3.4.3 NERVE IMPULSES AND SYNAPTIC TRANSMISSION
EQ: During an action potential. The permeability of the cell-surface membrane of an axon changes. The graph shows changes in permeability of the membrane to sodium ions (Na+) and to potassium ions (K+) during a single action potential. (a) Explain the shape of the curve for sodium ions between 0.5ms and 0.7ms. (3 MARKS) (b) During an action potential, the membrane potential rises to +40mV and then falls. Use information from the graph to explain the fall in membrane potential. (3 MARKS)
(a) - (Ion) channel proteins open - Sodium in - Changes membrane potential / makes inside of axon less negative / depolarisation / reaches threshold - More channels open/positive feedback (b) - Potassium channels open - Potassium out - Sodium channels close
Q: Synapses are unidirectional. Explain how acetylcholine contributes to a synapse being unidirectional. (3 MARKS)
- (Acetylcholine) released from/in presynaptic side - Diffusion from higher concentration/to lower concentration - Receptors in postsynaptic (side) / binds to postsynaptic (side)
Q: During an action potential, the permeability of the cell-surface membrane of an axon changes. Explain the change in permeability to sodium ions that takes place during a single action potential. (4 MARKS)
- (ion) channel proteins open - Sodium (move) in - Changes membrane potential / makes inside of axon less negative / positive / depolarisation / reaches threshold - More channels open/positive feedback
Synapses result in unidirectional nerve impulses. Explain how.
- (vesicles containing) Neurotransmitter only made in / released from pre-synaptic neurone/membrane - (Neuro)receptors only on post-synaptic membrane, none in pre-synaptic - Diffuse from high → low concentration across synaptic cleft - Neurotransmitter are removed from cleft so they response doesn't keep happening (broken down by enzyme)
Q: The black mamba's toxin kills prey by preventing their breathing. It does this by inhibiting the enzyme acetylcholinesterase aat neuromuscular junctions. Explain how this prevents breathing. (3 MARKS)
- Acetylcholine not broken down / stays bound to receptor - Na+ ions (continue to) enter / (continued) depolarisation / Na+ channels (kept) open / action potentials / impulses fired (continously) - (Intercoastal) muscles stay contracted / cannot relax
Q: Multiple sclerosis (MS) is a disease that involved damage to the myelin sheaths of neurones. Movement in MS sufferers may be jerky or slow. Damage to the myelin sheaths of neurones can lead to problems controlling the contraction of muscles. Suggest one reason why. (2 MARKS)
- Action potentials travel more slowly / don't travel / no salutatory movement of potentials - So delay in muscle contraction / muscles don't contract / muscles contract slower OR - Action potentials / depolarisation 'leaks' to adjacent neurones - So wrong muscle (fibres) contract
Q: Outline the importance of the junctions between neurones in the functioning of the nervous system. (3 MARKS)
- Allows neurones to communicate / cell signalling - Ensure transmission (between neurones) in one direction (only) - One neurone can connect to / transmit impulses to many neurones OR divergence - Summation OR convergence OR one neurone can receive multiple impulses from many neurones OR allows many low level stimuli to be amplified - Idea that filters out 'background' / low level stimuli OR ensures that only stimulation that is strong enough will be passed on OR prevents continuous stimulation of neurones OR prevents fatigue / prevents over-stimulation OR permits memory / learning / decision making
Describe how myelination affects the speed of axon diameter in a neurone.
- Bigger diameter means less leakage of ions + less resistance to flow of ions - So faster the speed of action potential as less resistance, and more surface rea for ion movement
Q: Outline the events following the arrival of an action potential at the synaptic knob until the acetylcholine has been released into the synapse. (5 MARKS)
- Calcium channels open - Ca2+ / calcium ions enter / diffuse in - Acetylcholine / ACh / neurotransmitter in vesicle(s) - (synaptic) vesicles move towards presynaptic membrane OR vesicles fuse with membrane - Release acetylcholine by exocytosis into synaptic cleft
Q: Serotonin is a neurotransmitter released in some synapses in the brain. It is transported back out of the synaptic gap by a transport protein in the pre-synaptic membrane. Serotonin diffuses across the synaptic gap and binds to a receptor on the post-synaptic membrane. Describe how this causes depolarisation of the post-synaptic membrane. (2 MARKS)
- Causes sodium ion channels to open - Sodium ions enter (cell and cause depolarisation)
Q: Describe the differences between the central nervous system and the peripheral nervous system. (4 MARKS)
- Central: brain and spinal cord / intermediate neurones - Has coordinating role / many synapses - Peripheral: nerves from sense organs / to muscles / to glands / sensory and motor neurones - Role in sensing stimuli / controlling effectors or conduction impulses to / from CNS
Compare the transmission across cholinergic synapses and neuromuscular junctions.
