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NEUR201 > Module 2 > Flashcards

Module 2 Flashcards

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1
Q

What are the 5 key molecular steps that underpin learning and memory?

A
  1. Neurotransmitter release
  2. Activation of postsynaptic receptors
  3. Trafficking of receptors of the PSD
  4. Local translation of proteins
  5. Altered gene expression
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2
Q

What is the main difference between chemical and electrical synapses?

A
  • Chemical use neurotransmitters
  • Electrical use gap junctions for direct ionic current flow
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3
Q

What are small synaptic vesicles?

A
  • ~50nm, electron lucent
  • Found at chemical synapses
  • Contain classical neurotransmitters (glutamate, GABA)
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4
Q

What are large dense core vesicles?

A
  • ~100nm, electron dense
  • Contain neuropeptides, neurotrophins, catecholamines
  • Released slowly
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5
Q

Where are large dense core vesicles primarily found?

A
  • Peripheral nervous system
  • Hypothalamus
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6
Q

What is the tripartite synapse?

A

Synapse model
1. Presynaptic terminal
2. Postsynaptic region
3. Astrocyte processes regulating transmission

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7
Q

How are neuropeptides in LDCVs synthesised and processed?

A
  1. Synthesised in RER
  2. Modified in Golgi
  3. Packaged and transported
  4. Pro-peptides are cleaved
  5. Released and slowly recycled
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8
Q

What roles do LDCVs play in the CNS?

A

Modulate or synchronise activity via GPCRs or tyrosine kinase receptors

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9
Q

What are some molecules released by LDCVs?

A
  • Adrenaline, noradrenaline
  • Neuropeptide Y, Brain derived neurotrophic factor
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10
Q

What is the importance of receptor trafficking to the PSD in memory?

A

Strengthens synaptic connections, allowing long term changes in signalling - key process in memory formation

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11
Q

What triggers neurotransmitter release at the presynaptic terminal?

A

An action potential opens voltage gated calcium channels, causing calcium influx that triggers exocytosis`

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12
Q

What are SNARE proteins and their role in exocytosis?

A

SNAREs mediate vesicle docking and fusion. v-SNARE pairs with t-SNAREs

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13
Q

What is the synaptotagmin and its role?

A

It is a calcium sensor on synaptic vesicles that triggers fusion upon calcium influx`

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14
Q

What are the three pools of synaptic vesicles?

A
  • Readily releasable
  • Reserve
  • Recycling
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14
Q

What is the function of Rab proteins in exocytosis?

A

Assist in vesicle translocation and docking at the presynaptic membrane

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15
Q

Where are synaptic vesicles formed?

A

Golgi apparatus, then transported to axon terminals

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16
Q

How are neurotransmitters loaded into vesicles?

A

Vesicular transporters using a proton gradient

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17
Q

What is full collapse fusion?

A

Mode of exocytosis where the vesicle fully merges with the membrane and releases all content

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18
Q

What is kiss and run fusion?

A

Brief vesicle fusion where the pore opens and closes, releasing only part of the content

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19
Q

What is the role of clathrin in endocytosis?

A

Forms a coated pit that helps retrieve vesicle membrane from the plasma membrane

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20
Q

What does dynamin do during endocytosis?

A

A GTPase that pinches off the forming vesicle by wrapping around its neck

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21
Q

What ensures fast neurotransmitter release at synapses?

A

Close proximity of vesicles to calcium channels, pre docked vesicles and fast calcium triggered fusion via SNAREs

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22
Q

Why is endocytosis essential in the synaptic vesicle cycle?

A

Recycles vesicle membrane to maintain neurotransmission during sustained activity

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23
Q

What is the synaptic vesicle cycle?

