Nervous Coordination Flashcards
1
Q
Neurones
A
Specialised cells adapted to rapidly carrying electrochemical changes called nerve impulses
2
Q
Resting Membrane Potential
A
- When neurone isn’t being stimulated, outside of membrane is more positively charged
- More positive ions outside of cell
- Voltage when membrane at rest
3
Q
Movement of sodium and potassium ions
A
- Resting potential is created and maintained by sodium-potassium pumps and potassium ion channels in a neurone’s membrane
- Sodium-potassium pumps use active transport to move 3 sodium ions out of the neurone for every 2 potassium ions moved in (ATP needed)
- Potassium ion channels allow facilitated diffusion of potassium ions out of the neurone, down their concentration gradient
- 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 (creates a sodium ion electrochemical gradient because more positive sodium ions outside cell than inside)
- Sodium-potassium pumps also move potassium ions in to the neurone
- When the cell’s at rest, most potassium ion channels are open
- Means that the membrane is permeable to potassium ions, so some diffuse back out through potassium ion channels
- In total, more positive ions move out of cell
- Phospholipid bilayer of axon plasma membrane prevents sodium and potassium ions diffusing across it
4
Q
Sequences that lead to an action potential
A
- Stimulus= excites neurone cell membrane, causing sodium ion channels to open. Membrane becomes more permeable to sodium, so sodium ions diffuse into the neurone down the sodium ion electrochemical gradient. Makes inside of the neurone less negative.
- Depolarisation= if potential difference reaches threshold,more sodium ion channels open so more sodium ions diffuse into the neurone.
- Repolarisation= (+30mV) sodium ion channels close and potassium ion channels open. 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.
- Hyperpolarisation= potassium ion channels are slow to close so there’s a slight ‘overshoot’ where too many potassium ions diffuse out of the neurone. Potential difference becomes more negative than the resting potential.
- Resting potential= ion channel are reset. Sodium-potassium pump returns the membrane to its resting potential by pumping sodium ions out and potassium ions in, and maintains the resting potential until the membrane’s excited by another stimulus.
5
Q
Why are sodium-ion channels voltage-gated?
A
Only open when the potential difference reaches a certain voltage
6
Q
Refractory Period
A
- After an action potential, the neurone cell membrane can’t be excited again straight away
- This is because the ion channels are recovering and they can’t be made to open-sodium ion channels are closed during repolarisation and potassium ion channels are closed during hyperpolarisation
- Period of recovery is called the refractory period
- Refractory period acts as a time delay between one action potential and the next (makes sure action potentials don’t overlap and are discrete impulses)
- Also means there is a limit to the frequency at which the nerve impulses can be transmitted, and that action potentials are unidirectional (they only travel in one direction)
7
Q
Passive and active process
A
- Resting potential is maintained by active transport (active)
- Action potential= movement of sodium ions due to diffusion (passive)
8
Q
Waves of depolarisation
A
- When an action potential happens, some of the sodium ions that enter the neurone diffuse sideways
- Causes sodium ion channels in the next region of the neurone to open and sodium ions diffuse into that part
- Causes a wave of depolarisation to travel along the neurone
- Wave moves away from the parts of the membrane in the refractory period because these parts can’t fire an action potential
- K+ channels open and Na+ channels close
9
Q
All-or-nothing principle
A
- Once threshold is reached, an action potential will always fire with the same change in voltage, no matter how big the stimulus is
- If threshold isn’t reached, an action potential won’t fire
- Bigger stimulus won’t cause a bigger action potential but it will cause them to fire more frequently
- Different neurones have different threshold values
- This principle stops the brain from getting over-stimulated by not responding to very small stimuli
10
Q
Factors that affect speed of conduction
A
Myelination, salatory conduction, axon diameter and temperature
11
Q
Myelination
A
- Some neurones are myelinated (have myelin sheath which is an electrical insulator)
- In the peripheral nervous sytem, the sheath is made of a type of cell called a schwann cell
- Between schwann cells are tiny patches of bare membrane called the nodes of Ranvier
- Sodium ion channels are concentrated at the nodes of Ranvier
12
Q
Structure of a myelinated motor neurone
A
- Dendrons= extensions of cell body which subdivide into dendrites that carry nerve impulses towards cell body.
- Schwann cells= surround axon, protecting it and providing electrical insulation. Carry out phagocytosis and play a part in nerve regeneration. Schwann cells wrap around loads so layers of membrane build up.
- Axon= single fibre that carries nerve impulses away from cell body.
- Cell body= associated with production of proteins and neurotransmitters.