- Cholinergic synapse - neurone to neurone WHEREAS neuromuscular - neurone to muscle - Neuromuscular junction: ACh is always excitatory in muscle response and never inhibitory, so always triggers generator/action potential - No summation in muscle (neuromuscular) - Action potential in neurone and no action potential in muscle/sacrolemma - Neuromuscular junction: Post-synaptic membrane has more receptors than other synapses → an action potential is always generated in the post-synaptic membrane - Some neuromuscular junctions have different neurotransmitters - Neuromuscular junction: Lots of folds on post-synaptic membrane which form clefts to store enzyme (Acetylcholinerase / AChE) to break down neurotransmitter (Acetylcholine / Ach)
Q: There are a number of differences between myelinated and non- myelinated neurones. One difference is the distribution of voltage-gated sodium ion channels in the membrane. Myelinated neurone: - voltage-gated sodium ion channels only occur at gaps between Schwann cells - each gap is approximately 2 um long - gaps occur at approximately 1000 um intervals Non-myelinated neurone: - voltage-gated sodium ion channels occur along the total length of the neurone. Use the information above to explain the difference in the speed of conduction of an action potential along the length of a myelinated neurone and a non-myelinated neurone. (4 MARKS)
- Conduction faster in myelinated neurone - Depolarisation / action potential can only travel where channels present OR movement / transfer can only take place at the gaps / nodes OR action potential jumps from node to node - Idea that myelinated neurones have long(er) sections with no (voltage-gated / Na(+)) channels present - Saltatory conduction
Nervous communication is...
- Fast - Short lived - Localised
Give examples of inhibitory neurotransmitters.
- GABA → binds to receptors, causing potassium ion channels to open on the postsynaptic membrane, hyperpolarising the neurone - Acetylcholine → in cholinergic synapses in the heart, bind to receptors here, causing potassium ion channels to open on the postsynaptic membrane, hyperpolarising it
Q: The image shows a synaptic bulb. State the correct labels for H, I, J and K. (4 MARKS)
- H = vesicle containing neurotransmitter - I = mitochondrion - J = axon - K = presynaptic membrane
Describe how temperature affects the speed of an action potential / impulse in a neurone.
- Higher temperature increases rate of movement of ions Na+ and K+ as more kinetic energy so more active transport / diffusion, so further speeds action potential - Higher rate of respiration (enzyme activity faster) so ATP produced faster and energy released faster → active transport faster - But proteins could denature at a certain temperature (above optimum)
Q: Explain what is meant by repolarisation of a cardiac muscle cell or a nerve cell. (3 MARKS)
- Idea of redistribution of ions - Across the cell membrane - Causes change in / different potential difference / return to resting potential
Q: The chemical nature of synaptic transmission makes it susceptible to disruption by toxins. Atropine is a toxin produced by the deadly nightshade plant, Atropa belladonna. Atropine is a similar shape to acetylcholine. The presence of atropine prevents the initiation of an action potential in the post-synaptic neurone. Explain how the presence of atropine in the synapse will prevent the initiation of an action potential. (5 MARKS)
- Idea that atropine binds to / occupies / competes for (ACh) receptor on postsynaptic membrane / neurone OR prevents ACh binding / blocks binding site / blocks receptor - Ion gates / ion channels / sodium channels do not open - Na+ cannot enter / K+ cannot leave neurone / (nerve) cell - No / insufficient depolarisation / postsynaptic potential / excitatory postsynaptic potential / generator potential - (so) does not reach threshold (value / potential)
Q: Explain how the structure of the axon cell membrane is related to the conduction of nerve impulses. (4 MARKS)
- Idea that phospholipid restricts ion movement - Proteins span the membrane - Idea that sodium potassium pump moves ions - (protein) gates / channels allow diffusion / allow movement
What is the 'all or nothing' law?
- If a generator potential reaches threshold → trigger an action potential - All action potentials are same size - Strong stimulus generates more frequent action potentials
Q: Describe the differences in the structure of a myelinated sensory neurone and a myelinated motor neurone. (3 MARKS)
- In sensory neurone: dendron longer - Axon shorter - Cell body not at the end / towards the middle / to the side OR reference to no motor end plate
Describe and explain spatial summation.
