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LCRS-Neuroscience > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

what are some properties of synaptic transmission?

A
  • Rapid timescale:
  • diversity
  • adaptability
  • plasticity: synapse changes with experience
  • learning and memory
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2
Q

Features of a neurone

A
  • Spine are protrusions from dendrites (information receptor)
  • Soma: cell body. All the integration. Can modify all the integration
  • axon: transmits action potential to the nerve terminal. Communication between cells-neurotransmitter release.
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3
Q

Where does integration of the signals coming down the dendrites occur?

A

In the soma

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4
Q

What is the width of a synaptic cleft?

A

20-100nm wide

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5
Q

Where is the action potential generated?

A

Axon hillock

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6
Q

Why are there lots of mitochondria in the axon terminal?

A

Energy is required to release neurotransmitter

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7
Q

Describe the process of neurotransmission

A
  • Action potential comes along
  • Activates calcium channels
  • Calcium enters the nerve terminal
  • Exocytosis of the neurotransmitter contained in the vesicle
  • Diffuses across the synaptic cleft and binds to receptors on the postsynaptic neuron
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8
Q

How is a neurotransmitter removed from the synaptic cleft?

A
  • This is done by transporters (for amino acid transmitters)
  • These take amino acids back into the terminal
  • Other transporters take it back into the synaptic cleft
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9
Q

What are the three classes of neurotransmitter? Give examples.

A
  1. Amino Acids e.g. glutamate, GABA, glycine
  2. Amines e.g. noradrenaline, dopamine
  3. Neuropeptides e.g. opioid peptides
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10
Q

What is the main inhibitory and excitatory neurotransmitter in the CNS

A

Excitatory- Glutamate

inhibitory- GABA

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11
Q

Describe the process of synaptic transmission.

A

The vesicles dock on the pre-synaptic membrane and await a signal before the contents of the vesicles are expelled into the synaptic cleft.

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12
Q

Where are the vesicles present in the presynaptic synapse?

A
  • Some vesicles are docked in the active zone at the site of the synapse
  • Others are floating in the terminal region
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13
Q

How are the vesicles docked stably?

A
  • There is an interaction between the presynaptic membrane and the vesicle proteins which allows the vesicles to be docked stably
  • Interaction allows a rapid response
  • There are alpha-helical structure which interact together to form a super helix
  • Net effect of this interaction = stable complex of the vesicle at the synapse full of neurotransmitter
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14
Q

What drives the release of the neurotransmitter into the synaptic cleft?

A
  • Vesicle requires a signal for release and the signal is calcium
  • High concentration of calcium channels at the sites of docking of the vesicles
  • Calcium enters through these channels
  • Causes a calcium dependent change in a calcium sensor protein on the vesicle
  • Causes conformational change in the complex
  • Drives release of neurotransmitter
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15
Q

State three toxins that target synaptic vesicle proteins and the effects that they have

A

Tetanus

  • causes spastic paralysis
  • has zinc-dependent endopeptidases that inhibit transmitter release

Botulinum
- causes flaccid paralysis

Alpha-latrotoxin (from black widow spider)
- prevents recycling of the vesicles and hence releases the transmitter to total depletion

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16
Q

What is required for transmitter release?

A

Docking - transmitter filled vesicles must be docked on the presynaptic membrane

Protein complex formation - between vesicle, membrane and cytoplasmic proteins - this allows vesicle docking and a rapid response to calcium entering the axon terminal

ATP and vesicle recycling

17
Q

What are the two types of receptor and what is the most important difference in their properties?

A
  1. Ion channel receptor
    - Fast (milli seconds)
  2. G-protein coupled receptors
    - Slow (sec/min)
18
Q

What are examples of Ion channel receptors?

A

CNS

  • Glutamate
  • Gamma Amino Butyric Acid (GABA)

Neuromuscular Junction
- Acetylcholine at nicotinic receptors

19
Q

What are examples of G-protein coupled receptors?

A

CNS and PNS

  • Acetylcholine at muscarinic receptors
  • Dopamine
  • Noradrenaline
  • 5-hydroxytryptamine
  • Neuropeptides (e.g. enkephalin)
20
Q

What is the effect of glutamate on the postsynaptic membrane?What is the effect of GABA on the postsynaptic membrane?

A

Glutamate is excitatory - causes influx of Na+

GABA in inhibitory - causes influx of Cl-

21
Q

What are the two main types of glutamate receptors and their properties?

A
  1. AMPA Receptors
    - Responsible for the majority of FAST excitatory synapses
    - Rapid-acting
    - Rapid onset, offset and desensitization
  2. NMDA Receptors
    - Slower acting (despite still being excitatory and fast)
    - Requires two conditions for activation:
  3. Depolarisation of membrane
  4. Glutamate must bind
    - Lets in Ca2+
22
Q

Where is glutamate formed?

A

Glutamate is a product of intermediary metabolism (e.g. glycolysis and TCA cycle)
- Formed from the transamination of alpha-ketoglutarate

23
Q

How is an excitatory synapse mediated by glutamate?

A
  • Interacted with the receptor and causes entry of sodium and calcium through the NMDA receptor
  • Transporters on the presynaptic membrane and on glial cells causes the uptake of glutamate once it has fulfilled its role
24
Q

What is the main transporter of glutamate and where is it found?

A
  • Main transporter is EAAT2 (Excitatory Amino Acid Transporter 2)
  • Found on glial cells and on the presynaptic membrane
25
Q

How is glutamate inactivated in the glial cells?

A
  • Once in glial or in neurons, glutamate is then inactivated by glutamine synthetase to make glutamine by simply adding a mino acid
26
Q

What causes epilepsy?

A

Increased release of glutamate causing hyperexcitability

27
Q

Describe the structure of GABA and state how it is produced

A

GABA has the same structure as Glutamate but with the carboxyl group removed. So GABA is produced from glutamate by the action of GLUTAMIC ACID DECARBOXYLASE (GAD)

28
Q

What transporter takes GABA up into the glial cells?

A

GABA Transporter (GAT)

29
Q

Describe the inactivation of GABA in the glial cells.

A

GABA is converted to SUCCINATE SEMIALDEHYDE by GABA Transaminase

30
Q

Describe how the GABA receptor can be manipulated to create treatments for epilepsy.

A

There are binding sites on the pentameric GABA receptor for

  • benzodiazepines,
  • steroids,
  • barbiturates etc.
  • These sites can be manipulated to facilitate the activity of GABA and produce antiepileptic drugs.

LCRS-Neuroscience (12 decks)

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