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202 Theme 1: Fundamental Neuroscience and the Brain > L1 Synaptic Transmission > Flashcards

L1 Synaptic Transmission Flashcards

1
Q

What is a synapse?

A

Specialised junction where one part of a neurone contacts another neurone, muscle of glandular cell.

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2
Q

How common are chemical synapses?

A

Majority of synapses in the adult brain are chemical.

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3
Q

How is an electrical synapse different to chemical?

A

Simpler structure and function
Faster
Passive signal transmission (can’t amplify)
Bidirectional

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4
Q

How common are electrical synapses?

A

Minority but common in development and the retina..

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5
Q

What do electrical synapses allow for?

A

Synchronised electrical activity among populations of neurones.

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6
Q

How is a drug different to hormones?

A

Must be exogenously administered rather than released endogenously. Hormones can be drugs when intentionally administered.

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7
Q

What are psychoactive drugs?

A

Cross blood brain barrier and act on the CNS, changing brain function.

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8
Q

What is an axodendritic synapse?

A

Axon of the presynaptic neurone -> dendrite of the postsynaptic neurone.

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9
Q

What is an axosomatic synapse?

A

Axon of the presynaptic neurone -> soma of the postsynaptic neurone.

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10
Q

What is a axoaxonic neurone?

A

Axon of the presynaptic neurone -> Another presynaptic neurone axon -> the postsynaptic neurone

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11
Q

How does location of the synapse affect function?

A 
Axodendritic= many inputs Axosomatic= powerful synaptic weight 
Axoaxonic= may cancel out if one is excitatory and the other is inhibitory (signal integration) to the final target
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12
Q

What is the synaptic bouton?

A

Presynaptic element (axon terminal).

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13
Q

What structures are in the presynaptic terminal?

A

Mitochondria, vesicles, secretory granules (chemicals), cytoskeleton.

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14
Q

What is the active zone?

A

Membrane differentiations of the pre and postsynaptic terminals, allowing communication.

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15
Q

What is the synaptic cleft?

A

Gap between the active zone and the postsynaptic densitY. Larger in chemical synapses.

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16
Q

How does a neuromuscular junction differ in structure from a chemical synapse?

A

The postsynaptic membrane is called the motor end plate and contains folds to increase SA.

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17
Q

What is direct neurotransmission?

A

Excitatory or inhibitory, the membrane of the next cell is either slight hyper or depolarised.
On or off switch.

18
Q

What is neuromodulation?

A

Alters the presynaptic cell’s ability to release more NT or the postsynaptic cell’s ability to respond.
Wide range of possibilities.

19
Q

Why is neuromodulation important?

A

Development, learning and memory, allowing for changes to synapses as they are created or removed when no longer used.

20
Q

What defines a neurotransmitter?

A

Synthesised in neurone
Released from presynaptic terminal in an amount enough to cause a defined effect on a postsynaptic neurone/organ
Exogenously administered drug mimics endogenous NT
Specific mechanism to remove from cleft

21
Q

How is a chemical synapse transmission signalled?

A

AP depolarises the presynaptic terminal and opens voltage gated Ca2+ channels.

22
Q

How does Ca2+ affect vesicles?

A

Causes vesicles to fuse with the presynaptic membrane, releasing the NT.

23
Q

How does the neurotransmitter affect the postsynaptic membrane?

A

Binds to receptors and either opens or closes channels causing an excitatory or inhibitory current that changes excitability of the cell.

24
Q

How is neurotransmitter removed from the cleft?

A

Glial uptake or enzymatic degradation.

25
Q

How are vesicles anchored?

A

In pools above the AZ, to the cytoskeleton by synapsin.

26
Q

How are vesicles released?

A

Ca2+ influx activates Calcium calmodulin activated kinase II (CaMKII) which phosphorylates synapsin. P-synapsin can no longer bind to the cytoskeleton.

27
Q

What are SNARE complexes?

A

Allow vesicles to fuse and communicate with the membrane, NT can’t be released without.

28
Q

What are the two types of SNARE?

A

v-SNARE: vesicle
t-SNARE: target
They come together to allow exocytosis of the NT.

29
Q

What catalyses membrane fusion?

A

Ca2+ binding to synaptotagmin which then binds to the SNAREs and plasma membrane.

30
Q

How are vesicles recycled?

A

The membrane is rapidly recovered by endocytosis, new vesicles bud off and are refilled with the NT.

31
Q

What is priming?

A

Docked vesicles are not ready for fusion as the SNARE complexes must be assembled to allow rapid response to Ca2+ concentration.

32
Q

What is the affect of Botulinum?

A

Proteolysis of amino acids in SNARE prevents neuromuscular transmission of acetylcholine causing constant relaxation and paralysis.

33
Q

What is the affect of Tetanus?

A

Proteolysis of AAs in SNARE preventing the release of inhibitory GABA and Gly in interneurones at the spinal cord. This causes permanent muscle contraction due to dis-inhibition of cholinergic neurones.

34
Q

What diseases affect the presynaptic terminal?

A

Congenital myasthenia syndromes: imparted vesicle recycling
Latrotoxin: extreme and constant vesicle fusion (similar to Botox and Tet)
Cognitive disorders: impair transsynaptic signalling
LEMS: attacks presynaptic Ca2+ channels

35
Q

What are vesicular transporters?

A

Powered by proton gradient, ATPase proton pump loads vesicles with H+ making them acidic and then are traded with glutamate (counter transport).
Mainly allow transport into the vesicles.

36
Q

What are plasma membrane transporters?

A

Powered by electrochemical gradient, Glutamate is co-transported with Na+ as there’s a higher conc outside.
Mainly allow transport into the presynaptic terminal.

37
Q

What do membrane transporters mainly transport?

A

Amino acids, amines and acetylcholine.

38
Q

What site allows the action of a number of drugs?

A

Membrane transporters.

39
Q

What are astrocytes?

A

A form of glial cell that wrap around synapses that receive the NT, causing as Ca2+ increase and release their own NT that can enhance or inhibit synaptic activity.
Tri-partite synapse.

40
Q

Why are glia important?

A

Control synapse formation, function, plasticity and elimination. Crucial during development, learning, memory and disease.

41
Q

Which diseases are glia linked to?

A

Reactive gloss following an injury (CNS regeneration potential)
Aberrant synapse formation (epilepsy and neuropathic pain)
Brain cancer
HIV-induced dementia
Neuroinflammatory response of depression
Neurodegenerative diseases (Alzheimer’s, glaucoma, prion disease) through aberrant synaptic stripping

202 Theme 1: Fundamental Neuroscience and the Brain (6 decks)

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