- Many pre-synaptic neurones share the same synaptic cleft / post-synaptic neurone - Collectively release sufficient neurotransmitter to reach threshold to trigger an action potential in a post-synaptic neurone - This is because a weak stimulus may only create a few action potentials → doesnt always trigger an action potential in the post-synaptic neurone
What is the role of a motor neurone in the reflex arc?
- Many short dendrites - Single long axon - Ends with a neuromuscular junction - Cell body outside and at the end - Transmit nerve impulse from intermediate OR sensory neurone to effector; gland/muscle
Q: The figure represents part of the axon of a neurone. Describe the structure of the feature labelled A. (3 MARKS)
- Myelin / myelinated / lipid/fatty (sheath) - (Schwann) cell wrapped around / surrounds axon - Except at nodes of Ranvier / (sheath) not continuous / presence of gaps (in the sheath)
Q: Fewer action potential occur along a myelinated axon than along an unmyelinated axon of the same length. Explain why. (2 MARKS)
- Myelin insulates axon / ions can only pass through (plasma membrane of axon) to gaps in myelin sheath - (Gaps in sheath are called) nodes of Ranvier
What are the different factors affecting the speed of conductance in a neurone?
- Myelination - Axon diameter - Temperature
Describe and explain temporal summation.
- One pre-synaptic neurone releases neurotransmitter many times over a short period / in rapid succession to add to produce an action potential - A single action potential doesnt always trigger an action potential in the post-synaptic membrane → a strong stimulus will cause more frequency action potentials → releasing more neutransmitter → add up to trigger an action potential in the post-synaptic membrane
Q: Multiple sclerosis (MS) is a disease that involves damage to the myelin sheaths of neurones. Movement in MS sufferers may be jerky or slow. Damage to the myelin sheaths of neurones can lead to problems controlling the contraction of muscles. Suggest one reason why. (2 MARKS)
- One suitable suggestion explained e.g. action potentials travel more slowly / don't travel OR action potentials/depolarisation 'leaks' to adjacent neurones - So delay in muscle contraction / muscles dont contract / muscles contract slow(er) OR so wrong muscle (fibres) contract
Q: During an action potential, the membrane potential rises to +40 mV and then falls. Use your knowledge of the movement of sodium ions and potassium ions to explain the fall in membrane potential. (3 MARKS)
- Potassium channels open - Potassium (move) out - Sodium channels close
Q: Scientists investigated the use of substances called cannabinoids to control muscle problems caused by multiple sclerosis (MS). Cannabinoid receptors are found in the pre-synaptic membrane of neuromuscular junctions. When a cannabinoid binds to its receptor, it closes calcium ion channels. Suggest how cannabinoids could prevent muscle contraction. (4 MARKS)
- Prevents influx of calcium ions (into pre-synaptic membrane) - (synaptic) vesicles don't fuse with membrane / vesicles don't release neurotransmitter - Neurotramsitter does not diffuse across synapse/does not bind to receptors (on post-synaptic membrane) - No action potential/depolarisation (of post-synaptic membrane) / sodium (ion) channels do not open/prevents influx of sodium ions
Describe the importance of the refractory period.
- Produces discrete and discontinuous impulses → action potentials don't overlap, ensures 'new' action potentials are generated ahead - Limits frequency of impulse transmission at a certain intensity (limits strength of stimulus that can be detected); higher intensity stimulus causes higher frequency of action potentials but only up to certain intensity - Unidirectional action potential - can't be propagated in a region that is refractory, cannot move baclwards
Q: The figure is a diagram representing the neuromuscular junction in mammals. 1. What type of molecule forms ion channels W and X? 2. Identify region Y. 3. Name the enzyme found in region Y. (3 MARKS)
- Protein - (synaptic) cleft - acetylcholinesterase
Q: The peripheral and central nervous systems work together to enable mammals to respond to changes in their external environment. Outline the roles of the peripheral and central nervous systems in responding to changes in the environment from stimuli to response. The names and functions of regions in the brain are not required. (7 MARKS)
- Receptor detects stimulus / change in environment - Sensory neurones conduct action potentials - (from receptors) to CNS - CNS / brain coordinates response / has coordinating role - Relay / intermediate neurones conduct action potentials (from sensory to motor neurones) - Motor neurones conduct action potentials - To effector
Describe how myelination affects the speed of conductance in a neurone.
