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Physiological concepts > Wk8 - communication > Flashcards

Wk8 - communication Flashcards

1
Q

Cells are believed to communicate in 3 ways; state them.

A
  1. Gap junctions.
  2. Plasma-membrane bound signalling molecules (influence cells in direct contact).
  3. Secretion of chemicals (influence cells some distance away).
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2
Q

Chemical communication occurs in 3 ways; state and briefly explain them.

A
  1. Paracrine signalling - local chemical mediators, only act on cells in immediate vicinity.
  2. Endocrine signalling - specialised endocrine cells release hormones which travel through the blood, influencing target cells far away.
  3. Neurotransmitters - nerve cells release NT into chemical synapses, which are received by the target cell.
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3
Q

Contrast between paracrine and autocrine signals.

A

Paracrine chemical signals are those chemical mediators which act on cells in the immediate vicinity.
Autocrines are a subdivision of paracrine signals, which involve chemical mediators acting only on the SAME TYPE of cell which released them.

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4
Q

What structure(s) are known for to quickly destroy paracrines?

A

Extracellular enzymes.

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5
Q

t/f: a chemical may, in some circumstances, act as both a paracrine and an autocrine signal.

A

true.

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6
Q

What forms paracrines/ autocrines?

A
  1. Proteins (ie. cytokines).

2. Steroids.

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7
Q

Explain what is meant by the following term(s):

Cytokines.

A

Cytokines are chemical messengers (paracrines) produced by proteins, which play an important role in the immune response.

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8
Q

Explain what is meant by the following term(s):

Eicosanoids.

A

Eicosanoids are paracrines derived from cell membrane lipids, they come in 3 classes.

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9
Q

What’re the 3 classes of eicosanoids?

A
  1. Prostaglandins.
  2. Leukotrienes.
  3. Thromboxanes.
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10
Q

Some cells are specialised for paracrine signalling. Provide an example of this.

A
  • Mast cells (found in CT) secrete histamine.
  • Histamine is stored in large secretory vesicles, which can be rapidly released.
  • Histamine causes local BV to dilate and become leaky.
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11
Q

How often are prostaglandins released in mammals? How often are they degraded - and by what?

A

Prostaglandins are continuously released in mammalian tissues. They are also continuously degraded by enzymes in the ECF.

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12
Q

State the derivative structure of prostaglandins.

A

Prostaglandins are 20C fatty acid derivatives of ARACHIDONIC acid.

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13
Q

How many different types of prostaglandins (PG) exist; and how many ‘classes’ do these fall into?

A

There are 16 or more PG’s, which fall into 9 classes. The different types of PG’s produce different biological responses as they bind to different cell surface receptors.

(general ass vague ass info but wtv phil).

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14
Q

What causes increased PG secretion?

A

Cells are activated to increase PG synthesis and release due to:

  1. Local tissue damage.
  2. Chemical stimuli.
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15
Q

State the general known biological activities of PG’s. (4)

A
  1. Inflammation.
  2. Contraction of SM.
  3. Platelet aggregation.
  4. Contraction of uterine SM.
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16
Q

What may reduce inflammation which is brought about by increased levels of PG’s?

A

The drug aspirin inhibits PG synthesis, and so reduces inflammation.

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17
Q

State Nitric Oxide’s (NO)…

a. ) Structure.
b. ) Permeability.
c. ) Potency.

A

a. ) Structure - small, gaseous.
b. ) Permeability - membrane permeable (lipophillic).
c. ) Potency - high (powerful biological effects).

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18
Q

What is the half life of NO?

A

2-30 seconds (very short!).

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19
Q

What enzyme is responsible for the local synthesis of NO? What substances are required for this synthesis?

A

Nitric oxide synthase (enzyme) produces NO. It requires:

  • Ca+2 (cofactor)
  • calmodulin (cofactor)
  • L-arginine (substrate)
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20
Q

In what cell is NO synthesized?

A

Vascular endothelial cells.

