synapses Flashcards

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1
Q

What is synaptic transmission?

A

process of signal travelling from a neuron to a muscle.

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2
Q

Where does the process of action potential transmission occur?

A

-in the axon of the pre-synaptic neuron

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3
Q

Where does the process of synaptic transmission occur?

A
  • occurs in the synaptic region- where information is transferred from the pre-synaptic neuron to the post synaptic neuron.
  • A similar process occurs at the junction between a motor neuron and a muscle fibre.
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4
Q

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

A
  1. Electrical - potential goes directly from one cell to next
  2. Chemical- chemical is released by presynaptic neuron.
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5
Q

What is the evidence for chemical synaptic transmission?

A
  1. Synaptic cleft- as its the section between the 2 neurones and if neurones are not touching each other then it cant be electrical
  2. Synaptic delay- there is a delay of 0.5-0.8msec which means that a chemical must be involved unlike an electrical signal which is fast
  3. Classic Otto Loewi experiment- 1 heart attached to a vagus nerve, whenn stimulating vagus nerve the heart would slow down. Then he attached 2 hearts with the vagus nerve and they both slow down. This could only happen from a chemical being released from a vagus nerve
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6
Q

What is the classic Otto Loewi experiment?

A
  • Take heart with a vagus nerve attached to it
  • kept heart alive in a perfusion chamber
  • when stimulated vagus nerve -heart slowed down
  • however when he connected the perfusion beaker to another perfusion beaker with a heart in it- when he stimulated the vagus nerve on the first heart the 1st and 2nd heart both slowed down
  • shows synaptic transmission mediated by chemicals.
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7
Q

What are electical synapses?

A
  • adjacent cells joined via gap junctions (membrane proteins of 2 cells fuse and make a channel) , thus ionic continunity between cells
  • fast (transmission of a.p)
  • Gap junctions are inflexible- can’t modify the A.P
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8
Q

What do gap junctions act as?

A

electrical synapses

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9
Q

What does it mean if the electrical synapse is inflexible?

A

you can transmitt action potential but cant modify action potential

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10
Q

Why are electrical synapses fast?

A

No neurotransmitter is released

action potential potential will go from neurone directly to the post synaptic neurone

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11
Q

Where are electrical synapse?

A

You have them in your heart and muscles of eye

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12
Q

What is the structure of a chemical synapse?

A

mitochondria
vesicles ( containing neurotransmitter)
synaptic cleft- 30-40nm wide
post synaptic receptors- for neurotransmitters to bind onto protein receptors

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13
Q

Why does the presynaptic area has lots of mitochondria?

A

its very energy intense

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14
Q

What are the inital stages of chemical synaptic transmission?

A
  1. the arrival of an action potential causes the influx of ca2+- when synaptic ending is depolarised
  2. this causes the vesicle to migrate towards the presynaptic membrane
  3. here it fuses with the meembrane and releases the neurotransmitter via exocytosis into synaptic cleft
  4. the transmitter diffuses down the concentration gradient across the synaptic cleft and binds to post synaptic receptors changing the shape of the protein and ion channels open and diffuse
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15
Q

What can a single post synaptic cell receive their synaptic input from?

A

from several thousand presynaptic neurons

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16
Q

What is motor endplate?

A
  • junction between nerve cell and muscle cell

- a neuromuscular junction

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17
Q

What is the experiment of recording from 2 points on a muscle fibre following neural stimulation?

A

1, A motor neurone is stimulated

  1. 2 electrodes put on muscle cell
  2. action potential recorded on the muscle cell

-if you record a.p far away from synaptic region- normal looking a.p
if you record a.p close to motor endplate- you Geta. small positive bump- which is known as the endplate potential- which triggers a.p

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18
Q

What is an endplate?

A

when recording the action potential close to where the stimulus was, you have a positive bump

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19
Q

What did the drug curare do?

A

Used a drug curarae
It stopped action potential in muscle cells/skeletal- paraylsis/not able to move
Ended in endplate potential

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20
Q

What is an endplate potential?

A

when the action potential on a muscle fibre can be abolished by curare, revealing the endplate potential (triggering the action potential)

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21
Q

What is a neurotransmitter?

A

ACH

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22
Q

how does ACH trigger action potential at neuromuscular junction ?

What happens at synapses between neuromuscular junction?

A

-Presynaptic area full of vesicles with ACH
-At the neuromuscular junction bind to receptors on the sarcolemma, opening sodium channels (change shape and open)
leading to influx of sodium ions (strong driving force of Na ) and an EPP
-Inside cell depolarises- EPP- reaches threshold and opens Na channels
(If threshold is reached), an action potential is generated

23
Q

What happens when ACH is on the muscle cell?

A

it will contract as ACH is released and triggered EPP, initiating depolarisation which triggers action potential on the muscle

24
Q

What was the experiment between 2 neurones?

A

stimulated motor neurons in the spinal cord of a cat

then recorded from post synaptic neuron

25
Q

What are the 2 neurons he used?

