Extracellular signalling Flashcards

1
Q

Why do cells communicate together

A
  • regulate development
  • control growth & division
  • co-ordinate function
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2
Q

What happens when cellular communication goes wrong

A
  • signal lost (diabetes 1)
  • target ignores signal (diabetes 2)
  • signal doesn’t reach target (multiple sclerosis)
  • too much signal (brain damage)
  • multiple breakdowns (cancer)
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3
Q

What happens in diabetes 1

A
  • signal (insulin) lost

- pancreatic B cells no longer synthesise

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4
Q

What happens in diabetes 2

A
  • insulin ignored by defective target receptor
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5
Q

What happens in multiple sclerosis

A
  • nerve impulse not reach target

- breakdown of myelin sheath surrounding neurone

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6
Q

What happens in brain damage

A
  • excitetoxicity
  • too much glutamate neurotransmitter
  • neural degeneration
  • death
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7
Q

What happens in cancer

A
  • over-active
  • under-active
  • confused signalling
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8
Q

What are the three ways in which cells communicate (signal)

A
  • remote by secreted proteins
  • contact by plasma membrane-bound molecules (juxtacrine)
  • contact via gap junctions
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9
Q

What happens in contact via gap junctions

A
  • GJ join cytoplasm of interacting cells

- passage of signals

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10
Q

Give an example of gap junction

A

cardiomyocyte contraction (cc)

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11
Q

How do gap junctions in cc form

A
  • connexin protein expressed by adjacent cells
  • channel —> cytoplasmic content movement (2nd messenger)
  • rapid electrical; coupling
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12
Q

What protein make the gap junctions in the cardiac muscle

A

Connexin-43

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13
Q

What are the stages of remote signalling

A
  • reception
  • transduction
  • response
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14
Q

What are extracellular signal molecules referred to as

A

1st messenger

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15
Q

Give examples of 1st messenger

A
  • growth factors
  • neurotransmitters
  • hormones
  • cytokines
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16
Q

What are 1st messengers synthesised by

A

Signalling cells

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17
Q

What do 1st messengers have

A
  • specific response in target cells

- specific receptors

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18
Q

What are the four types of intercellular signalling

A
  • autocrine
  • paracrine
  • endocrine
  • neuronal
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19
Q

What happens in autocrine

A
  • cells respond to self-signals
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20
Q

What happens in paracrine

A
  • signalling acting on nearby cells
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21
Q

What happens in endocrine

A
  • signal released in blood
  • circulate
  • act on specific target
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22
Q

What happens in neuronal

A
  • response to nerve impulse
  • neurotransmitters released
  • act on target cells
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23
Q

What are hormones

A

Chemical messengers transport signal from one cell to another

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24
Q

Name two types of hormones

A
  • endocrine

- paracrine

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25
Q

Where are endocrine hormones released into

A
  • blood

- by endocrine glands

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26
Q

Where are paracrine hormones released into

A
  • diffuse thru intestinal tissue
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27
Q

What do hormones regulate

A
  • energy needs
  • protein & nucleic acid metabolism
  • mineral and electrolyte metabolism
  • synthesis and release of hormones
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28
Q

How is hormone activity regulated

A
  • positive feedback

- negative feedback

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29
Q

Give examples of hydrophilic hormones

A
  • catecholamines

- peptide hormones

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30
Q

Give examples of lipid-based hormones

A
  • steroids
  • thyroid hormones
  • sterol hormones
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31
Q

Give examples of catecholamines

A
  • adrenaline
  • noradrenaline
  • dopamine
  • serotonin
  • histamine
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32
Q

Give examples of peptide hormones

A
  • insulin
  • glucagon
  • angiotensin II
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33
Q

Give examples of steroids

A
  • oestrogen
  • testosterone
  • cortisol
  • aldosterone
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34
Q

Give examples of thyroid hormones

A
  • thyroxine (T4)

- tri-iodothyronine (T3)

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35
Q

Give examples of sterol hormones

A
  • calcitrol (Vitamin D)
36
Q

What has to happen to signal of extracellular in order to have an effect

A
  • convert into intercellular signal
37
Q

What are receptors and what do they do

A
  • co-ordinate functions of cells in response to signals

- shape complementary to messenger for interaction

38
Q

Give an example of receptor subtype specific

A

Adrenaline

  • liver, muscle: glycogen degeneration
  • adipose: fatty acid production
  • cardiovascular: heart rate, bloop pres. up
39
Q

What determines the class of a receptor

A
  • molecular structure

- transduction mechanism

40
Q

What are the two types of receptions

A
  • cell-surface - hydrophilic

- intracellular - lipid-based

41
Q

Name cell-surface membranes

A
  • ligand-gated ion channel
  • G-protein coupled
  • tyrosine kinase
42
Q

Name intracellular receptor

A
  • nuclear hormone receptor
43
Q

Describe ligand-gated ion channels

A
  • ionotropic
  • very fast
  • synaptic transmission
44
Q

Explain mechanism of ligand-gated ion channels

A
  • binding —> conformational change
  • ions flow
  • cell electrical potential altered
45
Q

Where are ligand-gated channels found

Where is binding site

A
  • electrically excitable cells

- extracellular side

46
Q

What is the structure of ligand-gated ion channels

A

4 or 5 heteromeric subunits

Central pore

47
Q

Give examples of ligand-gated ion channels

A
  • nAChR
  • GABAa
  • GlyR
  • 5-HT3R
48
Q

How does nicotine acetylcholine receptor (nAChR) work

A
  • in. Na+ & K+ permeability
  • Na+ in, K+ out
  • depolarisation
49
Q

What are G-protein-coupled-receptors (GPCR)

