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Principles of Med Neuroscience > L.7 > Flashcards

L.7 Flashcards

1
Q

What are the 2 main types of synapses

A

electrical and chemical

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2
Q

Name 5 features of chemical synapses

A
  • unidirectional
  • majority (most common)
  • complex structure
  • slower
  • amplification
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3
Q

Why do chemical synapses have complex structures

A

they need vesicles, receptors & neurotransmitters

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4
Q

Why do chemical synapses have slower transmission

A

there is a synaptic delay because neurotransmitters need to be released and then bind to receptors

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5
Q

Name 5 features electrical synapses

A
  • bidirectional
  • minority
  • simpler structure
  • faster
  • no amplification
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6
Q

What does axodendritic mean

A

axon connects to dendrite of post-synaptic neuron

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7
Q

What does axosomatic mean

A

axon connects to soma of post-synaptic neuron

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8
Q

What does axoaxonic mean

A

axon connects to axon of post-synaptic neuron

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9
Q

TRUE or FALSE: axosomatic gives the most power signal between the 3 types

A

FALSE
- axoaxonic because the closer the axon connect to axon (post-synaptic) = more powerful signal is going to be

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10
Q

What is a synaptic button/terminal

A

where NTs are released

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11
Q

What is the function of the cytoskeleton in chemical synapses

A
  • keeps vesicles in place
  • maintains structure of synaptic button
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12
Q

Why are there mitochondria in chemical synapses

A

provides energy for NT release ad vesicle recycling

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13
Q

What is the active zone in chemical synapses

A

where synaptic vesicles dock and release NTs into synaptic cleft

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14
Q

What is the synaptic cleft

A

gap between post and pre-synaptic neurons where NTs are released

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15
Q

What is a neuromuscular junction

A

synapses between motor neuron and muscle fibre

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16
Q

What are the features of neurotransmitters

A
  • needs to be synthesised in neurons
  • it needs to mimic the action endogenously released transmitter
  • needs to be a specific mechanism for removing chemical from synaptic cleft
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17
Q

What is the effect of an excitatory neurotransmitter

A
  • depolarises membrane
  • neuron more likely to fire action potential
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18
Q

What is the effect of inhibitory neurotransmitter

A
  • (hyper)repolarises membrane
  • neuron less likely to fire action potential
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19
Q

What initiates vesicle release in the presynaptic terminal?

A
  • An action potential
  • opening Ca²⁺ channels, allowing Ca²⁺ to influx
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20
Q

What happens when Ca²⁺ binds to calmodulin?

A

It forms a Ca²⁺-calmodulin complex that activates CAMKII

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21
Q

What does CAMKII phosphorylate during vesicle release

A

CAMKII phosphorylates synapsin

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22
Q

What is the effect of phosphorylating synapsin?

A

It causes the release of vesicles from the cytoskeleton

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23
Q

What occurs after vesicles are released from the cytoskeleton?

A

The vesicles dock to the active zone

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24
Q

How is vesicle membrane recovered after neurotransmitter release?

A

endocytosis

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25
Q

What happens to vesicles after they are recovered?

A

They are refilled with NTs

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26
Q

What is the role of SNARE proteins

A

essential for vesicle fusion

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27
Q

How do toxins affect synaptic transmission?

A

They cleave SNARE proteins, disrupting synaptic transmission

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28
Q

What is the effect of BoTX on neurotransmitter release?

A

prevents release of Ach causing decreased/blocked muscle contraction

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29
Q

What does TeTX block in the nervous system?

A

blocks release inhibitory NTs, decreasing interneuron activity

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30
Q

What is the effect of Latrotoxin on neurotransmitter release?

A

triggers excessive vesicle fusion, causing NT depletion

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31
Q

What condition can cause impaired vesicle recycling?

A

Congenital myasthenic syndromes.

32
Q

What channels are attacked in LEMS?

A

Pre-synaptic Ca²⁺ channels

33
Q

How do cognitive disorders affect synaptic communication?

A

impair trans-synaptic signalling (NT flow in the synaptic cleft)

34
Q

How do Botulinum and Tetanus toxins affect vesicle fusion?

A

They disrupt SNARE proteins, preventing neurotransmitter release

35
Q

What powers vesicular transporters in synaptic vesicles?

A

A proton (H⁺) gradient created by ATPase pumping H⁺ into vesicles.

36
Q

How does a proton gradient aid vesicular transport?

A
  • It increases acidity inside the vesicles
  • transporters use the energy from H+ gradient to carry molecules into the vesicles
37
Q

What drives plasma membrane transporters?

A

electrochemical gradient

38
Q

What enzyme maintains the electrochemical gradient across the plasma membrane?