A

Docking → Priming → Fusion (exocytosis) → Recycling (endocytosis) of synaptic vesicles at presynaptic terminal

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24
How does an action potential trigger neurotransmitter release?
Opens voltage gated calcium channels → Calcium influx activates SNARE-mediated vesicle fusion and neurotransmitter release
25
How does Botulinum toxin block neurotransmission?
Cleaves SNAP25 or synaptobrevin, preventing synaptic vesicle fusion and acetylcholine release, causing paralysis
26
How does tetanus toxin differ from botulinum toxin?
Targets inhibitory neurons, cleaving synaptobrevin and blocking inhibitory neurotransmitter release, causing muscle rigidity
27
How does α-latrotoxin affect neurotransmitter release?
It forms Ca²⁺ pores via neurexin binding and activates intracellular signalling, triggering massive exocytosis
28
What is synapsin and why is it important?
A phosphoprotein that tethers vesicles to the actin cytoskeleton - phosphorylation releases vesicles from the reserve pool for exocytosis.
29
How does CaMKII regulate synapsin function?
Ca²⁺ activates CaMKII, which phosphorylates synapsin, detaching vesicles from actin and making them available for release.
30
What are the consequences of impaired synapsin function?
Reduced vesicle availability, faster synaptic fatigue, and neurological disorders like epilepsy and schizophrenia.
31
Why is knowledge of presynaptic mechanisms clinically relevant?
A: It helps explain effects of neurotoxins, disease pathogenesis, and pharmacological targets in disorders like epilepsy and schizophrenia.
32
What is a neurotransmitter?
a chemical messenger that transmits signals between neurons or from neurons to muscles, typically across a synaptic cleft
33
What are the four main classes of neurotransmitters?
1. Amino acids (glutamate, GABA) 2. Amines and purines (dopamine, acetylcholine) 3. Neuropeptides (substance P) 4. Gases (NO, CO)
34
What are the criteria for identifying a neurotransmitter?
1. Present in the brain 2. Stored in synaptic vesicles 3. Synthesized by specific enzymes 4. Released upon depolarization 5. Binds specific receptors 6. Mimicked/inhibited by drugs 7. Has uptake/metabolism mechanisms
35
What type of transmitter is dopamine and how is it synthesised?
It's a TYPE II amine neurotransmitter, synthesised from tyrosine via the enzyme tyrosine hydroxylase forming L-DOPA then dopamine
36
How does dopamine signalling end?
Dopamine is taken up by dopamine transporters (DAT) and broken down by monoamine oxidase (MAO)
37
What are dopamine receptors and what type are they?
They are GPCRs, including D1 and D2 which initiate intracellular signalling cascades
38
How is dopamine invloved in parkinsons disease?
Loss of dopiminergic neurons in the substantia nigra leads to movement defects typical of parkinsons disease
39
How do drugs like L-DOPA and haloperidol interact with dopamine?
L-DOPA - dopamine precursor used to treat parkinsons Haloperidol - D2 receptor antagonist used to treat schizophrenia
40
How to stimulants like cocaine affect dopamine?
They block dopamine reuptake, increasing its synaptic presence, which enhances euphoria and alertness
41
Q: What role does α-synuclein play in dopamine-related disorders?
It regulates dopamine release and vesicle fusion. Toxic aggregates (Lewy bodies) of α-synuclein contribute to Parkinson’s disease.
42
What are the three major classes of neurotransmitter receptors?
GPCRs, Enzyme linked and ion channels
43
What determines the effect of a neurotransmitter?
The type and location of the receptor it binds to
44
What are GPCRs and how do they signal?
Metabotropic receptors that activate G-proteins, which dissociate into Ga and GBy to modulate second messenger systems
45
Are GPCRs fast or slow acting
Slow
46
What is the effect of D-like dopamine receptors?
Excitatory - stimulate adenylyl cyclae via Gs proteins
47
What is the effect of D2-like dopamine receptors?
Inhibitory - inhibit adenylyl cyclase via Gi/Go proteins
48
What type of receptor is the GABA-A receptor and what is its effect?
Ionotropic chloride channel - causes hyperpolarisation and inhibition (IPSP)
49
What type of receptor is the GABA-B receptor?
Metabotropic GPCR - slow inhibitory signalling
50
What enhances GABA-A receptor function?
Benszodiazepines, ethanol, barbiturates and neurosteroids
51
What are the two main types of acetlycholine receptors?
