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Biological Sciences > Lecture 8 - Part 2 - Synapses and drugs > Flashcards

Lecture 8 - Part 2 - Synapses and drugs Flashcards

1
Q

What happens at a synapse

A
  • Information is transferred from one neuron to another, neurons join each other here
  • Pre synaptic neuron attaches to post synaptic neuron at synapse
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2
Q

Where does action potential transmission occur

A

In axon of pre - synaptic neuron

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3
Q

What are the 2 alternatives to explain the process of synaptic transmission

A

Electrical - potential goes directly from one cell to next- action potential jumps from one neuron to another
Chemical - chemical is released by presynaptic neuron - acts on postsynaptic neuron

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4
Q

Evidence for chemical synaptic transmission

A

Synaptic cleft (30-40 nm) - too wide for action potential to jump across. If neurons arent touching each other i.e. there’s a gap, it can’t be electrical transmission

  • Synaptic delay (0.5-0.8 msec) when stimulate pre synaptic neuron, theres a delay before postsynaptic response
  • Classic Otto Loewi experiment
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5
Q

What is synaptic cleft

A

Gap - separates pre/post membrane

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6
Q

What is the more common synapse

A

Chemical

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7
Q

What is Classic Otto Loewi experiment

A

Connected heart in beaker to another heart in 2nd beaker - only if chemical released - neurotransmitter
Attached to 1st heart was a nerve - vagus nerve - stimulate this = heart slow down

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8
Q

What is electrical synapse/gap junction

A

Proteins of one cell joined to protein of another cell = ionic continuity between cells

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9
Q

How are adjacent cells joined in electrical synapse

A

Via gap junctions

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10
Q

What do gap junctions allow

A

Ionic continuity between cells

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11
Q

What does electrical synapses allow

A

Action potential directly from one neuron to post synaptic neuron

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12
Q

Advantage of electrical synapse

A

Fast - no release of neurotransmitter

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13
Q

Disadvantage of electrical synapse

A

Inflexible - can’t modify action potential

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14
Q

Where are electrical synapses used

A

Heart - contracts quickly - dont have to change it

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15
Q

What is synaptic transmission

A

Neurons join each other at synapses - action potential transferred

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16
Q

What is difference between electrical and chemical synapse

A

Electrical: Gap junction - very quick - straight from pre to post membrane
Chemical: Slow - due to release of transmitter

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17
Q

Structure of a chemical synapse

A
  • Mitochondria - energy ( PRE )
  • Vesicles (containing neurotransmitter) ( PRE )
  • Synaptic cleft ( gap )
  • Post synaptic receptors ( POST ) -
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18
Q

What are the initial stages of chemical synaptic transmission

A
  1. The arrival of an action potential at pre - synaptic neuron causes influx of Ca+ as Ca channels open
  2. This causes the vesicle with neurotransmitter to migrate towards the presynaptic membrane
  3. Here it releases its content via exocytosis
  4. Neurotransmitter diffuses across the synaptic cleft (down its concentrationtransmitter gradient) and binds to postsynaptic receptors.
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19
Q

Single post synaptic cell receiving info from neurons

A

A single post-synaptic cell can receive synaptic input from several thousand pre-synaptic neurons

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20
Q

What do muscle cells conduct action potentials like

A

Nerve cells

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21
Q

What is a neuromuscular junction

A

Nerve cell and muscle cell

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22
Q

What is neuromuscular junction also called

A

Motor endplate

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23
Q

How many neurons does each muscle fibre receive input from

A

Only one

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24
Q

What is found in pre - synaptic region

A
  • Vesicles
  • Mitochondria
  • Synaptic cleft
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25
Q

Recording from 2 points on a muscle fibre following neural stimulation

A
  • Motor neuron stimulated

- 2 electrodes on muscle cell - action potential recorded

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26
Q

What does action potential long way from nerve show

A

Regular action potential

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27
Q

What does action potential close to stimulus show

A

Little and bump = EPP

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28
Q

What is Endplate potential ( EPP)

A

Triggers action potential ( by depolarisation - Na = inside neuron

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29
Q

How can action potential in a muscle fibre be abolished

A

By curare

30
Q

What happens when action potential in a muscle fibre is abolished

A

Endplate potential is revealed - triggers action potential

31
Q

What is curare

A

Drug stopping action potential in muscle cells - abolished action potential leaving EPP only

32
Q

What happens at neuromuscular junction

A

Ach binds to the receptors on the sarcolemma, opening sodium channels = influx of Na+

33
Q

What does influx of Na+ cause

A

EPP

If threshold reached- action potential

34
Q

Summary of EPP

A

Action potential - releases AcH - AcH binds to protein receptor which changes shape - opens ion channel - Na+ into neuron - small depolerisation - EPP - action potential