- Schwann cells make myelin sheath, which is an electrical insulator → preventing depolarisation and prevents the movement of ions in and out of the neurone - Depolarisation at Nodes of Ranvier only → lots of Na+ and K+ ion channels, saltatory conduction → impulse jumps from node to node - Impulse doesn't travel whole axon / no need to depolarise along whole length of axon unlike non-myelinated neurone, so speeds up transmission of nerve impulses as cytoplasm conducts enough charge to depolarise the next node
What is the role of a sensory neurone in the reflex arc?
- Single long dendron → carries impulse towards cell body - Single short axon → carries impulse away from cell body - Cell body is presented outside (little bit beyond middle) - Transmit nerve impulses from receptor to intermediate OR motor neurone
Q: Which three specific types of transmembrane proteins are involved in establishing a resting potential in a neurone? (3 MARKS)
- Sodium-potassium pumps - Voltage-gated sodium ion channels - Potassium ion channels
What is the role of a receptor in the reflex arc?
- Specific receptor will only detect one type of stimulus - Cell OR protein - Transform stimulus into an electrical nerve impulse
State the features of a synapse.
- Unidierctionality - Summation: spatial + temporaal
What is the role of a relay neurone in the reflex arc?
- Within CNS - Many short dendrites - Many short axons - Cell body inside and in the middle - Transmit impulses between neurones, e.g. from sensory to motor
Give an example of an excitatory neurotransmitter.
Acetylcholine is an excitatory neurotransmitter → binds to cholinergic receptors to cause an action potential in the postsynaptic membrane) at cholinergic synapses in the CNS and at neuromuscular junctions
Give and example of inhibition by inhibitory synapses.
Acetylcholine is an inhibitory neurotransmitter at cholinergic synapses in the heart
Q: The figure represents a sensory neurone connected to its associated receptor cells. 1. Identify the parts of the neurone labelled A to D. (4 MARKS) 2. What is represented by the arrows on the figure? (1 MARK)
1. A: dendrite 2. B: dendron 3. C: cell body (of neurone) 4. D: axon 2. Direction of (conduction / travel / transmission) impulse / action potential
Describe the transmission across a neuromuscular junction.
1. Action potential arrives at pre-synaptic neurone, causing voltage-gated calcium ion channels to open (Ca2+) → calcium ions diffuse into pre- synaptic neurone 2. Causing vesicles containing neurotransmitter / acetylcholine (which is made only in the presynaptic neurone) to fuse to pre-synaptic membrane → release acetylcholine into synaptic cleft by exocytosis 3. Neurotransmitters/acetylcholine diffuse across synaptic cleft → bind to specific neurotransmitter nicotinic cholinergic receptors found only on the sarcolemma membrane, sarcolemma membrane has more receptors than other synapses 4. Lots of folds / pits on post-synaptic membrane (sarcolemma) which form clefts to store enzyme (Acetylcholinerase / AChE) to break down neurotransmitter (Acetylcholine / Ach) 5. Some sodium ion (Na+) channels open → sodium ions diffuse into post-synaptic membrane (sacrolemma) → if thereshold is reached, voltage-gated Na+ channels open, depolarization initiates/triggers action potential (excitatory synapse) 6. Neurotransmitter removed from cleft so response doesn't keep happening e.g. broken down by an enzyme called acetylcholinesterase (AChE) and the products are reabsorbed by the presynaptic neurone and recycled. 7. Sacrolemma is depolarised, generating an action potential that passes down the T-tubules towards the centre of the muscle fibre 8. These action potentials cause voltage-gated calcium ion channels proteins in the membranes of the sarcoplasmic reticulum (which lie very close to the T-tubules) to open 9. Calcium ions bind to troponin molecules, stimulating them to change shape → this causes the troponin and tropomyosin proteins to change position on the thin (actin) filaments 10. The myosin-binding sites are exposed to the actin molecules, the muscle now contracts
Describe the transmission across a cholinergic synapse.
1. Depolarisation of presynaptic membrane / action potential arrives at the pre-synaptic knob of presynaptic neurone, 2. Causing voltage-gated calcium ion channels to open in (Ca2+) → calcium ions enter axon by facilitated diffusion into pre-synaptic knob down electrochemical gradient 3. Causing vesicles containing neurotransmitter / acetylcholine to diffuse down the cytoplasm and fuse to pre-synaptic membrane → release the neurotransmitter acetylcholine into synaptic cleft by exocytosis 4. Neurotransmitters/acetylcholine diffuse across synaptic cleft 5. Bind to specific neurotransmitter/cholinergic receptors found only on post-synaptic membrane 6. Some sodium ion (Na+) channels open as a result → sodium ions diffuse + enter into post-synaptic knob → if threshold is reached, voltage-gated Na+ channels open, depolarization initiates/triggers action potential (excitatory synapse) 7. Neurotransmitter/ACh removed from synaptic cleft so response doesn't keep happening → broken down by an enzyme called acetylcholinesterase (AChE) to form acetate and choline → the products are reabsorbed by the presynaptic neurone and recycled and reassembled.