A
  • metabotropic

- heptahelical

50
Q

What is the structure of GPCR

A
  • single polypeptide chain
  • 7 a-helical regions —> intracellular & extracellular loops
  • NH2 terminus
  • COOH cytosolical terminus
51
Q

What is a 2ry messenger

A
  • small intracellular molecule

- formed in reception to receptor activation

52
Q

What is Renin-Angiotensin system (RAS)

A
  • feedback system
53
Q

What does RAS control

A
  • blood pressure
  • blood vol.
  • electrolyte homeostasis
54
Q

What does RAS consist of

A
  • renin

- angiotensin-converting enzyme (ACE)

55
Q

What does renin (made in kidney) do

A
  • cleaves a decapeptide from N-terminus from angiotensinogen (made in liver)
56
Q

What is ACE

A

Membrane-bound dipeptidyl carboxypeptidase

57
Q

What does ACE do

A
  • cleaves C-terminal dipeptides from angiotensin

- producing angiotensin 2

58
Q

What does Ang 2 do

A
  • in. Sympathetic activity
  • water retention
  • aldosterone secretion
  • arteriolar vasoconstriction
  • in. Bp
  • ADH secretion
59
Q

What is the structure of Ang 2

A
  • peptide hormone

- octapeptide

60
Q

What are the receptors of Ang 2

A
  • GPCRs

- AT1, AT2

61
Q

What effect does Ang ii have if bound to AT1

A
  • vasoconstriction
  • increased NA
  • Na+ reabsorption
  • aldosterone secretion
  • vascular growth
62
Q

What effect does Ang ii have if bound to AT2

A

Opposite AT1

63
Q

What strategies are used to control RAS against HF

A
  • inhibit renin release/ activity
  • ACE inhibitors
  • AT1 receptor antagonists (losaratan)
  • aldosterone receptor antagonists
64
Q

What is the structure of kinase-linked receptors

A
  • single transmembrane helix
  • large extracellular domain
  • intracellular catalytic domain
  • large & heterogeneous
65
Q

Explain catalytic receptors (kinase-linked)

A
  • receptor is enzyme
  • tyrosine kinase receptors
  • activated by insulin & growth factors
66
Q

Explain non-catalytic receptors (kinase-linked)

A
  • receptor act thru cytoplasmic tyrosine kinases
  • cytokines
  • growth hormones
67
Q

What happens after ligand binding in kinase linked receptors

A
  • receptor dimerisation
  • indirectly regulate transcription
  • cell division
  • tissue repair
  • apoptosis
68
Q

What is the structure of nuclear hormone receptors

A
  • monomeric
  • lipophilic hormones
  • separate ligand ; DNA binding domains
69
Q

What do nuclear hormones receptors do

A
  • regulate gene transcription
70
Q

Examples of hormones that are acted on by nuclear receptors

A
  • steroid hormones

- thyroid hormones

71
Q

How do hormones affect gene transcription in nuclear receptors

A
  • hormones diffuse across memb.
  • interact with cytosolic/nuclear receptors
  • hormone-receptor complexes
  • bind to DNA —> affect transcription
72
Q

What do dendrites, cell bodies and axons do

A
  • receive info.
  • assimilates info.
  • ends at nerve terminal
73
Q

Describe neurotransmission

A
  • action potential
  • synaptic vesicles fusing synaptic memb.
  • Ca2+ diff. in
  • neurotransmitter (ACh) released by exocytosis
  • neurotransmitter across syn cleft
  • binds to post-syn cleft
  • initiates response
74
Q

What are neurotransmitters

A

Chemical messengers of nervous system

75
Q

Give examples of neurotransmitters

A
  • ACh
  • monoamines
  • amino acids
  • peptides
  • lipids
76
Q

Give examples of monoamines neurotransmitters

A
  • noradrenaline
  • adrenaline
  • dopamine
  • histamine
  • serotonin
77
Q

Give examples of amino acids neurotransmitters

A
  • glutamate
  • aspartate
  • glycine
  • GABA
78
Q

Give examples of peptides neurotransmitters

A
  • endorphins
  • substance P
  • neuroticisms
  • neurotensin
79
Q

Give examples of lipids neurotransmitters

A
  • anandamide
80
Q

What is the life cycle of a neurotransmitter

A
  • synthesis
  • storage
  • release
  • receptor activation
  • neurotransmitter inactivation
81
Q

What are the two types of depression

A
  • unipolar

- bipolar affective disorder

82
Q

What neurotransmitters are deficited in depression

A
  • noradrenaline
  • dopamine
  • serotonin
83
Q

What are the treatments for depression

A
  • monoamine reuptake inhibitors
  • Monoamine oxidase inhibitors (MAOIs)
  • miscellaneous antidepressants
  • electoconvulsive therapy (ETC)
  • mood-stabilising drugs
84
Q

Give examples of monoamines reuptake inhibitors

A
  • TCAs: tricyclics antidepressants
  • SSRIs: selective serotonin reuptake inhibitors
  • SNRIs: serotonin/noradrenaline reuptake inhibitors
85
Q

What are the harmful effects of CO

A
  • highly toxic
  • 50% of fatal poisoning
  • long term neurological & cardiovascular disorders
86
Q

What are the benefits of CO

A
  • endogenous signalling molecule
  • cardioprotective
  • neuroprotective
87
Q

what is the role of antidepressants

A

increase monoaminergic transmission within the synaptic cleft