Neurotransmission II Flashcards

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1
Q

What is myelination?

A

A fatty type placed around the axon by either an oligodendrocyte or a Schwann cell. In between the myelin sheath have Node’s of Ranvier.

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2
Q

What are Oligodendrocytes and Schwann Cells?

A

Oligodendroglial cell = forms myelin around axons in the brain and spinal cord.
Schwann cell = wraps around peripheral nerves to form myelin.
Basically do the same job, but are different cells.

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3
Q

What are differences in the propagation of the AP along the axon in unmyelinated compared to myelinated neurons?

A

Unmyelinated - get the same response along the neuron - all or nothing response.
Myelinated - no ion exchange in the fatty sheath - AP only happens at the Node of Ranvier, and is therefore much more efficient - AP jumps.

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4
Q

What are the advantages of a myelinated axon?

A

The action potentials jump and impulses are quicker. It doesn’t have to occur at many places.

Communication can become more synchronous. Your movements become fast. So it’s important for coordination.

When sodium pump is working hard it uses lots of energy – therefore want this to be efficient. Myelinated neurons are more efficient than unmyelinated neurons; get less APs, signal jumps.

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5
Q

What happens with multiple sclerosis?

A

Get damage in the myelin, therefore won’t be as efficient. Symptoms are loss of sensitivity, muscle weakness, difficulty with coordination and balance.

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6
Q

What toxins affect AP?

A

Tetrodotoxin - blocks voltage gates Na+ channels, results in paralysis.
Dendrotoxin - blocks voltage gated K+ channels, results in convulsions.

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7
Q

What are the different types of synapse?

A
  1. Electrical synapse - very rare in adult mammalian neurons, junction between neurones is small, gap is spanned by proteins which are used to communicate between the neurons (ions move freely).
  2. Chemical synapse - common in adult mammalian neurons, junction between the neurons 20-50nm (synaptic cleft), chemicals (neurotransmitters) are released from the presynaptic neuron to communicate with the postsynaptic neurons.
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8
Q

What kind of synapses do we have?

A

Androdendritic - axon controls the postsynaptic neuron
Axosomatic - axon controls the soma
Axoaxonic - axon controls another axon, and modulates the signal.
Majority are androdendritic.

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9
Q

Why does synapse location matter?

A

Activation of an excitatory synapse leads to local and small (1mV) depolarisation of the postsynaptic cell known as an EPSP (excitatory postsynaptic potential). EPSP decays over the length of the dendrite (decremental decay). Therefore the closer the synapse is to the soma the greater its influence on the production of an action potential in the axon. All inputs are summated at the soma (cell body). If there is enough excitation then an action potential is generated at the axon hillock.

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10
Q

What are the processes at the chemical synapses?

A
  1. Action potential travels down the axon
  2. When it gets to the synapse, depolarisation opens voltage-dependent calcium channels
  3. Influx of calcium leads to neurotransmitter release
  4. Neurotransmitter binds to and activates receptors on the dendrites of the postsynaptic cell
  5. This leads to depolarisation or hyperpolarisation of the postsynaptic cells.
  6. This spreads to the postsynaptic soma, where summation occurs.
  7. If there is enough depolarisation, then an action potential is generated at the axon hillock.
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11
Q

What are neurotransmitters?

A

A chemical that is used to transmit information from the presynaptic neuron to the postsynaptic neuron.

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12
Q

What is the criteria for a neurotransmitter?

A
  1. Chemical synthesised presynaptically.
  2. Electrical stimulation leads to the release of the chemical.
  3. Chemical produces physiological effect e.g. switch on or off the neuron.
  4. Terminate activity.
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13
Q

What is Dales Law

A

If a particular neurotransmitter is released by one of a neuron’s synaptic endings, the same chemical is released at all synaptic ending of that neuron.
(But the dendritic field can receive signals from multiple transmitters).

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14
Q

What happens during neurotransmitter release?

