resting Potential
The Waves of Depolarisation
When an Action Potential happens, some of the Sodium ions that enter the neurone diffuse sideways. This causes the Sodium ion channels in the next region of the neurone to open, and the Sodium ions diffuse into that part. This causes a Wave of Depolarisation to travel along the neurone. The wave moves from parts of the membrane in the Refractory period because these parts can’t fire Action Potentials
All or Nothing Principle
Once the Threshold is reached an Action potential will always fire with the same charge in voltage, no matter how big the stimulus is. If the stimulus is strong, a higher frequency of Action Potentials will be fired. If the threshold isn’t reached, an Action Potential won’t fire.
Speed of Conduction - Myelination
Some neurones, including Motor Neurones, are Myelinated; They have a Myelin Sheath. It is an electrical insulator. In the Peripheral Nervous System it is made from a type of cell called a Schwann cell. Between the Schwann cells, there is bare membrane, called Nodes of Ranvier - The Sodium ion channels are concentrated here.
What is Saltatory Conduction?
In Myelinated neurones, depolarisation only happens at the Nodes of Ranvier. The Neurones cytoplasm conducts enough electrical charge to depolarise the next node, so the impulse ‘jumps’ from node to node. In Non-Myelinated neurones, the impulse has to travel along the whole length of the neurone, so therefore it is slower than Saltatory Conduction, although still pretty quick.
Factors affecting Impulse conduction
- Axon Diameter - The bigger the Diameter of an Axon, the quicker an Action Potential is conducted, as there’s less resistance to the flow of ions than in the cytoplasm of a smaller Axon. With less resistance, depolarisation reaches other parts of the neurone cell membrane quicker
- Temperature - the higher the temperature, the higher the rate of conduction as ions can diffuse faster as well as an increased ATP supply for Active Transport from the increased
Respiration Rate is. The temperature must only increase up to 40 degrees, as any higher an the proteins will denature, and the channels won’t be able to produce an Action Potential
Draw and Label a Myelinated Neurone
Cell Body, Dendrons and Dendrites, Axon, Myelin Sheath - Schwann Cells, Axon Terminals and nodes of Ranvier
Synapses and Neurotransmitters
A synapse is the junction between a neurone and another neurone, or between a neurone and an effector cell. The tiny gap between the cells at a synapse is called the Synpatic Cleft. The Presynaptic neurone has a swelling called the presynaptic knob. This contains vesicles willed with the neurotransmitters
The Effect of an Action Potential on Synpase’s
When an action potential reaches the end of a neurone, it causes the neurotransmitters to be released into the synoptic cleft. They diffuse across to the postsynaptic membrane, and bind to specific receptors. When they bind to the receptors they might trigger an AP, causing muscle contraction or a hormone to be secreted from a gland. The neurotransmitters are then removed once the stimulus stops to ensure the response doesn’t keep happening
How do we know synapses ensure the impulses are Unidirectional?
The Presynaptic knob doesn’t have receptors, and only releases the neurotransmitters, whilst the Postsynaptic membrane inly has receptors which the neurotransmitters bind too
What is Acetylcholine?
it is a neurotransmitter which binds to Cholinergic receptors. Synpases that use Acetylcholine are called Cholinergic Synapses
What happens at a Cholinergic Synapse? 1. The Arrival of an Action Potential
When an AP arrived at the presynaptic knob, it depolarises the cell membrane, stimulating the Voltage-Gated Calcium ion channels to open. The Calcium ions diffuse into the synoptic knob.
What happens at a Cholinergic Synapse? 2. Fusion of the vesicles
The influx of Calcium ions into the synoptic knob causes the vesicles, containing the neurotransmitter to fuse with the presynaptic membrane. The vesicles release the neurotransmitter (Acetylcholine - ACh) into the synaptic cleft via exocytosis.
What happens at a Cholinergic Synapse? 3. Diffusion of ACh
ACh diffuses across the synaptic cleft and binds to specific cholinergic receptors on the postsynaptic membrane. This causes the Sodium ion channels in the postsynaptic membrane to open. An influx of Sodium ions into the postsynaptic membrane causes depolarisation. If the Generator Potential reaches its threshold, it causes an Action Potential. Each is removed from the synaptic cleft so the response doesn’t keep happening. It is broken down into Choline and Ethanoic Acid catalysed by an enzyme called Acetylecholinesterase (AChE) and the products are re-absorbed by the presynaptic neurone and used to make more ACh
Excitatory and Inhibitory Neurotransmitters
Neurotransmitters can be excitatory, inhibitory, or both. Excitatory neurotransmitters depolarise the postsynaptic membrane, making it fire an AP if the threshold is reached, Whilst inhibitory neurotransmitters hyperpolarise the postsynaptic membrane by causing protein channels carrying chloride ions to open, making the potential difference more negative, preventing it from firing an AP. Acetylcholine is both Excitatory (In Cholinergic synapses in the CNS and at neuromuscular junctions) and Inhibitory (In Cholinergic synapses in the heart)
Another Inhibitory neurotransmitter is GABA, Which binds to receptors and causes Potassium Ion channels to open.