Nicotinic (ionotropic) and Muscarinic (metabotropic)
52
Where are the nicotine ACh receptors found and what is their role?
A: At the neuromuscular junction - mediate fast synaptic transmission and muscle contraction.
53
What is the TrkB receptor and its ligand?
Enzyme linked receptor tyrosine kinase - binds BDNF
54
What is the role of mature BDNF vs proBDNF?
Mature BDNF promotes survival and LTP - proBDNF promotes apoptosis and LTD
55
What are some long term effects of BDNF-TrkB signalling?
Changes in gene expression, protein synthesis and synaptic plasticity
56
What is the difference between fast and slow neurotransmission?
Fast - ionotropic receptors Slow - metabotropic and enzye linked receptors
57
What is synaptic plasticity?
Acitivity-dependent modification of synaptic strenth - underpins learning and memory
58
What is the difference between habituation and sensitisation in Aplysia?
Habituation - Weakened response due to decreased neurotransmitter release Sensitisation - Enhanced response due to increased neurotransmitter release
59
What reflex is used in Aplysia to model learning and memory?
The siphon gill withdrawal reflex
60
What neurotransmitter mediates presynaptic facilitaion in Apylsia?
Serotonin (5-HT), released by interneuron L29
61
What is the molecular pathway of short term sensitisation in Aplysia?
5-HT → cAMP → PKA → phosphorylation of K⁺ channels → prolonged AP → ↑Ca²⁺ influx → ↑neurotransmitter release.
62
How does long term sensitisation differ from short term in Aplysia?
Long-term involves PKA entering the nucleus → altered gene expression → new proteins → synaptic growth.
63
What role does phosphorylation of K⁺ play in Aplysia sensitisation?
It closes K⁺ channels, prolonging the action potential and enhancing neurotransmitter release
64
What is long term potentiation (LTP) and where is it studied?
A persistent, activity dependent increase in synaptic strenth - studied in the hippocampus of rodents
65
What are the three pathways in the hippocampal trisynaptic circuit?
1. Entorhinal cortex → dentate gyrus (perforant path) 2. Dentate gyrus → CA3 (mossy fibers) 3. CA3 → CA1 (Schaffer collaterals)
66
What molecular changes underlie LTP in the hippocampus?
Increased glutamate receptor sensitivity (e.g. NMDA/AMPA) and changes in gene expression
67
What are the two main types of glutamate receptors?
Ionotropic and metabotropic
68
What ions flow through AMPA receptors when activated?
Na⁺ influx and K⁺ efflux - GluA2-lacking AMPARs also allow Ca²⁺ influx
69
What is required fro NMDA receptor activation?
Binding of glutamate and removal of the MG²⁺ block via depolarisation
70
What does phosphorylation of GLUA1 at SER831 by CaMKII do?
Increases single channel conductance
71
What does phosphorylation of GLUA1 at Ser845 by PKA do?
Enhances open probability and retention at the plasma membrane
72
How do AMPA receptors contribute to synaptic plasticity?
By trafficking to the post synaptic density (PSD), increasing synaptic strength
73
What is lateral mobility in relation to AMPARs?
Movement of AMPARs along the cell surface between synapatic and extra synaptic regions
74
What is the retrograde messenger in LTP?
A signal that travels from the postsynaptic to presynaptic cell (like nitric oxide)
75
How is NO synthesised and what does it do?
Synthesised on demand by neuronal nitric oxide synthase (nNOS) - diffuses to enhance presynaptic glutamate release
76
Where does local protein synthesis occur during LTP?
Dendritic spines, using mRNA and polyribosomes already present in dendrites
77
How does BDNF affect local protein synthesis?
Enhances it, contributing to long term synaptic changes
78
What transcription factor is activated for long term LTP maintenance?
CREB (cAMP response element binding protein)
79
What triggers CREB activation in LTP?
Elevated cAMP levels and calcium influx through NMDA receptors
80
What structural chance accompanies long term LTP?
Growth of new dendritic spines
81
Q: How does amyloid-β (Aβ) initially affect glutamatergic transmission?
Causes hyper-excitability and excessive glutamate release?
82
How does amyloid-β (Aβ) contribute to synaptic loss?
By promoting NMDA overstimulation and AMPAR endocytosis, disrupting receptor trafficking
83
What are other mechanisms of amyloid-β (Aβ) neurotoxicity?
Disruption of actin dynamics and synaptic adhesion molecules - impairing synaptic integrity

NEUR201 (3 decks)

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