13
Q
Saltatory Conduction
A
- In a myelinated neurone, depolarisation only happens at the nodes of Ranvier (where sodium ions can get through the membrane)
- Neurone’s cytoplasm conducts enough electrical charge to depolarise the next node, so the impulse ‘jumps’ from node to node
- Known as saltatory conduction and it’s really fast
- In a non-myelinated neurone, the impulse travels as a wave along the whole length of the axon membrane (so you get depolarisation along the whole length of the membrane)
- This is slower than saltatory conduction
14
Q
Axon diameter
A
- Action potentials are conducted quicker along axons with bigger diameters beacuse there’s less resistance to the flow of ions than in the cytoplasm of a smaller axon (less leakage of ions and leakage makes membrane potentials harder to maintain)
- With less resistance, depolarisation reaches other parts of the neurone cell membrane quicker
15
Q
Temperature
A
- Energy for active transport comes from respiration which is controlled by enzymes (as well as sodium-potassium pump)
- Enzymes function rapidly at higher temperatures up to a point (can denature)
- Ions can diffuse quickly at higher temperatures
- Temperature also affects speed and strength of muscle contractions
16
Q
Myelin sheath as electrical insulator
A
- Preventing an action potential forming in the part of axon covered in myelin (increases speed of conductance)
17
Q
Hormonal system VS Nervous system
A
18
Q
What is a synapse?
A
- Junction between a neurone and another (or effector cell)
- Space between synapse is called the synaptic cleft
- Presynaptic neurone has a swelling called a synaptic knob (possesses many mitochondria and endoplasmic reticulum that helps make neurotransmitters)
- Contains synaptic vesicles filled with chemicals called neurotransmitters (made in presynaptic neurone)
19
Q
Effect of an action potential
A
- Causes neurotransmitters to be released into the synaptic cleft
- They diffuse across to the postsynaptic membrane and bind to specific receptors
- When neurotransmitters bind to receptors they might trigger an action potential (in a neurone), cause muscle contraction (muscle cell), or cause hormone to be secreted (gland cell)
- Because receptors are only on the postsynaptic membranes, synapses make sure impulses are unidirectional (can only travel in one direction)
- Neurotransmitters are removed from the cleft so the response doesn’t keep happening (taken back into presynaptic neurone or broken down by enzymes-products taken back into neurone)
20
Q
Nerve impulse across cholinergic synapse
A
- Action potential arrives at synaptic knob
- Voltage-gated ion channels open
- Calcium ions diffuse into the synaptic knob (pumped out afterwards by active transport)
- Calcium ions cause the synaptic vesicles to move to and fuse with the presynaptic membrane
- Acetylcholine released by exocytosis
- Acetylcholine diffuses across cleft
- Acetylcholine binds to the receptor sites on the sodium ion channels in the postsynaptic membrane (complementary)
- Sodium channels open
- Sodium ions diffuse across post synaptic membrane into postsynaptic neurone (excitatory postsynaptic potential created)
- EPSPs can combine, reaching the threshold potential
- New action potential created in the postsynaptic neurone
- ACh removed from synaptic cleft so response doesn’t keep occuring
- Broken down by acetylcholinesterase and products are re-absorbed back into presynaptic neurone, ready to make more ACh
21
Q
Exocytosis
A
Vesicle inside cell moves to the cell-surface membrane, fuses with the membrane and releases its contents outside the cell
29
Q
Spatial summation
A
- Where 2 or more presynaptic neurones release their neurotransmitters at the same time onto the same postsynaptic neurone
- The small amount of neurotransmitter released from each of these neurones can be enough altogether to reach the threshold in the postsynaptic neurone and trigger an action potential
- If some neurones release an inhibitory neurotransmitter than the total effect of all the neurotransmitters might be no action potential
30
Q
Temporal summation
A
- Where 2 or more nerve impulses arrive in quick succession from the same presynaptic neurone
- Makes an action potential more likely because more neurotransmitter is released into the synaptic cleft
31
Q
Neuromuscular junctions
A
- Specialised cholinergic synapse between a motor neurone and a muscle cell
- Neuromuscular junctions use the neurotransmitter acetylcholine, which binds to cholinergic receptors called nicotinic cholinergic receptors
37
Q
Role of skeletal muscle
A
- Skeletal muscles are attached to bones by tendons
- Ligaments attach bones to other bones, to hold them together
- Pairs of skeletal muscles contract and relax to move bones at a joint-the bones of the skeleton are incompressible (rigid) so act as levers, giving muscles something to pull against
- Muscles that work together to move a bone are called antagonistic pairs
- The contracting muscle is called the agonist and the relaxing muscle is called the antagonist
- When your bicep contracts your triceps relaxes (pulls the bone so arm bends at elbow)
- Biceps are agonist and triceps are antagonist