35
Q

What chemical is found in vesicles at pre - synaptic neuron

A

AcH

36
Q

What happens when AcH is released

A

EPP = small depolarisation - triggered action potential on muscle - contracts

37
Q

What does EPP result in

A

Action potential

38
Q

What causes receptor to change shape

A

Binding of neurotransmitter

39
Q

What determines whether a postsynaptic cell will fire

A

EPSPs and IPSPs sum

How much excitation it has - sometimes they fire, sometimes they dont

40
Q

What is excitatory postsynaptic potential ( EPSP)

A

Small depolarisation in post synaptic cell = opens Na+ channels but not enough to trigger action potential

41
Q

What is inhibitory postsynatpic potential ( IPSP )

A

Small depolarisation, not enough to trigger action potential

42
Q

What happens If both IPSP and EPSP added together

A

threshold reached - action potential

43
Q

Ionic mechanisms of IPSP

A

Open Cl- channels - INTO neurone
Open K+ channels - OUT of neurone
Post synaptic cell negative
Hyperpolarise postsynaptic cell

44
Q

Ionic mechanisms of EPSP

A

Open Na+ channels = Na+ into neurone = depolerisation = action potential
Inside negative

45
Q

What happens when neurotransmitter binds to ion channel

A

Ion channel changes shape = opens = ion flows -

46
Q

How can neurotransmitters alter ionic permeability

A

Binding directly onto postsynaptic membrane protein receptors.
e.g.cation channel is normally shut, but when Ach binds to it, it changes shape allowing the passage on Na+ and K+.

47
Q

What is the mode of action of transmitters

A

-Direct activation of an ionic channel
-Use of a secondary messenger (i.e. cGMP,
phospholipase C etc.)

48
Q

What are the mechanisms of transmitter inactivation

A
  • Diffusion
  • Reuptake
  • Enzymatic breakdown
49
Q

How does diffusion inactivate transmitter

A
  • Falls of and diffuses
50
Q

How does reuptake inactivate transmitter

A
  • Pre-synaptic neuron sucks it back up
51
Q

How does enzymatic breakdown inactivate transmitter

A

Enzymes in synaptic cleft break down neurotransmitter into component parts
e.g. acetlycholinesterase

52
Q

Why inactivate transmitter

A

Neurotransmitter can’t stay bound - get rid of it - or it overstrimulates postsynaptic neuron

53
Q

Summary of events at a chemical synapse

A
  • Arrival of potential causes influx of calcium
  • Calcium causes vesicles containing neurotransmitter to migrate to presynasptic membrane
  • Transmitter released via exocytosis
  • Transmitter migrates to postsynaptic receptors
  • Activation of receptors causes change in postsynaptic ionic permeability
  • Neurotransmitter inactivation
  • IPSP, EPSP (EPP)
54
Q

Examples of neurotransmitters

A

Neuroactive peptides - short chains of amino acids

- Nitric oxide - gas - dilation of blood vessels

55
Q

Colocalisation of more than one neurotransmitter to a single neuron

A

Neurons have many neurotransmitters - in single pre - synaptic cell - releasing different ones at different times

56
Q

What are 2 basic types of Acetylcholine receptor

A

Nicotinic

Muscarinic

57
Q

Nicotinic receptor

A
  • Occur at neuromuscular junction = open Na+ channels = are therefore excitatory
58
Q

Muscarinic receptor

A

Occur on heart = open K+ and Cl- channels = inhibitory

Heart slows down

59
Q

What does receptor determine

A

Whether you get ISP or ESP

60
Q

Examples of diseases due to defects in synaptic transmission

A
  • Parkinson’s - lack of dopamine
  • Schizophrenia - too much dopamine
  • Myasthenia gravis destruction of Ach receptors
  • Depression- low levels of serotonin and nor-adrenalin
61
Q

What are drugs that enhance effectiveness of a neuron

A

Agonists

62
Q

What are drugs that suppress specific neurons

A

Antagonists

63
Q

What is L - dopa

A

Precursor for dopamine synthesis to alleviate the symptoms of Parkinson’s

64
Q

What happens in botox

A

Botulinum toxin cleaves synaptic vesicles

65
Q

What happens in Atropine

A

Ach receptor blocker
Dilates pupils - muscle of iris
Ach can’t bind to receptor = pupil can’t restrict

66
Q

What is prozak

A

Serotonin reuptake blocker

67
Q

What happens during transmission

A

Action potential is transferred

68
Q

Why can’t you use dopamine instead of L - dopa

A

Dopamine is big = can’t get into brain

69
Q

How does L dopa work

A

Smaller
Make dopamine - gets into brain
Astrocytes = blood brain barrier

70
Q

How does botox work

A

Cosmetic industry
Relaxes skeletal muscle and muscles of face
Only lasts 6 weeks
Squinting - use in eye, relax lateral rectus muscle - inject with botox = relax = eye points forwards

Biological Sciences (27 decks)

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