Give ways in which specific drugs inhibit the nervous system in relation to the synapse.
1. Inhibit nervous system → fewer action potentials e.g. block receptors so cant be activated by neurotransmitters 2. Inhibit nervous system → fewer action potentials e.g. inhibit release of neurotransmitter
What are all the steps in the changes in membrane permeability that lead to the depolarisation and generation of an action potential?
1. Resting potential (polarisation): neurones default state --> -65 mV 2. Generator potential / stimulus 3. Threshold --> -55 mV 4. Depolarisation 5. Hyperpolarisation: (-70 mV) 7. Resting potential restored
Describe step one in the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
1. Resting potential (polarisation): neurones default state → -65 mV - Sodium potassium ion pump - Active transport (ATP) - Na+ out - K+ in - Some K+ diffuses out through K+ channels - Sodium voltage-gated channels are closed - Voltage-gated K+ channel is closed
Describe step two in the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
2. Generator potential / stimulus - Weak stimulus - Membrane more permeable to sodium ions as some voltage-gated Na+ channels open - Some Na+ diffuses into neurone, down electrochemical gradient - Does not reach threshold - Na+/K+ pump restores resting potential - Voltage-gated K+ channel is closed - Some K+ diffuses out through K+ channels
Describe the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
1. Resting potential (polarisation): neurones default state → -65 mV - Sodium potassium ion pump - Active transport (ATP) - Na+ out - K+ in - Some K+ diffuses out through K+ channels - Sodium voltage-gated channels are closed - Voltage-gated K+ channel is closed 2. Generator potential / stimulus - Weak stimulus - Membrane more permeable to sodium ions as some voltage-gated Na+ channels open - Some Na+ diffuses into neurone, down electrochemical gradient - Does not reach threshold - Na+/K+ pump restores resting potential - Voltage-gated K+ channel is closed - Some K+ diffuses out through K+ channels 3. Threshold - Generator potential reaches threshold (-55 mV), action potential generated - As many more voltage-gated Na+ channels open - Na+ diffuse into axon rapidly down electrochemical gradient - Positive feedback - Voltage-gated K+ channel is closed - Some K+ diffuses out through K+ channels 4. Depolarisation - Changes to membrane potential - More voltage-gated Na+ channels open due to sodium ions diffusing into axon - More Na+ diffuse into the neurone (influx) → positive feedback - K+ channels close - Voltage-gated K+ channel is closed - Some K+ diffuses out through K+ channels 5. Repolarisation → (+40 mV) - Voltage-gated K+ channels open - K+ diffuses out of neurone, down the potassium ion concentration gradient, causing repolarisation - Voltage-gated Na+ close (membrane less permeable to sodium ions) - Some K+ diffuses out through K+ channels 6. Hyperpolarisation: movement of cell's membrane potential to a more negative value (the inside is more negative than the outside) → (-70 mV) - When membrane potential is more negative than resting potential - Voltage-gated Na+ are still closed - K+ channels are slow to close so there's slight overshoot → too many potassium ions diffuse out of neurone - Some K+ diffuses out through K+ channels - *Refractory period: time in which a nerve cell is unable to fire an action potential (nerve impulse), this is important as it allows for discrete impulses - Another action potential cannot be started, Makes action potentials: → discrete (don't overlap) → unidirectional (one-way) 7. Resting potential restored by sodium-potassium ion pump Note: bigger stimulus will cause more frequent action potentials but they will all be the same size
Describe how a resting potential is established/maintained.
1. Sodium-potassium ion pump in neurone's membrane actively transports using ATP: - 3 sodium (Na+) ions out of axon - 2 potassium (K+) ions into axon - Electrochemical (concentration) gradient created e.g. higher conc. Of potassium ions inside axon than outside, higher conc. of sodium ions outside axon than outside 2. Voltage-gated sodium ion channel is closed so sodium ions cannot diffuse back into axon, but Membrane more permeable to potassium ions (open K+ channels) than sodium ions (closed Na+ channels) 3. Potassium ions in channels are open: Potassium ions can diffuse out of axon by facilitated diffusion, down the electrochemical gradient. 4. Inside of axon negatively charged relative to outside; axon is polarised = resting potential NOTE: Doesn't reach equilibrium because of the positive charge outside
Give ways in which specific drugs stimulate the nervous system in relation to the synapse.