A

EPSP and IPSP

26
Q

What is inhibitory?

A

When taking it further away from threshold (getting more negative)

27
Q

What does the post synaptic cell do?

A

takes a decision whether fire or not depending on the potentials (EPSP and IPSP) added together in the cell body
-adding together- get bigger depolarisation- reaches threshold and fires off a.p.

28
Q

What is EPSP?

A

excitatory postsynaptic potential

29
Q

What is IPSP?

A

Inhibitory postsynaptic potential

30
Q

How do you make postsynaptic cell negative IPSP?

A

-neurotransmitter dissue across post synaptic cleft
-caused by neurotransmitter opening CL channels and CL go in to neurone or
K+ open and K+ go out the cell
-Both would hyperpolarise the cell and cause IPSP

31
Q

How do you make the inside of a post-synaptic neuron positive EPSP?

A
Small depolarisation caused by neurotransmitter released
binding to receptors 
opening Na+ ion channels
Na+ go into the neurone
causes EPSP (depolarisation)
32
Q

What can neurotransmitters do?

A

alter ionic permability by binding onto postsynaptic membrane protein receptors (activation of receptors)
Only some neurotransmitters affect

33
Q

What are the 2 mode of action of transmitters?

A

Direct activation of an ionic channel (na+ etc)

Use of a secondary messenger

34
Q

What is a secondary messenger?

A

neurotransmitter released
binds to receptor which is not the ion channel, but it releases chemicals which act on ion channel and open or shut them.

35
Q

What are the 3 mechanisms of transmitter inacitvation (get rid of neurotransmitter such as ACH)?

A
  • Diffusion
  • Reputake- presynaptic neurone sucks neurotransmitter
  • Enzymatic breakdown (ACH-esterase)- breakdown of neurotransmitter
36
Q

Summary of events at a chemical synapse

A
  1. arrival of action potential causes influx of calcium ions
  2. calcium causes vesicles contraning neurotransmitter to migrate to presynaptic membrane
  3. transmitter is released via exocytosis
  4. transmitter migrates to postsynaptic receptors
  5. activation of receptors causes change in postsynaptic ionic permability
  6. transmitter inacitvation via reputake,diffusion and enzyme breakdown
  7. IPSP, EPSP (EPP)
37
Q

What is an example of another neurotransmitter?

A

nitric oxide

38
Q

What is dayls law

A

one neurone contains one neurotransmitter

39
Q

What are the 2 basic types of acetylcholine receptor?

A

nicotinic

muscarinic

40
Q

What does nicotinic receptor do?

A

it occurs at neuromuscular junction- ACH- open Na+ channels which therefore means its excitatory- muscles contract

41
Q

What does the muscarinic receptor do?

A

occur on heart-ACH- open K+ and Cl- channels- are therefore inhibitory

42
Q

What is the affect of ACH?

A

same neurotransmitter but 2 different effects depending on the receptor

43
Q

What is Agonists

A

drug that enhances effectiveness of a neuron- turn the neurone on

44
Q

What are antagonists

A

drug that supresses specific neurons- turn neuron off

45
Q

What do drugs do?

A

either enhance neurotransmission or depress

46
Q

What are the examples of the mode of action of a selection of therapeutic drugs?

A
  • L-dopa- precursor for dopamine, synthesis to alleviate symptoms of Parkinson’s
  • Botox- botulinum toxin cleaves synaptic vesicles
  • Atropine -ACH receptor blocker
  • Prozak- serotonin reuptake blocker
47
Q

What happens in the enzymatic breakdown of neurotransmitter?

A

AAcetylcholinesterase breaks ACH down into acetic acid and choline which are used to make new ACH
-Monoamine oxidase (neurotransmitter) breaks down monoamines (dopamine, serotonin and noradrenalin)

48
Q

What are some classic neurotransmitters?

A
  • ACH
  • glutamate
  • Aspartate
  • Glycine
  • GARA- Inhibtory neurotransmiter in CNS
  • Dopamine
  • Serotonin
  • Histamine
  • Norepinephrine
  • Epinephrine
49
Q

What are neuroactive [peptides?

A

can act as neurotransmitters

-very small proteins

50
Q

What can neurotransmitters be?

A

can be excitatory or inhibitory

51
Q

What are function of receptor?

A

determine which ion channels are open and shut and the action of that neurotransmitter

52
Q

What are neurotransmitter receptors?

A

proteins- bind with complementary shape

  • specific to a particular type of neurotransmitter
  • each neurotransmitter can have several different receptors which can determine whether that neurotransmitter is inhibitory or excitatory.
53
Q

What are the diseases that are the result of defects in synaptic transmission?

A
  • e.g Parkinsons- lack of dopamine
  • Schizophernia- too much dopamine
  • Myasthenia gravis- destruction of ACH resceptors
  • Depression- low levels of serotonin and nor-adrenalin
54
Q

What do therapeutic drugs have their effect?

A

by synaptic transmission