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Neurology (BRS) > Neurotransmission and pharmacology > Flashcards

Neurotransmission and pharmacology Flashcards

1
Q

What does information transfer across the synapse require?

A
  1. Release of neurotransmitters
  2. Interaction with postsynaptic receptors
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2
Q

4 key features of nervous transmission

A
  1. Rapid timescale
  2. Diversity (variety of NTs)
  3. Plasticity (the more often a signal is recieved, the stronger it gets)
  4. Learning and memory
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3
Q

In what time frame do APs happen?

A

milliseconds

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4
Q

What is the difference between electrical and chemical neurotransmission?

A

Electrical → neurons connected by gap junctions e.g. between two dendrites coming together

Chemical → neurotransmitters released across a synapse

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5
Q

How big is the synaptic cleft?

A

20 -100nm

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6
Q

3 stages of synaptic transmission

A
  1. Biosynthesis → packing and release of NT
  2. Receptor action
  3. Inactivation (deagradation/removal of NT)
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7
Q

What are the main types of NTs?

A
  1. Amino acids
  2. Amines
  3. Neuropeptides
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8
Q

Examples of amine NTs

A

Noradrenaline NA, Dopamine DA

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9
Q

Examples of amino acid NTs

A

Glutamate, GABA [gamma-aminobutyric acid], glycine

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10
Q

Examples of neuropeptide NTs

A

Opioid peptides

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11
Q

How quick are the effects NTs mediate?

A

May mediate rapid (micro to milliseconds) or slower effects (secs)

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12
Q

How abundant are NTs in CNS tissues?

A

from nM to mM conc-wise

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13
Q

How much of an increase in intracellular [Ca 2+] is required for transmitter release?

A

200mM

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14
Q

How quick is synaptic transmission?

A

Fast within ms

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15
Q

How many NT molecules are there per SV?

A

4 to 10 thousand molecules

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16
Q

What is synaptic transmission restricted to?

A

The synapse

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17
Q

Main steps of typical synaptic transmission in the CNS

A
  1. AP arrives at presynapic terminal
  2. Depolarisaion => VGCCs open
  3. Ca 2+ influx
  4. Vesicle exocytosis + NT release
  5. NT binds to receptors (on ion channels in postsynaptic membrane) => Na+ influx
  6. Reuptake of NTs
  7. NT repackaged into vesicles for further use
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18
Q

Activation of transmitter release…. [2]

A
  1. Calcium dependent
  2. Requires RAPID transduction
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19
Q

Detailed steps of NT release

A
  1. SVs are filled with NT and docked in the synaptic zone (presynaptic membrane)
  2. SVs are primed with special protein complex formation between vesicles, presynaptic membrane and cytoplasm proteins
  3. Rapid response to Ca 2+ entry ⇒ vesicle fusion and exocytosis
  4. ATP and vesicle recycling
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20
Q

From the diagram, key terms for vesicle formation, exocytosis and recycling

A
  1. Endosome budding
  2. Docking (following Ca2+ influx)
  3. Priming
  4. Fusion (exocytosis)
  5. Budding (endocytosis)
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21
Q

What are the main targets of neurotoxins?

A

Vesicular proteins

22
Q

What are the main targets of neurotoxins?

A

Vesicular proteins

23
Q

What does the venom of Black Widow spiders do?

A

Alpha latrotoxin activates Ca 2+ channels, causing massive NT release

24
Q

What are the physiological effects of alpha latrotoxin?

A

Massive muscle cramping, anxiety and overload

25
Q

What does the product of C. botulinum do?

A

Botulinum toxin interferes with vesicle exocytosis, causing v. little NT release

26
Q

What are the physiological effects of the botulinum toxin?

A

Paralysis, death by asphyxiation

27
Q

What is NT action defined by?

