Synapses and the NMJ Flashcards Preview

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Flashcards in Synapses and the NMJ Deck (25)
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1
Q

Whats an electrical synapse

A

Direct contact between two adjacent cells through gap junctions

2
Q

How are electrical synapses formed?

A

Via 6 connexins joining to form 1 connexion which lines up with connexion in adjacent membrane to form pore

3
Q

Where are electrical synapses found? What are their proterties?

A

Found in glial neurone, Glial glial communication
Also between Cardio myocytes

Fastest form of communication
bidirectional
allow synchronous activity between cells

4
Q

What type of synapse is found between two neurones?

A

Chemical Synapse

5
Q

What are the properties of a chemical synapse?

A

no direct contact between neurones
unidirectional transport
uses neurotransmitters
Fast but slower than gap junctions

6
Q

How do chemical synapses work in terms of the presynaptic membrane?
Why is Ca2+ so important?

A

Action potential arrives in synaptic bouton

depolarisation

opening of VG Ca2+ ion channels

Results in secretory vesicle movement and release of NT via exocytosis into the synaptic cleft

NT release is Ca2+ dependant

7
Q

What happens from the release of NT in a chemical synapse?

A

Diffusion across synaptic cleft
binds to specific comp receptor
allostery
opening of ion channels

for excitatory NT = Na+ influx and depolarisation

For inhibitory NT= Cl- influx and hyperpolarisation

8
Q

How is the message form a chemical synapse terminated?

A

Dependant on NT either:
Enzymatic breakdown
Reuptake of NT

9
Q

How do excitatory ionotropic receptors work?

A

Nt binds usually 2 molecules
conformational change
channel opening
Na+ influx
Depolarisation
generation of a small excitatory postsynaptic potential (EPSP)
If threshold is met lots of Depolar –> AP generated

10
Q

How do inhibitory ionotropic receptors work?

A
NT release binding 
conformational change
channel opening
Cl- ion influx
hyperpolarization
small inhibitory postsynaptic potential
11
Q

GPCRS

What kind of response does this produce?

A

NT can also bind to GPCR’s

conformational change in receptor

activation of heterotrimeric g protein GDP-GTP

Dissociation

subunits can go on to activate enzymes 2nd messenger systems or open g protein gated ion channels

Slower longer lasting response

12
Q

What is spatial summation?

How can it lead to the generation of an AP

A

if one synaptic event occurs some inotropic Na+ ion channels open –> EPSP does’t overcome threshold so no AP generated

Multiple synaptic inputs opening of VG Na+ channels depolarisation–> spatial summation of EPSP’s, additive depolarisation, threshold easily overcome generation of AP

If you have a excitatory and inhibitory event of equal magnitude they can cancel out through spacial summation

13
Q

What is Temporal Summation

A

summing of EPSP’s at the same synapse as long as they occur in rapid succession
keep adding to each other additive depolarisation until threshold is overcome and an AP is generated

14
Q

What is the NMJ

How is it specialised?

A

Specialised synapse

Neruomuscular junction
located between a motor neurone and the motor end plate

Presynaptic membrane thousands of vesicles containing ACh

postsynaptic membrane lots of invaginations of the sarcolemma to form junctional folds
increases the SA and the no of nAChR’s and Vg Na+ channels

15
Q

What the role of Ca2+ at the NMJ

A

AP arrives at presynaptic terminal
depolarisation
Ca2+ influx
causes vesicles to fuse with the presynaptic membrane and ACh release via exocytosis

16
Q

What happens on the post synaptic membrane once ACh has been released at the NMJ?

A

ACh binds to nACh receptors (2 molecules)
results in conformational change of ionotropic channel resulting in Na+ influx

thousands of ACh molecules and thousands of receptors causes massive depolarisation due to opening of ligand gated Na+ channels

result in Em changing from–90mV up to -20mV

this is known as the end plate potential

17
Q

Why is there such a large influx of Na+ at the NMJ

A

So many nAChR’s on postsynaptic membrane and loads of ACh released
and
Concentration gradient wants Na+ to enter and there is a larger electrostatic difference across the membrane Em is -90mV
therefore there is a larger ionic driving force acting on Na+

18
Q

What is the Em of a myocyte

A

-90mV

19
Q

How does the large EPP generated result in an action potential

A

Huge EPP form -90mV to -20mv due to opening of ligand gated ion channels easily overcomes threshold and therefore voltage gated Na+ ion channels open leading to further depolarisation and the generation of an action potential.

20
Q

Why does the EPP decay ?

A

there are no nAChR’s away from the end plate thereof must cause AP as there are abundant VG Na+ ion channels on the sarcolemma

21
Q

What is important about Ca2+ inside myocytes

A

Ca2+ binds to troponin causing a conformational change thus rotating tropomyosin and exposing acting binding sites for myosin heads

I.e. muscle contraction is ca2+ dependant

22
Q

How is Ca2+ released from the sarcoplasmic reticulum?

A

AP propagates down T-tubule system causing depolarisation of sarcolemma

Affects the DHP (dihydrpyridine) receptor that is tethered to another ryanodine receptor.

Depolarisation results in DHP conformational change and the pulling of ryanodine receptor out of the sarcoplasmic reticulum leading to Ca2+ efflux into sarcoplasm

23
Q

What is the fate of ACh in the NMJ?

A

ACh broken down by acetylcholinesterase breaks ACh into choline and acetyl groups

Choline taken back up by specific receptors on the presynaptic membrane and recycled

24
Q

What is Myasthenia Gravis

A

Autoimmune condition that targets nAChR’s on the postsynaptic membrane
results in poor synatpic transmission

Symptoms include muscle weakness particularity noticeable around the eyes

25
Q

How is Myasthenia Gravis treated?

A

AChE inhibitors means ACh present for longer at NMJ therefore allowing muscle contraction

neostigmine