What are the synapses called when the neurotransmitters released from the presynaptic membrane are inhibitory?
Inhibitory Synapses
What is Summation at Synapses?
If a stimulus is weak, only a small amount of neurotransmitter is released from a neurone into the synaptic cleft. This might not be enough to excite the postsynaptic membrane to the threshold level. Summation is where the effect of neurotransmitters released from many neurones is added together
The two types of Summation
- Spatial Summation - Where two or more presynaptic neurones release their neurotransmitters at the same time onto the same, single postsynaptic neurone. If some neurones release inhibitory neurotransmitters and some release excitatory neurotransmitters, then it is down to adding up the total effect of all the neurotransmitters
- Temporal Summation - Two or more nerve impulses arrivals quickly at the same single presynaptic neurone. This makes the AP more likely as more neurotransmitter will be released into the synaptic cleft
What are Neuromuscular junctions?
Specialised Cholinergic synapse between a motor neurone and a muscle cell. It uses Acetylcholine, which binds to Cholinergic receptors called Nicotinic Cholinergic Receptors
The differences between a Neuromuscular junction and a Cholinergic synapse
- The postsynaptic membrane has lots of folds that form clefts. These clefts store AChE
- The postsynaptic membrane has more receptors than other synapses
- ACh is always excitatory, so when a motor neurone fires an AP, it normally triggers a response in a muscle cell
Drugs at Synapses
Drugs can affect transmission. They do this in various ways:
- Some are the same shape as the neurotransmitter, so they mimic the action at receptors
- Some block the receptors so they can’t be activated
- Some inhibit the enzyme from breaking the neurotransmitter down, meaning more neurotransmitter in the synaptic cleft to bind to receptors and they’re there for longer
- Some stimulate the release of a neurotransmitter so more receptors are activated
- Some inhibit the release of neurotransmitters from the presynaptic neurone so fewer receptors are activated
Types of Muscle
- Smooth Muscle - Contracts without conscious control, Its found in walls of internal organs (apart from the heart)
- Cardiac Muscle - Contracts without conscious control, only found in the heart
- Skeletal Muscle - also called Striated, is a type of muscle you can move
Role of Skeletal muscle
Skeletal muscles are attached to bones by tendons. Ligaments (Bands of strong connective tissue) attach the bones to other bonds to hold them together. Pairs of skeletal muscles contract and relax to move at a joint - the bones act as a levers, giving the muscles something to pull against
Antagonistic Pairs
Muscles that work together to move a bone are called Antagonistic pairs. The contracting muscle is called agonist and the relaxing muscle is called antagonist. E.g. Biceps and Triceps - When the biceps contracts, the triceps relaxed, pulling the bone so the arm bends, and vice versa
Structure of Skeletal Muscle
Made up of large bundles of long cells, called muscle fibres. The cell membrane of the muscle fibres is called the Sarcolemma. Bits of the Sarcolemma fold inwards across the muscle fibre and stick into the Sarcoplasm (muscles cytoplasm) These folds are called T-Tubules, and they help spread the electrical impulses throughout the sarcoplasm so they reach all parts of the muscle fibre. A network of internal membranes called the Sarcoplasmic Reticulum runs through the Sarcoplasm, and it stores and releases Calcium ions needed for muscle contraction.
What are the muscle fibres like?
They have many nuclei (Multinucleate) and lots of mitochondria to provide ATP for muscle contraction. They have lots of long, cylindrical organelles called Myofibrils, made up of proteins and are highly specialised for contraction
What are Myofibrils and their role
-They are organelles which contain bundles of thick (Myosin) and thin (Actin) proteins, which move past each other to make muscles contract
- Dark bands contain Thick Myosin Filaments overlapping Thin Actin Filaments.
Slightly lighter bands are just Myosin Filaments and the thin bands are just Actin Filaments
The Structure of a Sarcomere (Short units of myofibrils)
Remember:
- Sarcomere
- Z-lines
- I-band
- A-band
- H-zone
What happens to the cross section of a Sarcomere when it contracts?