A

Receptor kinetics

28
Q

Two main types of NT receptors

A
  1. Ion channel linked receptors
  2. G protein coupled receptors
29
Q

Compare the speed of the response with ion channel linked and G protein coupled receptors

A

Ion channel linked ⇒ Fast response (msecs)
G protein coupled ⇒ Slow response (secs/mins)

30
Q

Key features of G-protein coupled receptors

A
  1. Slower response
  2. More adapatable physiology due to multiple steps
31
Q

What are the effectors for G protein coupled receptors?

A

Enzymes e.g. adenylyl cyclase, phospholipase C, cGMP-PDE
Channels (Ca 2+ or K+)

32
Q

Key features of ion channel linked receptor

A
  1. Rapid activation (micro to milli secs)
  2. Rapid info flow, mediating all fast excitatory or inhibitory transmission
  3. Multiple subunit combos of the same receptor in different parts of the brain ⇒ distinct functional properties
33
Q

Examples of ion channel linked receptors

A

CNS ⇒ GABAR, GlyR
NMJ ⇒ nACHR

34
Q

Examples of G protein coupled receptors

A

CNS & PNS ⇒ ACh at muscarinic receptors
DA, NA, serotonin [5HT], neuropeptides e.g. enkephalin

35
Q

What does a NT binding to an excitatory NT receptor cause?

A

Positive ion influx ⇒ depolarisation

36
Q

What does a NT binding to an inhibitory NT receptor cause?

A

Negative ion influx ⇒ hyperpolarisation

37
Q

What are 2 types of glutamate receptors found at most glutamate synapses?

A

AMPA receptors
NMDA receptors

38
Q

What do both glutamate receptors require?

A

Glycine as co-agonist

39
Q

AMPA receptors

A

Na+ ion channel linked receptor
⇒ Majority of FAST excitatory synapses
⇒ Rapid onset, offset and desensitisation

40
Q

NMDA receptors

A

Na+ ion channel linked receptor with Ca 2+ as second messenger
⇒ SLOW component of excitatory transmission

41
Q

Describe an excitatory GLUTAMATE synapse

A
  1. Glutamate synthesised from glucose via TCA cycle and transamination
  2. Glutamate reversibly binds to postsynaptic receptors linked to ion channels
  3. Rapid uptake of glutamate by excitatory AA transporters [EAATs] into presynaptic cell and glial cells
  4. Glutamate enzymatically modified by glutamine synthetase into glutamine in glial cells
42
Q

What protein is responsible for the rapid uptake of glutamate?

A

Excitatory amino acid transporters EAATs

43
Q

How is glutamate synthesised in the first place?

A

Glutamate synthesised from glucose via TCA cycle and transamination

44
Q

What enzyme modifies glutamate into glutamine in glial cells?

A

Glutamine synthetase

45
Q

Describe an inhibitory GABA synapse

A
  1. GABA synthesised by decarboxylation of glutamate by glutamic acid decarboxylase GAD
  2. GABA reversibly binds post-synaptic receptors linked to ion channels
  3. Rapid uptake of GABA by GABA transporters GATs
  4. GABA enzymatically modified by GABA transaminase (GABA-T) to succinic semialdehyde SSA (glial cells and GABA nerve terminals)
46
Q

What protein is responsible for rapid uptake of GABA?

A

GABA transporters GATs

47
Q

What enzyme modifies GABA to succinic smeialdehyde SSA?

A

GABA transaminase GABA-T

48
Q

How is GABA synthesised in the first place?

A

Decarboxylation of glutamate by glutamic acid decarboxylase GAD

49
Q

How can seizures be measured?

A

Electroencephalography EEG → measuring electrical activity in the brain

50
Q

What might cause the abnormal cell firing that leads to seizures?

A

Excess glutamate in the synapse e.g. due to a reduction in glutamine synthetase sometimes seen in head injury

51
Q

What is epilepsy characterised by?

A

Recurrent seizures due to abnormal neuronal excitability

52
Q

Symptoms of epilepsy [6]

A
  • Loss of consciousness
  • Anxiety
  • Weakness
  • Staring
  • Contraction and jerking of muscles
  • Confused speech

Neurology (BRS) (12 decks)

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