7 Neurotransmission Flashcards
Q: Draw a simple diagram of a neuron and label. (5) Describe simple functions.
A: spine: receives inputs
dendrite
soma: involved in integration of signals
axon: action potential is generated at the AXON HILLOCK
nerve ending/terminal: lots of mitochondria in the axon terminal because energy is needed to release neurotransmitter
Q: What has high resistance?
A: synapse
Q: How wide is the synaptic cleft? How long does it take for the action potential to get from one cell to the next?
A: about 20 - 100 nm wide
about 2 ms
Q: Describe the mechanism of neurotransmission. (6)
A: 1. Action potential comes along (wave of depolarisation) and the calcium channel gets activated
- Calcium enters the nerve terminal and you get exocytosis of the neurotransmitter
- It diffuses across the gap and interacts with the receptors
- You have to get rid of the transmitter - this is done (for the amino acid transmitters) by TRANSPORTERS
- These take the amino acids back into the terminal and other transporters take it back into the synaptic vesicles
- You then use sodium-potassium pumps to bring it back to resting membrane potential
Q: What are the 3 stages of synaptic transmission?
A: 1. biosynthesis, packaging and release of neurotransmitter into synapse
- receptor action
- inactivation
Q: What are the 3 classes of neurotransmitter? Give examples (3,2,1).
A: Amino Acids (e.g. glutamate= widespread use and is vital, GABA, glycine= localised to brain stem and spinal cord)
Amines (e.g. noradrenaline, dopamine)
Neuropeptides (e.g. opioid peptides)
Q: How do neurotransmitters vary? (2) What’s the result of a neurone receiving multiple transmitter influences?
A: (There’s a lot of diversity in the transmitters and their receptors)
- They may cause rapid or slow effects
- They vary in abundance from mM to nM CNS tissue concentration
integrated to produce diverse functional responses
Q: What are the essential components to synaptic transmission? (4)
A: -restricted to specialised structures=synapse
- fast within ms
- calcium is essential= transmitter release requires a local increase in intracellular Ca2+
- synaptic vesicles provide source of NT
Q: What does the activation of NT release require?
A: -calcium (dependant)
-rapid (electro mechanical) transduction (200us) = mu seconds =10^-6
Q: How can rapid release of NT occur? (3)
A: 1. synaptic vesicles are filled with NT and docked in the synaptic zone ‘primed’ (some are floating in the terminal region) = interaction between synaptic vesicle and synaptic membrane proteins allows rapid response
- Ca2+ entry activates a Ca2+ sensor in the protein complex -> calcium sensor protein on the vesicle making the complex undergo conformational change
- leads to membrane fusion of vesicles and NT release into the synaptic cleft
Q: Why is vesicle docking stable? (2)
A: tails are present on vesicular pre synaptic membrane which can cross over -> form super alphahelical coils
The net effect of this interaction is a stable complex of the vesicle at the synapse full of neurotransmitter
Q: What are synaptic vesicular proteins targets for?
A: neurotoxins
Q: What effect does tetanus have on synaptic vesicular proteins? What is the effect that botulinum has? What can inhibit NT release?
A: SPASTIC paralysis
FLACID paralysis
Zn2+ dependent endopeptidases
Q: What effect does alpha latrotoxin have on synaptic vesicular proteins? Explain.
A: (from the black widow spider)
Alpha latrotoxin binds to the protein at the site of release and prevents the vesicle closing down and recycling and the transmitter is released to complete depletion
Q: What is neurotransmitter action defined by? Describe. (2) Speed?
A: receptor kinetics
Ion Channel Receptor = FAST (msecs)
- mediate ALL fast excitatory and inhibitory transmission
G protein coupled receptor = slow (secs/mins)
-effectors may be enzymes (eg adenyl cyclase, phospholipase C, cGMP–PDE) or channels (Ca2+, K+)
