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psc3011 - gastrointestinal tract 1 > lecture 18 > Flashcards

lecture 18 Flashcards

1
Q

what is substance P?

A
  • active neuropeptide found in gut
  • 11 amino acids long
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2
Q

how was substance P found by Von Euler?

A
  • found intestinal extract contained material that stimulated atropine-resistant contractions of ileum
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3
Q

what are the 3 major mammalian tachykinins?

A
  • substance P
  • substance K (neurokinin A)
  • neurokinin B
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4
Q

which two tachykinins are most similar?

A
  • substance P and K are cosynthesised and coreleased
  • have common feature at C terminus
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5
Q

what does the amino acid residue at position 4 from the C terminus mean?

A
  • determines the affinity
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6
Q

what neurones are immunopositive for substance P?

A
  • neurones in myenteric plexus (MY) that extend in orad direction to the circular muscle
  • neurones found to contain neuropeptides
  • project short distances
  • VIP negative but some contain ACh
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7
Q

what does electrical stimulation of substance P neurones cause?

A
  • smooth muscle contraction
  • excitatory junction potentials which are resistant to atropine
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8
Q

what are excitatory junction potentials?

A
  • rapid, temporary depolarisations that occur in smooth muscle cell arteries
  • occur when sympathetic nerves are stimulated
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9
Q

what does depolarising stimuli in myenteric neurones cause?

A
  • release of substance P (detected by radioimmunoassay)
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10
Q

what is the stimulus for substance P (and K) release?

A
  • distension
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11
Q

what does substance P cause direct excitation (contraction) of?

A
  • gastrointestinal smooth muscle
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12
Q

what experiment did Grider and Makhlouf test the effects of in 1989?

A
  • measuring the effects of ascending contraction
  • using the glass rod experiment, stretching at the caudad end
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13
Q

what did figure 2 show?

A
  • the greater the caudad stretch, the larger the increase in ascending contraction
  • reaches a plateau at caudad stretch of 10g
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14
Q

what is the response in figure 2 blocked by?

A
  • tetrodotoxin -> shows its a neuro-reflex
  • hexamethonium -> blocks nicotinic cholinergic receptor so blocks the interneurones
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15
Q

what does caudad stretch activate?

A
  • neuro-reflex
  • activates enteric nervous system in wall of colon
  • causes release of neurotransmitters to cause contraction of tissue above the point of stimulus
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16
Q

what occurred when atropine was added?

A
  • effective at low levels of stretch to block (almost completely inhibits)
  • less effective when greater stretch occurs
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17
Q

what is the neurotransmitter used at low stretch levels?

A
  • acetylcholine
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18
Q

what happens when substance P antagonist is added?

A
  • at low stretch, antagonist doesnt do much
  • the greater the stretch, the bigger the effect of the antagonist
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19
Q

what does this tell us?

A
  • substance P neurotransmitter is important at large stretch
20
Q

what happens when both neurotransmitters are combined?

A
  • almost completely blocks the response of ascending contraction
  • effects are specific
  • neither effect the descending relaxation
21
Q

what did Grider find in 1989?

A
  • both P and K released during ascending contraction
  • substance P and K are neither released during orad stretch in descending relaxation
  • levels decrease from basal
  • shows baseline tachykinins are being inhibited by orad stretch
22
Q

what does figure 5 in Griders 1989 experiment show?

A
  • no significant difference between substance P and K release
23
Q

what does treating with antibody for substance P cause?

A
  • decrease in response for both substance P and K
  • contractile response
24
Q

what does caudad stretch cause?

A
  • ascending contraction
25
Q

what is ascending contraction inhibited by?

A
  • antibodies for substance P and K
26
Q

what is contraction a combination of?

A
  • substance P
  • substance K
  • acetylcholine
27
Q

what blocks the release of substance P and K?

A
  • tetrodotoxin
  • hexamethonium
  • shows its released from the neural pathway
28
Q

what is CGRP?

A
  • calcitonin gene related peptide
29
Q

what has CGRP been immunolocalised to?

A
  • primary sensory/afferent neurones in GI tract
30
Q

where do the neurones releasing CGRP extend into?

A
  • myenteric plexus
31
Q

when is CGRP released?

A
  • when afferent neurones are stimulated
32
Q

how is CGRP release detected?

A
  • by radioimmunoassay
33
Q

where is serotonin (5-HT) found in?

A
  • paracrine cells -> enterochromaffin cells in the mucosa
34
Q

when is serotonin released?

A
  • through chemical stimulation
  • or increased pressure locally due to distension
35
Q

what does serotonin cause?

A
  • release of CGRP from the sensory neurones
36
Q

what did Grider test in 1998?

A
  • neurotransmitter release during contraction and relaxation
37
Q

what is the method Grider used to test this?

A
  • cut intestine tissue open and pinned to bottom of tissue bath
  • separate into separate compartments (central, orad, caudad)
  • measure what’s been released from tissue therefore what’s been stimulated
38
Q

what is the central compartment the point of?

A
  • distension
39
Q

what is the caudad section the point of?

A
  • descending relaxation
40
Q

what is the orad component the point of?

A
  • ascending contraction
41
Q

what happened when a 5-HT selective agonist was added to central compartment?

A
  • dose deponent increase in CGRP in central compartment
  • substance P was released from orad compartment
  • VIP released from caudad compartment
42
Q

what was added next alongside the 5-HT agonist?

A
  • hexamethonium
43
Q

what occurred with the addition of hexamethonium?

A
  • no effect on the CGRP release
44
Q

what does this tell us about CGRP?

A
  • that its released before the neurones are activated
  • release is early in the pathway
45
Q

what does the addition of CGRP antagonist cause?

A
  • blocked effects of CGRP (blocking the ascending contraction and descending relaxation)
46
Q

what does this tell us about CGRP?

A
  • has to be released to allow the activation of interneurone

psc3011 - gastrointestinal tract 1 (5 decks)

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