A
  1. Synaptic vesicle containing neurotransmitter ‘docked’ at the synaptic membrane
  2. Depolarisation of the presynaptic neurone leads to the opening of
    calcium channels and calcium influx (concentration gradient)
  3. Vesicles fuse with the synaptic membrane and releases neurotransmitter
    into the synapse
  4. Vesicle detaches from the docking zone
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15
Q

What is the postsynaptic action of the neurotransmitter?

A

Neurotransmitter binds to receptors on the postsynaptic membrane, which affects the activity of the postsynaptic cell. The configuration of the receptors make them specific for different neurotransmitters.
Ionotropic receptor - opening of an ionic channel, e.g. sodium and potassium channel.
Metabotropic receptor - Activates an internal 2nd messenger systems that goes on to affect the functioning of the postsynaptic cells. Produces an amplified signal.

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16
Q

What are ionotropic receptors?

A

Fast transmission - ion movement leads to an immediate change in the postsynaptic cell.
Excitatory fast transmission:
Ion channel opens
Movement of positive ions into the neurone (Na+)
(e.g. Glutamate receptors)
Depolarisation
Excitatory post synaptic potential (EPSP)
Inhibitory fast transmission:
Ion channel opens
Movement of negative ions into the neurone (Cl-)
(e.g. GABAA receptors)
Hyperpolarisation
Inhibitory post synaptic potential (IPSP).

17
Q

What is a metabotropic receptor?

A

Allows neurotransmitters to bind, and attaches G-protein.

  1. Neurotransmitter binds to receptor and activates the G-protein (exchange GDP for GTP).
  2. G protein splits and activates other enzymes.
  3. The breakdown of GTP turns off G protein activity.
  4. Series of chemical reactions that leads to an amplification of the signal – second messenger system.
18
Q

What is amplification?

A

Size of AP. G-rpotein activation is slower, but has a larger effect.

19
Q

What is neurotransmitter deactivation?

A

Neurotransmitters must be inactivated after use to remove them from the synaptic cleft. Something needs to stop it to prevent too much signalling - this is done by either deactivating enzymes or reuptake.

20
Q

What is glutamate?

A

Major fast excitatory neurotransmitter in the CNA. Very widespread through the CNA. If don’t have glutamate, won’t be able to turn on any neurotransmitters. Many neurons in the cortex have glutamate receptors - all excitatory.

21
Q

What is involved in normal neuronal transmission of glutamate?

A

Presynaptic release of glutamate leads to postsynaptic activation of AMPA receptors, which leads to an influx of Na+, which leads to depolarisation (EPSP).
This is involved in learning and memory processes.

22
Q

How can EPSPs (excitatory postsynaptic potential) be boosted?

A

EPSPs can be boosted by two ways: spatial and temporal. Spatial is done location wise, temporal is done time wise.

23
Q

What is GABA?

A

GABA = (gamma aminobutyric acid). Major inhibitory neurotransmitter. Activates an ionotropic receptor (GABAA receptor) which opens a chloride channel (Cl-) leading to hyperpolarisation (IPSP).
If GABA binds chloride comes in, and then you get an inhibition.

24
Q

What drugs/hormones enhance GABA’s function?

A

-ethanol (alcohol) binds to GABA a receptor.
-neurosteroids
-benzodiazepine
-barbiturate
Involved in anxiety.

25
Q

What is the interaction of excitatory and inhibitory inputs in neural integration?

A

EPSP decays over the length of the dendrite. Synapses close to the soma have a greater influence as there is less opportunity for the signal to decay. EPSP can be decreased or abolished by IPSPs from inhibitory neurons that are active at the same time or can be enhanced by EPSPs from excitatory neurons that are active at the same time.
Neural integration = all processes happen at the same time, and signals have to be inhibited.

26
Q

What are auto receptors?

A

Part of a negative feedback mechanism - can self-regulate. Prevent neurotransmitters from being released. Help regulate neurotransmission. Respond to neurotransmitters in the synaptic cleft, and are located on the presynaptic terminal.

27
Q

How is neuronal communication controlled?

A

At the level of the neurotransmitter: different types of neurotransmitters.
At the receptor: types of receptors, modulatory binding sites on the receptor.
At the synapse: auto receptors (presynaptic).
At the individual neuron: neuronal integration (EPSP/IPSP), neuromodulation.