Section 6: Nervous co-ordination Flashcards
How is the resting potential established?
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Sodium potassium ion pump actively transports
- 3 sodium ions out of the axon
- 2 potassium ions into axon
- Electrochemical gradient established - higher conc of K+ ions in axon
- Membrane more permeable to potassium ions (K+ channels open/ Na+ channels closed)
- K+ ions move out of axon by facilitated diffusion. Therefore inside more negative than outside. Axon is polarised - resting potential
What is the stimulus in membrane permeability leading to depolarisation?
- Membrane more permeable to Na+ ions as the channels open
- Sodium diffuse into neurone down electrochemical gradient
What is depolarisation part of the graph mean?
- P.d reaches threshold, action potential generated
- Because more voltage-gated sodium ion channels open and sodium diffuse rapidly
What is repolarisation part of the graph mean?
- Sodium ion channels close (membrane less permeable to sodium ions) whilst voltage gated potassium ion channels open so potassium ion s diffuse out of neurone
What is hyperpolarisation part of the graph mean?
- Potassium ion channels are slow to close so there is a slight overshoot - too many potassium ion diffuse out of neurone
What is the importance of the refractory period
- The refractory period is the time to restore axon to resting potential/ no further action potential can be generated
- Importance:
- Produces discrete impulses - action potentials cant overlap
- Limits frequency of transmission at a certain intensity
- Unidirectional action potential
What are the factors that affect the speed of conductance?
- Myelination
- Axon diameter
- Temperature
How does Myelination affect the speed of conductance?
- Depolarisation occurs at nodes of Ranvier only - saltatory conduction
- Impulse does not travel whole axon/ no need to depolarise along whole length of axon
How does the axon diameter affect the speed of conductance?
- Bigger diameter means less leakage of ions/ less resistance to the flow of ions
How does temperature affect the speed of conductance?
- Increases rate of movement of ions Na+ and K+ as more kinetic energy
- Higher rate of respiration so ATP is produced faster - active transport faster
- But proteins could denature at a certain temperature
What is the passage of an action potential along non-myelinated axons
- Action potential passes as a wave of depolarisation
- Influx of sodium ions in 1 region increases permeability and causes voltage gated sodium ion channels to open so region depolarises
What is the passage of an action potential along a myelinated axon?
- Depolarisation of an axon at nodes of ranvier only
- Resulting in saltatory conduction
- So there is no need for depolarisation along whole length of axon
What is the passage of an action potential along a myelinated axon?
- Depolarisation of an axon at nodes of ranvier only
- Resulting in saltatory conduction
- So there is no need for depolarisation along whole length of axon
Exam Question: Damage to the myelin sheaths of neurones can lead to problems controlling the contraction of muscles. Suggest 1 reason why? (2)
- Action potentials travel more slowly/ no saltatory conduction
- So delay in muscle contraction/ muscles dont contract
OR
- Action potentials/ depolarisation “leaks” to adjacent neurones
- So wrong muscle contracts
What is the sequence of steps of the transmission across a cholinergic synapse?
- Action potential arrives causing calcium ion channels to open - calcium ions diffuses into pre-synaptic neurone
- Causing vesicles of neurotransmitters/ acetylcholine to fuse to pre-synaptic membrane - release acetylcholine into synaptic cleft (exocytosis)
- Neurotransmitters diffuse across synaptic cleft - bind to neurotransmitter receptors on post synaptic membrane
- Sodium ion channels open - sodium ions diffuse into post-synaptic knob - depolarisation initiates action potential
- Neurotransmitter removed from cleft so response does not keep happening - broken down by acetylcholinesterase and products reabsorbed by presynaptic neurone.
What is the comparison between the transmission across cholinergic synapses and neuromuscular junctions?
- Cholinergic synapse - neurone to neurone WHEREAS neuromuscular is neurone to muscle
- Neuromuscular junction: ACh is always exitatory so always triggers action potential
- Neuromuscular junction - post-synaptic membrane has more receptors than other synapses
- Neuromuscular junction - lots of folds on post-synaptic membrane which forms clefts to store enzyme AChE to break down ACh
Why synapses result in unidirectional nerve impulses?
- Neurotransmitter only made in presynaptic neurone
- Receptors only on post-synaptic membrane
What is summation?
- Addition of a number of impulses converging on a single post-synaptic neurone
What is spatial summation?
- Many pre-synaptic neurones share the same synaptic cleft/ post-synaptic neurone
- Collectively release sufficient neurotransmitter to reach threshold and trigger an action potential
What is temporal summation?
- 1 pre-synaptic neurone releases neurotransmitter many times over a short period of time/ in rapid succession
- Sufficient neurotransmitter to reach threshold to trigger action potential
How does inhibition happen at inhibitory synapses?
- Inhibitory neurotransmitters hyperpolarise the post-synaptic membrane (K+ channels open and diffuse out, Cl- channels open, Cl- diffuse in)
- Inhibits formation of action potential/ transmission of nerve impulses by post-synaptic membrane - can’t be depolarised
- Example: Acetylcholine is inhibitory at cholinergic synapses at the heart
What are the effects of specific drugs on a synapse?
- Stimulate nervous system - more action potentials e.g minimic neurotransmitter/ stimulate release of more neurotransmitter/ inhibit enzyme that breaks down neurotransmitter
- Inhibit nervous system - fewer action potentials e.g inhibit release of neurotransmitter/ block receptors
What is the effect of this drug on the synapse
Black Mamba’s toxin prevents breathing. Inhibiting acetylcholinesterase at neuromuscular junctions
- ACh not broken down/ stays bound to receptor
- Na+ continues to enter/ depolarisation continues
- Intercostal muscles stay contracted/ can’t relax
What is the effect of this on the synapse?
Dopamine is a neurotransmitter. Cocaine has a similar shape. Cocaine can bind to dopamine transporter (dopamine transported back to pre-synaptic knob) It is released in parts of brain where pleasure is received.
- Dopamine and cocaine have similar shapes/ so 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 membrane
