3.6.2.2 Synaptic transmission (C15) Flashcards
What is the myelin made up of?
Schwann cells
What is saltatory conduction?
In myelinated neurones, depolarisation can only occur at the nodes of Ranvier, so the impulse ‘jumps’ from node to node.
What are the nodes of Ranvier?
Bare areas of neurones that are not insulated with myelin.
Give three factors that affect the speed of conduction of action potentials.
- Axon diameter
- Myelination
- Temperature
Why does increasing temperature increase the speed of transmission?
Ions diffuse faster when temperature increases.
Give one function of the refractory period
It produces discrete impulses that are unidirectional.
What is a synapse?
The junction between a neurone and the next cell.
What ensures that impulses cross the synapse in one direct only?
Vesicles of neurotransmitter are only found in the presynaptic knob.
Receptors for the neurotransmitter is only found on the post synaptic membrane.
What are Cholinergic synapses?
Synapses that use acetylcholine.
What happens to the neurotransmitter once they have attached to the receptors on the post synaptic membrane?
They are broken down by enzymes and their products are taken back into the neurone.
What stimulates the synaptic vesicles to move towards the presynaptic membrane in a cholinergic synapse?
Calcium ions diffuse into the synaptic knob causing the synaptic vesicles to move towards and fuse with the presynaptic membrane.
What happens when the acetylcholine bind with the receptors on the post synaptic membrane?
Sodium ion channels open and sodium ions flood in. If the threshold is reached and action potential is generated.
How is acetylecholine removed from the synaptic cleft?
Acetylcholinesterase breaks acetylcholine and the products are reabsorbed to make more acetylcholine.
What is temporal summation?
It is where there are two or more nerve impulses that arrive in quick succession from the same presynaptic membrane and action potential is more likely to occur..
What is spatial summation?
When many neurones connect to one neurone. The small amount of neurotransmitter released from each of these neurones can be enough to reace the threshold value.
Describe how calcium ions are involved in synaptic transmission.
(Nerve impulse causes) Ca2+ to enter presynaptic neurone/membrane;
(Ca2+ entry) causes fusion of vesicles with presynaptic membrane /
causes exocytosis / release of transmitter;
Describe how a nerve impulse causes the release of neurotransmitter from the vesicles in the presynaptic knob
- (Nerve impulse/depolarisation of membrane) causes Ca2+channel (proteins) to open;
- Ca2+enter by (facilitated) diffusion;
- Causes (synaptic) vesicles to fuse with (presynaptic) membrane;
GABA causes negatively charged chloride ions to enter post synaptic neurones - How does this inhibit post synaptic neurones?
- neurone becomes more negative/hyperpolarised
- not enough sodium ions enter (to reach threshold)
- for depolarisation to take place
Describe how a nerve impulse is transmitted across a cholinergic synapse
- Action potential arrives synaptic knob of presynaptic neurone
- AP stimulates calcium ion channels to open
- Calcium ions diffuse into synaptic knob
- Influx of calcium ions causes synaptic vesicles to move into presynaptic membrane + fuse with it
- Vesciles release acetylcholine into synaptic cleft
- Ach diffuses across synaptic cleft + binds specfic cholinergic receptors on postsynpatic membrane
- Causes sodium ion channels in postsynaptic neurone to open
- Influx of sodium ions causes depolorisation AP generated if threshold reached
- Ach broken down by acetylcholinesterase + products reabsorbed
How can more chloride ions entering the post synaptic neuron affect action potential propagation?
Cl-are negatively charged
They make the post synaptic neurone hyperpolarised
More Na+ needs to enter the post synaptic neuron for depolarisation of the neurone to pass threshold
Action potential is inhibited
How can potassium ions leaving the post synaptic neuron affect action potential propagation?
K+ are positively charged
When they move out they make the post synaptic neurone hyperpolarised
More Na+ needs to enter the post synaptic neuron for depolarisation of the neurone to pass threshold
Action potential is inhibited
How can drugs that bind to synaptic receptors affect neurotransmission?
Drugs bind receptors instead of Ach because they are complementary – they prevent Na+ from entering, threshold isn’t reached reducing action potentials.
How can drugs that inhibit acetylcholinesterase affective neurotransmission?
Drugs prevent acetylcholinesterase from breaking down Ach by aching as an inhibitor (inhibitor model answer applies here e.g. blocks active site or changes shape so the active site is no longer complementary) this prevents Ach from being removed from receptors, more Na+ diffuses in increases action potentials.
If a drug is complementary to the neurotransmitter, how might this affect neurotransmission?
Drugs may be complementary to the NT (substrate) and bind it, this changes shape of the substrate and means it can’t bind the receptor. Less Na+ moves in, doesn’t pass threshold reducing action potentials.
Describe the events at a NMJ (neuromuscular junction)
- Action potential reaches pre-synaptic membrane allowing Ca2+ channels to open and Ca2+ enters by facilitated diffusion
- Vesicles of neurotransmitter fuse with the pre-synaptic membrane
- Neurotransmitter e.g. Acetylcholine diffuse across the neuromuscular junction
- Neurotransmitters bind to the Na+ receptors causing Na+ to enter the sarcolemma (muscle tissue) depolarising it
- Depolarisation is transmitted through the T-tubules causing Ca2+ ions to be released from the sarcoplasmic reticulum
- Ca2+ binds to tropomyosin in the leading to muscle contraction
