Synaptic transmission (cells of NS) Flashcards

1
Q

What are the 2 types of synapses?

A
  • Chemical
  • Electrical
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2
Q

What is an electricl synapse like?

A
  • Has gap junctions where APs move thru
  • Creates a coupling potential in the post synaptic neurone
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3
Q

What moves through gap junctions?

A

Ions move through gap juntions to produce AP

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4
Q

What theory do electrical synapses fit well with?

A

The Retisular theory (Golgi)

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5
Q

What is the inferior olive?

A

Group of neurones in the medulla oblongata that is involved in motor coordination

  • Brain stem nucleus
  • Movement
  • Neurones form electrical synapses with eahc other to synchronise activity of networks
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6
Q

What are astrocytes?

A
  • Inter-connected via gap junctions to form syncytia
  • Ca+ signalling
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7
Q

What are the 2 components involved in electrical synapses?

A
  • Inferior olive
  • Atrocytes
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8
Q

Explain the stages of transmission at a chemical synapse:

A
  1. NT molecules are synthesised & packaged in vesicles
  2. An AP arrives at the presynaptic terminal
  3. Voltage gated Ca2+ channels open, Ca2+ enters
  4. Rise in Ca2+ triggers fusion of synaptic vesicles w the prsynaptic membrane
  5. Transmittter molecules diffuse across the synaptic cleft & bind to specific receptors on the postsynaptic cell
  6. Bound receptors activate postsynaptic cell
  7. A NT breaks down, is taken up by the presynaptic terminal or other cells or diffuses away from synapse
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9
Q

Rewatch lecture on slide 8 about vesicle docking

A

Apparently calcium is very important for this

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10
Q

What theory do chemical synapses fit well with?

A

The neurone doctrine (Cajal)

Sherrington coined the term synapse

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11
Q

Where are chemical synapses a prevalent mode of synaptic communication?

A

In the vertabrate central & peripheral nervous system

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12
Q

Give an example of a chemical synapse:

A

Neuromuscular junction

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13
Q

Summarise chemical synapses:

A
  • Neurotransmitters
  • Exocytosis and posy synaptic receptors
  • One way
  • Slow
  • Prevalent neurone junctions in the NS
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14
Q

Summarise electrical synapses:

A
  • Ions
  • Gap junctions
  • Two way
  • Fast
  • Neurone junction in certain areas of the NS & gap junctions connect astrocytes in syncytia
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15
Q

Who conducted the reaserch into chemical synapses?

A

Otto Loewi (1921)

Used a perfused frog heart

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16
Q

What was the process that Otto Loewi used when researching chemical synapses?

(Using the perfused frog heart)

A
  • Stimulated the atached Vagus nerve
  • Rapidly slowed the HR of the first heart
  • Delay slowed heartbeat of 2nd perfused heart, not directly attached to Vagus nerve
  • Conclusion: chemical released into the solution that inhibits heartbeat

Chemical later found to be ACh

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17
Q

What did Henry Dale study in 1936?

A

He studied chemical transmission at the neuromuscular junction

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18
Q

What are neuromuscular junctions also known as?

A

Motor end plates

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19
Q

What are neuromuscular junctions (NMJ)?

A

They are specialised chemical synapses between motor neurones axon terminal & muscle fibre

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20
Q

What is a motor unit?

A

A group of muscle fibres innervated by a single neurone

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21
Q

What are the agonists/antagonist that can work on the NMJ?

A
  • Eserine = agonist
  • Tubocurarine = antagonist
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22
Q

What does eserine do at the NMJ?

A
  • Blocks acetylcholinesterase
  • Prevents the breakdown

This increases the action of ACH

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23
Q

What does tubocuranine do at the NMJ?

A
  • Nicotinic receptor antagonist
  • Prevents action of ACh (blocks the action of ACh)
24
Q

What is the process of synaptic transmission at the NMJ?

A

1 - An AP arrives at the presynaptic terminal & causes voltage-gated Ca2+ channels in the presynaptic membrane to open

2 - Ca2+ ions enter the presynaptic terminal & initiate the release of the NT ACh from synaptic vesicles

3 - ACh is released into the synaptic cleft by exocytosis

4 - ACh diffuses across the synaptic cleft & binds to ligend-gated Na+ channels on the postsynaptic membrane

5 - Ligand-gated Na+ channels open & Na+ enters postsynaptic cell causing the postsynaptic membrane to depolarise –> if depolarisation passes threshold, an AP is generated along the postsynaptic membrane

Process contiunes with ACh reuptake (on another flashcard)

25
Q

What is the process of ACh re-uptake from the NMJ?

A

6 - ACh unbinds from the ligand-gates Na+ channels which then close

7 - Acetycholinesterase, which is attached to the postsynaptic membrane, removes ACh from the synaptic cleft by breaking it down into acetic acid and choline

8 - Choline is syported with Na+ into presynaptic terminal, where is can be recycled to make ACh–> acetic acid diffuse away from the synaptic cleft

9 - ACh is reformed within presynaptic terminal using acetic acid generated from metabolism & from choline recycled from th esynaptic cleft –> ACH taken up by synaptic vesicles

26
Q

What are end plate potentials?