A

Na⁺/K⁺ ATPase

39
Q

What are the three components of the tri-partite synapse?

A
  • Pre-synaptic neuron
  • post-synaptic neuron
  • astrocyte (glial cell).
40
Q

How do astrocytes participate in synaptic plasticity?

A
  • synapse formation/elimination
  • involved in learning and memory.
41
Q

What is reactive gliosis, and when does it occur?

A

It’s a glial response to injury, where glial cells become reactive.

42
Q

What are the categories of neurotransmitters

A
  • amino acids
  • monoamines
  • neuropeptides
43
Q

Where are amino acid neurotransmitters synthesised?

A

pre-synaptic terminal

44
Q

Where are monoamines stored

A

Stored in synaptic vesicles

45
Q

Where are neuropeptides synthesised

A

cell soma

46
Q

Where are neuropeptides stored

A

secretory granules

47
Q

What are the names of the main excitatory and inhibitory neurotransmitters

A

excitatory = glutamate
inhibitory = GABA (and glycine)

48
Q

Where is serotonin produced

A

Raphe nuclei (brainstem)

49
Q

What does serotonin regulate

A

mood, sleep, emotion & appetite

50
Q

What is a special feature of serotonin neurons

A

they have a large outreach (1 neurons contact 100 000 other neurons)

51
Q

How is glutamate stored in vesicles

A

by vesicular glutamate transporters (VGLUT)

52
Q

How is glutamate reabsorbed and recycled

A
  1. reabsorbed by excitatory amino acid transporters in pre-synaptic cell
  2. glial cells convert glutamate into glutamine
  3. glutamine is converted to glutamate (in nerve terminals)
53
Q

How is glutamate synthesised

A
  • from glucose in Krebs cycle
  • glutamine is converted to glutamate by glutaminase
54
Q

How is GABA synthesised

A

it is synthesised from glutamate by glutamic acid decarboxylase

55
Q

How is GABA stored

A

stored in vesicles by vesicular GABA transporter

56
Q

How is GABA cleared from the synaptic cleft?

A

Through reuptake mechanisms by transporters on glial cells and both GABAergic and non-GABAergic neurons

57
Q

TRUE or FALSE: a higher proportion of GABA is synthesised to novo rather than recycling

A

TRUE

58
Q

What happens to the electrochemical gradient during cerebral ischemia?

A
  • metabolic events maintaining gradient are disrupted
  • Na+/K+ gradient reverses –> releasing glutamate
  • Excessive calcium release causes excitotoxic cell death
59
Q

What is GHB?

A

a metabolite of GABA that can be converted back to GABA

60
Q

how does GHB affect GABA levels?

A

It increases the GABA levels

61
Q

What happens if there is an excess of GHB

A

unconsciousness and coma

62
Q

How do neuropeptides differ from small molecule neurotransmitters?

A
  • mediate slow transmission
  • differ in their synthesis and release methods
  • short polypetide chains
63
Q

how do soluble gases function as neurotransmitters?

A

They act quickly in the synaptic environment

64
Q

What is retrograde signalling by soluble gases?

A
  • Soluble gases are released from post-synaptic neurons
  • They diffuse back to pre-synaptic neurons, influencing neurotransmitter release
65
Q

What are endocannabinoids

A

active component of marijuana

66
Q

what effect do endocannabinoids have?

A

reduce GABA release

67
Q

What are the 4 main types of neurotransmitters?

A
  • amino acids
  • monoamine
  • acetylcholine
  • neuropeptides
68
Q

What are the two main types of post-synaptic receptors?

A

ionotropic & metabotropic

69
Q

How do ionotropic receptors work?

A
  1. NT bind to receptor to open it
  2. receptor changes conformation and ions flow through
70
Q

Which one has faster transmission: ionotropic or metabotropic

A

ionotropic

71
Q

How do metabotropic receptors work?

A

They transduce signals (relay signal from outside the cell to inside the cell) via activation of a G-protein triggering a series of intracellular events

72
Q

What is the difference between ionotropic and metabotropic receptors?

A
  • ionotropic: faster
  • metabotropic: longer lasting effects
73
Q

What does an antagonist do

A

blocks the normal activity of a neurotransmitter, preventing its effect

74
Q

What is the role of an agonist

A

enhances the effect of a neurotransmitter by mimicking or increasing its action

75
Q

How does kinetics affect neurotransmitter function?

A

how fast neurotransmitters bind to a receptor, which determines the duration of their effect

76
Q

What does selectivity in receptors mean?

A

refers to which ions (e.g., Na+, Cl-) pass through the receptor channels

77
Q

What is conductance in receptor function?

A

how quickly ions flow through the receptor, which determines the magnitude of the effect

Principles of Med Neuroscience (6 decks)

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