1. Stimulate nervous system → more action potentials e.g. mimic neurotransmitter as same shape, so more receptors activates 2. Stimulate nervous system → stimulate release of more neurotransmitter 3. Stimulate nervous system → inhibit enzyme that breaks down neurotransmitter, more neurotransmitters in synaptic cleft to bind to receptors and they're there for longer
Describe step three in the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
3. Threshold - Generator potential reaches threshold (-55 mV), action potential generated - As many more voltage-gated Na+ channels open - Na+ diffuse into axon rapidly down electrochemical gradient - Positive feedback - Voltage-gated K+ channel is closed - Some K+ diffuses out through K+ channels
Describe step four in the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
4. Depolarisation - Changes to membrane potential - More voltage-gated Na+ channels open due to sodium ions diffusing into axon - More Na+ diffuse into the neurone (influx) → positive feedback - K+ channels close - Voltage-gated K+ channel is closed - Some K+ diffuses out through K+ channels
Describe step five in the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
5. Repolarisation → (+40 mV) - Voltage-gated K+ channels open - K+ diffuses out of neurone, down the potassium ion concentration gradient, causing repolarisation - Voltage-gated Na+ close (membrane less permeable to sodium ions) - Some K+ diffuses out through K+ channels
Describe step six in the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
6. Hyperpolarisation: movement of cell's membrane potential to a more negative value (the inside is more negative than the outside) → (-70 mV) - When membrane potential is more negative than resting potential - Voltage-gated Na+ are still closed - K+ channels are slow to close so there's slight overshoot → too many potassium ions diffuse out of neurone - Some K+ diffuses out through K+ channels - *Refractory period: time in which a nerve cell is unable to fire an action potential (nerve impulse), this is important as it allows for discrete impulses - Another action potential cannot be started, Makes action potentials: → discrete (don't overlap) → unidirectional (one-way)
Describe step seven in the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
7. Resting potential restored by sodium-potassium ion pump
What is a neuromuscular junction?
A cholinergic synapse between a motor neurone and a muscle cell Use the neurotransmitter acetylcholine (ACh), which binds to cholinergic receptors called nicotinic cholinergic receptors
What is a synapse?
A junction between neurones
TIP!
ACh is always excitatory and never inhibitory, so always triggers generator/action potential
Describe the passage of an action potential along an myelinated neurone.
Action potentials only occur at Nodes of Ranvier. - Localised circuits therefore occur between adjacent nodes of Ranvier and the action potentials 'jump' from node to node by saltatory conduction, so they pass faster here than in unmyelinated neurones. - No need for depolarisation along whole length of axon
What is summation and what are the types?
Addition of a number of impulses converging on a single post-synaptic There is: - Spatial summation - Temporal summation
When generating an action potential, the bigger the stimulus...
Bigger stimulus will cause more frequent action potentials but they will all be the same size
TIP!!
By having both excitatory and inhibitory neurones forming synapses with the same post- synaptic membrane, this gives control of whether post-synaptic membrane 'fires' or not, therefore 'firing' is not inevitable and stimulation can be overridden
Q: Pufferfish produce a powerful poison, tetrodotoxin and some species store it in high concentrations in their body tissues. Unless these fish are correctly prepared, eating them can be fatal. Tetrodotoxin is poisonous to humans because it block gated sodium channels in cell membranes, preventing action potentials. This does not happen in the fish themselves. Suggest why tetrodotoxin is not toxic to the puffer fish. (1 MARK)
Channel / receptor / ion is different. Accept toxin confide to organelle / organ / part of the body / toxin not in general circulation / toxin stored in inactive form / contains a compound that neutralises toxin
What is moved between synapses?
Chemical transmission by neurotransmitters, e.g. acetylcholine (ACh)
What is the spinal cord?
Column or nervous tissues that runs along back and lies inside the vertebral column for protection. Emerging at intervals along the spinal cord are pairs of nerves.
What is an excitatory neurotransmitter?
Depolarise the postsynaptic membrane, making it achieve an action potential if threshold is achieved
Give an example of how specific drugs can stimulate the nervous system to release more neurotransmitter.