- Sarcomere shortens
- A-band stays the same
- I-Band gets shorter
- H-zone gets shorter
- Z-line closer together
- Dark band lengthens
Myosin and Actin Filaments
- Myosin filaments have globular heads that are hinged, and can move back and forth. Each Myosin has a binding site for Actin and a Binding Site for ATP
- Actin Filaments have binding sites for Myosin heads, called Actin-Myosin binding sites. Another protein called Tropomyosin is found between Actin Filaments, Preventing Myosin from binding when the muscle is relaxed
Sliding Filament Theory - Binding sites in Resting Muscles
For Myosin and Actin Filaments to slide past each other, the Myosin heads needs to bind to the Actin-Myosin binding site on the Actin Filament. In a resting (Unstimulated) muscle, the Actin-Myosin binding site is blocked by Tropomyosin. This means Myofilaments can’t slide past each other because the Myosin heads can’t bind to the Actin Filaments.
Sliding Filament Theory - The Process of Muscle Contraction - The arrival of an Action Potential
When an AP from a motor neurone stimulates a muscle cell, it depolarises the Sarcolemma. This spreads down the T-Tubules to the Sarcoplasmic Reticulum. This causes the stored Calcium ions in the Sarcoplasmic Reticulum to be released into the Sarcoplasm.
Calcium ions bind to the Tropomyosin, causing the protein to change its territory shape and pulls the Tropomyosin out of the Actin-Myosin binding site. This exposes the binding site, which allows the Myosin head to bind, forming a Actin-Myosin cross bridge.
Sliding Filament Theory - The Movement of an Actin Filament
Calcium Ions also activate the Enzyme ATP Hydrolase to catalyse the hydrolysis (Break down) of ATP to ADP, to provide the energy needed for muscle contraction. The energy released from ATP causes the myosin head to bend, pulling the Actin Filament along - this is known as the ‘Power Stroke’
Sliding Filament Theory - Breaking the Actin-Myosin Cross Bridge
Once the ATP has been hydrolysed to provide the energy for the Power Stroke, it detaches from the Myosin head. Therefore another ATP molecule binds to the Myosin head, and provides the energy to detach the Myosin head from the Cross Bridge after the Actin Filament has been moved. Also provides the energy for the Myosin head to return to its original position and the cycle is repeated.
Sliding Filament Theory - Returning to Resting State after Muscle Contraction
When the muscle stops being stimulated, Calcium ions leave their binding sites and are moved by Active Transport back into the Sarcoplasmic Reticulum. The Tropomyosin proteins move back, blocking the Actin-Myosin bind sites again, so both filaments slide back to their relaxed position again, lengthening the Sarcomere
Aerobic Respiration for Muscle contraction
Most ATP is generated via Oxidative Phosphorylation in cells Mitochondria. This ATP is used during the Sliding Filament Theory
Anaerobic Respiration for Muscle Contraction
ATP is made rapidly by Glycolysis. Pyruvate is then converted into Lactate by Lactate Fermentation. This quickly builds up in the muscles and causes muscle fatigue, so it is only good for short periods of hard exercise
ATP-Phosphocreatine (PCr) system
ATP is made by Phosphorylating ADP, taken from PCr. PCr is stored inside cells and the ATP_PCr system generates ATP very quickly. It runs out after a few seconds so it is used during short bursts of vigorous exercise. It doesn’t need oxygen and it doesn’t form any lactate.
ADP + PCr = ATP + Cr (Creatine) Creatine is broken down into creatine, which is removed from the body via the Kidneys.
Slow Twitch Muscle Fibres
- Contract slowly and can work for a long time without getting tired
- Less powerful contractions as less Myosin heads
- Smaller store of Calcium ions
- Energy is released slowly through aerobic respiration.
- Lots of Mitochondria (mainly found near the edge of muscle fibres so there’s a short diffusion pathway for oxygen from the blood vessels) and blood vessels.
- They are rich in Myoglobin, a protein which stores oxygen, so they have more of a reddish colour
- Found in muscles used for posture - E.g. Back and Calve muscles
Fast Twitch Muscle Fibres
- Contract very quickly
- Get tired very quickly
- More powerful contractions as thicker and more Myosin Heads
- Larger store of Calcium ions
- Good for short bursts of speed and power
- Normally found in your leg and arm muscles, as well as your eyes
- Energy is released through anaerobic respiration using Glycogen, and PCr.
- Few mitochondria and blood vessels, and not much myoglobin, so they can’t store much Oxygen, so they have more of a whitish colour