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21
Q

State the basic sequence of events involved with NO synthesis. (4)

A
  1. Stimuli such as ACh, bradykinin, thrombin, adenine nucleotides or Ca+2 bind to ligand receptor on endothelial cell.
  2. These substances trigger entry of Ca+2 into the cell.
  3. Ca+2 binds to cytosolic calmodulin, which then activates enzyme NOS.
  4. NOS produces NO, which rapidly diffuses out of the endothelial cell and crosses the membrane of neighbouring SM cell.
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22
Q

Synthesis of NO from NOS within a vascular endothelial cell is triggered by certain substances binding to ligand specific receptors on the membrane. State such stimulants. (5)

A
  • ACh
  • Ca+2
  • Bradykinin
  • Thrombin
  • Adenine nucleotides
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23
Q

List the 6 physiological effects of NO.

A

“LICCIN”
L - locally produced NT.
I - Immunity; released by WBC to kill bacteria/ tumour cells.
C - control BF/ pressure.
C - control renin release (JG cells).
I - Inhibit platelet aggregation.
N - Neural NT; may play role in learning/ memory.

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24
Q

Explain a clinical use of NO.

A

NO used to treat angina pectoris (chest pain due to coronary heart disease). NO relaxes SM of peripheral arterioles, reducing work of the heart and relieving associated pain.

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25
Q

As a NT, is NO released from presynaptic or postsynaptic nerves?

A

Both.

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26
Q

t/f: NO is contained within secretory vesicles within the pre-synaptic nerve terminals.

A

FALSE - NO is not contained within vesicles.

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27
Q

NO is not contained within secretory vesicles; what is the functional consequence of this?

A

As NO is not contained within secretory vesicles it does not require Ca+2 to stimulate its release.

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28
Q

Why is NO not considered to be a “normal” NT?

A
  1. NO isn’t stored within vesicles and thus doesn’t require Ca+2 to stimulate it’s release.
  2. NO doesn’t bind to any receptor on the surface of its target cell; it diffuses freely into the cell.
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29
Q

Endocrine cells rely on the diffusion of their chemical messengers in the blood. What is the functional consequence of this?

A

As substances must travel within the bloodstream, they are therefor heavily diluted. This means they must be able act at very low concentrations (<10^-8 M).

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30
Q

Endocrine chemicals must be able to act at very low concentrations. At the target tissue end of things, how are endocrine hormones received?

A

AMPLIFICATION - a single hormone molecule interacts with a receptor, leading to the formation of many active protein products.

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31
Q

The ability of a cell to respond to extracellular chemicals depends on the possession of what structural feature?

A

Substance-specific ligand receptors. These bind to their signalling molecules with high affinity.

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32
Q

What’re the 2 ways in which cell surface receptors are able to generate intracellular signals?

A
  1. Activating/ inactivating plasma bound enzyme (ie. adenyl(ate) cyclase.
  2. Opening/ closing gated ion channels in plasma membrane. This changes membrane potential.
33
Q

Many cells (which are not electrically active) have cell surface receptors that are functionally linked to __ channels in the membrane.

A

Calcium (Ca+2) channels.

34
Q

Signalling molecules may bind to ligand-gated ion channels to affect membrane permeability. However, they may instead bind to a receptor which is linked (coupled) to a certain type of protein. Expand on this.

A

Ligands may bind to ligand-specific receptors which are coupled to G-proteins. The G proteins can then…

  1. Open ion channels.
  2. Initiate 2nd messenger activation.
35
Q

t/f: the receptor and enzyme region on the intracellular side of the membrane may be two separate protein molecules, or the same protein molecule.

A

true.

36
Q

Explain the basic sequence of events involved with signal molecule binding to a surface receptor.

A
  1. Ligand binds to ligand gated surface receptor (ie. protein kinase), activating it.
  2. Receptor then activates enzyme (ie. tyrosine kinase) on cytoplasmic side.
  3. Enzyme produces protein(s).
37
Q

Collectively, what are the surface receptor (protein kinase) and intracellular enzyme known as?

A

Catalytic receptors.

38
Q

Explain what is meant by the following term(s):

Integrins.

A

Integrins are membrane-spanning receptors (protein), which attach to the cell cytoskeleton via anchor proteins.

39
Q

What does binding to integrins cause?

A
  • activation of intracellular enzymes

- altered structure of cytoskeleton

40
Q

What are integrins classed as?