- When triceps contract and bicep relaxes, this pulls the bone so your arm straightens at the elbow
- Triceps is agonist and biceps is antagonist
38
Q
Structure of skeletal muscle
A
- Skeletal muscle is made up of large bundles of long cells, called muscle fibres (cell membrane of muscle fibre is called sarcolemma)
- Bits of the sarcolemma fold inwards across the muscle fibre and stick into the sarcoplasm (muscle cell’s cytoplasm)
- These folds are called transverse tubules and help spread 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
- Sarcoplasmic reticulum stores and releases calcium ions that are needed for muscle contraction
- Muscle fibres have lots of mitochondria to provide the ATP that’s needed for muscle contraction
- They are multinucleate (contain many nuclei) and have lots of long, cylindrical organelles called myofibrils
- Myofibrils are made up of proteins and are highly specialised for contraction (organelles within the muscle fibre cell)
- Individual muscles are made up of millions of tiny muscle fibres called myofibrils (parallel to maximise force)
- Muscle fibres share nuclei and cytoplasm called sarcoplasm
40
Q
Myofibrils
A
- Contain bundles of thick and thin myofilaments that move past each other to make muscles contract
- Thick myofilaments are made of the protein myosin (long-rod shaped tails with bulbous heads on side) and the thin myofilaments are made of the protein actin (2 strands twisted around one another)
- Dark bands contain thick myosin filaments and some overlapping thin actin filaments (A-bands)
- Light bands contain thin actin filaments only (I-bands)
- Thick and thin filaments don’t overlap
- A myofibril is made up of many short units called sacromeres
- The ends of each sacromere are marked with a Z-line
- In the middle of each sacromere is an M-line
- M-line is the middle of the myosin filaments
- Around the M-line is the H-zone
- H-zone only contains myosin filaments
41
Q
Sliding filament theory (muscle contraction)
A
- Myosin and actin filaments slide over one another to make the sacromeres contract- myofilaments themselves don’t contract
- The simultaneous contraction of lots of sacromeres means the myofibrils and muscle fibres contract
- Sacromeres return to their original length as the muscle relaxes
- I-band becomes narrower
- Z-line move closer together (sacromere shortens)
- H-zone becomes narrower
- A-band remains same width
- Width of this band is determined by length of myosin filaments, myosin filaments don’t go shorter
- Discounts the theory that muscle contraction is due to filaments themselves shortening
42
Q
Myosin filaments
A
- (head and tail) Have globular heads that are hinged, so they can move back and forth
- Each myosin head has a binding site for actin and a binding site for ATP
43
Q
Actin filaments
A
- (globular protein, chains twisted around) Have binding sites for myosin heads, called actin-myosin binding sites
- Another protein called tropomyosin is found between actin filaments
- Helps myofilaments move past each other
45
Q
Process of muscle contraction
A
- Action potential from a motor neurone stimulates a muscle cell, it depolarises the sarcolemma (calcium ions diffuse into the synaptic knob, acetylcholine released in synaptic cleft and bind to receptors)
- Depolarisation spreads down the T-tubules to the sarcoplasmic reticulum
- This causes the sarcoplasmic reticulum to release stored calcium ions into the sarcoplasm
- This influx of calcium ions into the sarcoplasm triggers muscle contraction
- Calcium ions bind to a protein attached to tropomyosin, causing the protein to change shape (pulls the attached tropomyosin out of the actin-myosin binding site on the actin filament)
- This exposes the binding site, which allows the myosin head to bind
- Bond formed is an actin-myosin cross bridge
- Calcium ions also activate the enzyme ATP hydrolase, which hydrolyses ATP to provide energy for muscle contraction
- Energy released from ATP causes the myosin head to bend, which pulls the actin filament along in a kind of rowing action
- Another ATP provides energy to break actin-myosin cross bridge, so myosin head detaches from the actin filament after it’s moved
- The myosin head then returns to it’s starting position, and reattaches to a different binding site further along the actin filament
- A new actin-myosin cross bridge is formed and the cycle is repeated (attach,detach)
- Many actin-myosin cross bridges form and break very rapidly, pulling the actin filament along- which shorterns the sacromere, causing the muscle to contract
- Cycle will continue as long as calcium ions are present
52
Q
Slow twitch and fast twitch muscle fibres
A
Slow twitch
- Mitochondria are mainly found near edge of muscle fibres, so there’s a short diffusion pathway for oxygen from the blood vessels to the mitochondria
- Numerous mitochondria to produce ATP
- Aerobic to avoid build up of lactic acid which leads to less effective function
Fast twitch
- Stores of PCr so energy can be generated quickly when needed
- More powerful contractions
- High concentration of glycogen
- Thicker and more numerous myosin filaments
- High concentration of enzymes involved in anaerobic respiration which provides energy for muscle contraction