A

The depolarisations of skeletal muscle fibres caused by NTs binding to the postsynaptic membrane in the NMJ

27
Q

Who studied end plate potentials?

A

Fatt & Katz (1951)

Studied time course and spatial distribution of EPP

(Profile & decay)

28
Q

What process did Fatt & Katz (1951) use to study end plate potentials, profile & decay?

A
  • Simulated motor neurone
  • Recorded EPP of msucle fibre using intracellular electrode
  • Depolarisation larger in amplitude than needed to initiate an AP
  • Rapidly rose to a peak then slowly declined over 10-20ms
  • Further away along the muscle the intracellular electrode was from the end plate the smaller & slower the response
29
Q

What is Fatt & Katz conclude in their EPP experiment on profile & decay?

A

EPP breif surge of current into muscle fibre locally at the end plate that passively spreads in both directions becoming smaller

30
Q

What did Del Castillo & Katz (1955) study?

A

They mapped ACh sensitivity at NMJ

31
Q

What was the process that Del Castilo & Katz used to map ACh sensitivity in EPPs?

A
  • Applied ACH to muscle fibre by iontophoresis
  • Recorded EPP of muscle fibre using intracellular electrode
  • EPP only occured at end plate region
  • As distace of ACh application inc from the end plate the smaller & slower the response
32
Q

What did Del Castilo & Katz conclude in their mapping ACh sensitivity in EPPs study?

A

ACh postsynaptic receptors only on muscle fibre membrane drectly opposite presynaptic terminal

Now we know these receptors are nicotinic ACh receptors

33
Q

What sort of receptors are nicotinic ACh receptors?

A

Ionotropic

34
Q

What do nicotinic ACh receptors open in response to?

A

Channel opens in response to bidning of the ACh on its extracellular side

35
Q

When opened what do nicotinic ACh receptors do?

A
  • Allow Na+ to pass across the membrane
  • Results in depolarisation
  • Rapid response
  • In contrast to slower metabotropic (GPCRs)
36
Q

What is botox called?

A

Botulinum toxin

37
Q

How does botulinum toxin (botox) work?

A
  • Causes paralysis of muscle fibres
  • Interferes with SNARE proteins preventing ACh release
  • Transient effect - weeks

(botox prevents these synapses firing (freezes them) so stops the movement in that area)

38
Q

What is the main NT at a NMJ?

A

ACh

Nicotinic receptors are found on the opposite end plate

39
Q

What are the properties of EPPs?

A
  • Short synaptic delay (<1ms) between presynaptic AP arriving at axon terminal & EPP of muscle fibre
  • Suprathreshold response
  • Long time course
  • Passive spread - decremental decay w distance
  • Magnitude graded w stimulus
40
Q

What are the 3 main synaptic arrangements?

A
  • Axon terminal to dendrite
  • Axon terminal to soma
  • Axon terminal to axon terminal
41
Q

What are axon terminal to dendrite synapses like?

A

Likely excitatory

42
Q

What are axon terminal to soma synapses like?

A
  • Likely inhibitory
  • Greater effect - closer to hillock
43
Q

What are axon terminal to axon terminal synapses like?

A
  • Presynaptic inhibition (can stop another denrite from signalling to the cell if the terminals attach)
44
Q

What are the 2 types of synaptic potentials?

A
  • Excitatory Postsynaptic Potentials (EPSPs)
  • Inhibitory Postsynaptic Potentials (IPSPs)
45
Q

What is the principle NT in EPSPs?

A

Glutamate

46
Q

What are EPSPs a result of?

A

Result of NT opening channels which allow the movement of ions w positive reversal potentials

(e.g. Na+ & Ca2+)

47
Q

What sort of response does an EPSP produce?

A

Small response (sub threshold)

48
Q

What are the principle NTs for IPSPs?

A

GABA & glycine

49
Q

What is an IPSP the result of?

A

Result of NT opening channels which allow the movement of ions w -ive reverasl potentials positive

e.g. K+ & Cl-

50
Q

What sort of response do IPSPs cause?

A

Small response

51
Q

What will happen with the summation of EPSPs and IPSPs?

A

The summation of EPSP and IPSP cancel each other out

52
Q

EPP vs PSP:

Where are they found between?

A

EPP = motor neurones & muscle fibre

PSP = nuerone and neurone

53
Q

EPP vs PSP:

What is their magnitude?

A

EPP = Large (~20mV) suprathreshold

PSP = Small (1-2mV) subthreshold

54
Q

EPP vs PSP:

What are their NTs?

A

EPP = ACh

PSP = Glutamate, GABA, glycine

55
Q

EPP vs PSP:

Depolarising or hyperpolarising?

A

EPP = Depolarising

PSP = Either