Example: Amphetamines force a neurotransmitter called dopamine out of synaptic vesicles and into the synaptic cleft. This increases the effect of dopamine, e.g. it increases alertness
Give 2 examples of how specific drugs can inhibit the nervous system by inhibiting the release of the neurotransmitter.
Example: Cannabinoids prevent muscle contraction. They are hydrophobic and easily pass into neurones. Cannabinoid receptors are found in pre-synaptic membrane of neuromuscular junctions. When a cannabinoid binds to its receptor, it closes calcium ion channels. - Prevents influx of calcium ions into presynaptic membrane - Synaptic vesicles don't fuse with membrane / release ACh so ACh doesn't diffuse across synapse / bind to receptors on post-synaptic membrane - No action potential / depolarisation of post-synaptic membrane / sodium ion channels don't open / prevents influx of sodium ions Example: Opioids block calcium ions channels in the presynaptic neurone. This means fewer vesicles fuse with the presynaptic membrane so less neurotransmitter is released
Give 3 examples of how specific drugs can stimulate the nervous system to inhbit the enzyme that breaks down the neurotransmitter.
Example: GABA is a neurotransmitter produced by neurones in the brain and spinal cord. It binds to post-synaptic membranes and inhibits the production of nerve impulses. Epilepsy may result when there is increased neuronal activity in the brain. One form of epilepsy is due to insufficient GABA. GABA is broken down on the post-synaptic membrane by transaminase. Vigabatrin is a new drug being used to treat this form of epilepsy. It has a similar molecular structure to GABA. - Binds to GABA receptors → Inhibits neuronal activity/chloride ions enter neurone - OR inhibits enzyme which breaks down GABA → more GABA available Example: Black mamba's toxin prevents breathing. Inhibits Acetylcholinesterase at neuromuscular Junctions. - ACh not broken down / stays bound to receptor - Na+ ions continue to enter / depolarisation continues / Na+ channels kept open / action potentials or impulses fired continuously - Intercostal muscles stay contracted / can't relax Example: nerve gases stop acetylcholine from being broken down in the synaptic cleft. This can lead to loss of muscle control.
Give 3 examples of how specific drugs can inhbit the nervous system as they block receptors so cant be activated by neurotransmitters.
Example: Pancuronium binds to acetylcholine receptors on muscle fibres, causing muscle paralysis. - Pancuronium is a similar shape to acetylcholine so is complementary to / fits in receptor and can bind to - Not broken down / removed from receptor by AChE so blocks receptor site / prevents ACh from binding - Na+ channels on membrane don't open so no action potential, and no influx of Ca2+ ions to start contraction, so prevents unblocking of binding sites on actin Example: Enkephalins are neurotransmitters released by the brain and spinal cord in response to harmful stimuli. They're similar in shape to acetylcholine. They act as painkillers by inhibiting synaptic Transmission. - Bind to receptors on post-synaptic membrane as complementary to receptors - Acetylcholine can't bind so reduces/stops depolarisation Example: Curare blocks the effects of acetylcholine by blocking nicotinic cholinergic receptors at neuromuscular junctions, so muscle cells cant be stimulated, this results in the muscle being paralysed
Give 2 examples of how specific drugs can stimulate the nervous system to mimic a neurotransmitter.
Example: This synapse uses a neurotransmitter called dopamine. Cocaine is a similar shape to dopamine. Cocaine binds to the dopamine transporter (transports dopamine back to pre-synaptic knob). It is released in parts of the brain where pleasure is perceived and can result in feelings of pleasure. - Dopamine and cocaine have similar shapes / so it can fit into the transporter - Blocks transport of dopamine out of synaptic cleft into pre-synaptic knob - Dopamine concentration rises / remains and continues to bind to receptor - Continued firing of impulses in post-synaptic neurone Example: Nicotine mimics acetylchholine so binds to nicotinic cholinergic receptors in the brain
Q: Name the process by which acetylcholine leave the neurone. (1 MARK)
Exocytosis
What is an inhibitory neurotransmitter?
Hyperpolarise the postsynaptic membrane (make the potential difference more negative), preventing it from firing an action potential
Describe the passage of an action potential along an unmyelinated neurone.
If an action potential travels along an unmyelinated axon, it passes as a wave of depolarisation to the adjacent resting region where sodium ions trigger a change in potential difference, stimulating another action potential. Influx of sodium ions in one region increases permeability of adjoining region to sodium ions by causing voltage-gated sodium ion channels to open so adjoining region depolarises
Describe inhibition by inhibitory synapses.
