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
How are vesicles anchored?
In pools above the AZ, to the cytoskeleton by synapsin.
26
How are vesicles released?
Ca2+ influx activates Calcium calmodulin activated kinase II (CaMKII) which phosphorylates synapsin. P-synapsin can no longer bind to the cytoskeleton.
27
What are SNARE complexes?
Allow vesicles to fuse and communicate with the membrane, NT can't be released without.
28
What are the two types of SNARE?
v-SNARE: vesicle t-SNARE: target They come together to allow exocytosis of the NT.
29
What catalyses membrane fusion?
Ca2+ binding to synaptotagmin which then binds to the SNAREs and plasma membrane.
30
How are vesicles recycled?
The membrane is rapidly recovered by endocytosis, new vesicles bud off and are refilled with the NT.
31
What is priming?
Docked vesicles are not ready for fusion as the SNARE complexes must be assembled to allow rapid response to Ca2+ concentration.
32
What is the affect of Botulinum?
Proteolysis of amino acids in SNARE prevents neuromuscular transmission of acetylcholine causing constant relaxation and paralysis.
33
What is the affect of Tetanus?
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
What diseases affect the presynaptic terminal?
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
What are vesicular transporters?
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
What are plasma membrane transporters?
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
What do membrane transporters mainly transport?
Amino acids, amines and acetylcholine.
38
What site allows the action of a number of drugs?
Membrane transporters.
39
What are astrocytes?
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
Why are glia important?
Control synapse formation, function, plasticity and elimination. Crucial during development, learning, memory and disease.
41
Which diseases are glia linked to?
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