Inhibitory neurotransmitters hyperpolarise the postsynaptic membrane: - K+ channels open - K+ diffuse out - Cl- channels open, Cl- diffuse in - Inhibits formation of action potential / transmission of nerve impulses by post-synaptic membranes - Can't be depolarised as inside of postsynaptic membrane is even more negative than at resting potential → hyperpolarisation - Reduces the effect of sodium ions entering so much less likely to reach threshold
Describe what is open and closed when changes in membrane permeability that lead to the depolarisation and generation of an action potential occur.
Look at image and compare.
Draw a myelinated motor neurone.
Look at image and compare.
Draw and label the structure of a neuromuscular junction.
Look at image and compare.
Draw and label the structure of a synapse.
Look at image and compare.
Draw the graph of the changes in membrane permeability that lead to the depolarisation and generation of an action potential.
Look at image and compare.
Draw a motor neurone, sensory neurone, and intermediate (relay) neurone.
Look at the image and compare.
Q: Name the type of neurone that stimulates muscles. (1 MARK)
Motor
What is the role of a effector in the reflex arc?
Muscle or gland
Describe and explain the structural adaptations of a myelinated motor neurone.
Myelin sheath: - Schwann cells make myelin - Electrical insulator around axon → prevents depolarisation - Prevents movement of ions in and out of the neurone Nodes of Ranvier: - Gaps in myelin sheath - Lots of Na+ and K+ ion channels - Depolarisation can only happen at the nodes → action potentials jump between nodes in a process called saltatory conduction Cell body: contains a nucleus + many RER → associated with production of proteins and neurotransmitters Dendrons: small extensions of cell body that subdivide into smaller branched fibres called dendrites → carry nerve impulses towards the cell body Axon: single long fibre that carries nerve impulses away from cell body Schwann cells: surround the axon, protect it and provide electrical insulation. Also carry out phagocytosis and play a part in nerve regeneration. Wrap themselves around axon many times, so many layers around it.
What are the receptors in cholinergic synapses called?
Nicotinic cholinergic receptors.
Where does the generation of an action potential occur in a neurone?
Only occurs in unmyelinated neurones and in the Nodes of Ranvier in myelinated motor neurones.
What is membrane potential?
Potential difference inside of a neurone (in each nerve) which is determined by the amount of sodium and/or potassium ions.
State what a reflex arc consists of, drawing a diagram.
Stimulus → receptor → sensory neurone → relay neurone (CNS) → motor neurone → effector → response
Explain the importance of summation (temporal, spatial) for transmission between synapses.
Sufficient neurotransmitter to reach threshold to trigger an action potential: - Important because low frequency action potentials often release insufficient amounts of neurotransmitter to exceed threshold in post-synaptic neurone → summation allows an action potential to be generated by the build-up of neurotransmitter
What are cholinergic synapses?
Synapses that use acetylcholine (ACh)
Q: Name the part of a neurone from which acetylcholine is secreted. (1 MARK)
Synaptic knob / synaptic bulb / presynaptic membrane
Q: Synaptophysin is a protein involved in the production of synaptic vesicles. Scientists can use the presence or absence of synaptophysin to identify presynaptic and postsynaptic membranes in synapses. Explain why they are able to use synaptophysin for this purpose. (1 MARK)
Synaptic vesicles only found in presynaptic
Q: Give a way in which the function of a motor neurone differs from that of a sensory neurone. (1 MARK)
The motor neurone carries impulse(s) / action potential(s) from, brain / spinal cord / CNS / relay neurone to effector / muscle / gland
Describe how the nervous system is split.
The nervous system is split into - CNS: brain, spinal cord - Peripheral nervous system: Made up of pairs of nerves that originate from either brain or spinal cord, which split into The peripheral nervous system then splits to... - Sensory neurones: Carry nerve impulses from receptors to CNS - Motor neurones: Carry nerve impulses away from CNS to effectors The motor neurones are then split into... - Voluntary nervous system: Carries nerve impulses to body muscles and is under voluntary (conscious) control - Autonomic nervous system: Carries nerve impulses to glands, smooth muscle, and cardiac muscle and is involuntary (subconscious)
What is the refractory period?
The time to restore axon to resting potential / no further action potential can be generated (Repolarisation + Hyperpolarisation)
What is synaptic convergence?
When many neurones join a single neurone This amplifies the signal → this is called spatial summation
What is synaptic divergence?
When one neurone splits into many neurones This spreads the cation potential to other parts of the body
A synapse where inhibitory neurotransmitters are released from the presynaptic membrane following an action potential is called an _______ synapse.
inhibitory