A

Catalytic receptors.

41
Q

Integrins are able to activate intracellular enzymes and alter the structure of the cytoskeleton. Explain some of their actual roles in the body, by doing so?

A
  • blood clotting
  • wound repair
  • cell adhesion
  • cell movement (during development)
42
Q

State the solubility of all known NT/ most hormones/ local chemical mediators.

A

Water-soluble.

43
Q

Most hormones are water soluble, with the exception of what class(es)?

A
  1. steroid hormones

2. thyroid hormones

44
Q

Different solubility of hormones influences their mode of action. Briefly explain this with reference to WATER soluble molecules.

A

Water soluble molecules (lipophobic) aren’t able to pass through membrane; must bind to specific receptors on cell surface.

45
Q

Different solubility of hormones influences their mode of action. Briefly explain this with reference to LIPID soluble molecules.

A

Steroid and thyroid molecules are hydrophobic (lipophillic) and so are able to diffuse straight through membrane of target cell. This means they do not need to bind to a receptor on the surface of the cell.

46
Q

Hormones influence is to change the rate of existing processes. State 3 ways in which they may do this.

A
  1. Change enzyme activity.
  2. Affect enzyme directly.
  3. Change membrane transport.
47
Q

Explain the steps involved with signalling via a WATER soluble molecule.

A
  1. Water soluble molecule binds to specific surface receptor (HIGH AFFINITY).
  2. Cell surface receptor undergoes a CONFORMATIONAL change.
  3. Cell surface receptor activates many G-proteins (AMPLIFICATION).
  4. G-proteins LINK the binding of ligand to activation of adenyl cyclase.
  5. Adenyl cyclase converts ATP to secondary messenger; cAMP.
  6. cAMP activates protein kinases, bringing about intracellular response.
    (note: this pathway must refer to cAMP and not Ca+2 as calcium pathway is brought about by electrical stimulus)
48
Q

State the general intracellular [cAMP]. By how much can this change due to stimulation?

A

<10^-6 M (must be tightly regulated).

49
Q

State the chemical reaction regarding control of cAMP levels.

A

ATP –> cAMP (via adenyl(ate) cyclase).

cAMP –> 5AMP (via phosphodiesterase).

50
Q

Why is a G-protein so called?

A

G - protein (short for GTP binding regulatory protein) binds to guanosine nucleotides; which is how it gets it’s name.

51
Q

State the general role of G-proteins in the secondary messenger system.

A

G-proteins provide a link between ligand receptor binding (to cell surface receptor) and adenyl cyclase activity (and thus, cAMP production).

52
Q

Explain in which step of the signalling via a water soluble molecule AMPLIFICATION occurs.

A

Ligand binding to singular cell surface receptor activates many G-proteins. The result of this is a greater activation of adenyl cyclase (and thus more cAMP produced), and a stronger intracellular response.

53
Q

Each G-protein has binding spot for 2 molecules - what are they, and what’re their effects on the G-protein?

A

G-protein activity depends on which molecule binds:

  1. GDP - inactivates G-protein.
  2. GTP - activates G-protein.
    (note: when GTP binds to G-protein it uses the same binding site, so in doing so it dislodges the GDP).
54
Q

When does displacement of GDP in the G-protein occur, and what takes it’s place?

A

GDP is dislodged when ligand binds to cell surface receptor; GTP binds to the site.

55
Q

Each G-protein consists of 3 subunits; what are they?

A
  1. α
  2. β
  3. Y
56
Q

In active state, which G-protein subunits are present?

A

Only α.

57
Q

In inactive state, which G-protein subunits are present?

A

All three, α, β and Y.

58
Q

State the function of the α subunit in a G-protein.

A

α binds and hydrolyses GTP; which activates adenyl cyclase.

note: this is why this is the only subunit present in the active form

59
Q

State the function of the β and Y subunits in a G-protein.

A

β and Y anchor the G-protein to the plasma membrane.

note: this is why they’re only present in inactive form

60
Q

How is it cAMP is able to exert its effect?

A

cAMP activates cAMP-dependant protein kinases (enzymes).

61
Q

Why is it beneficial that the use of secondary messengers provides a mechanism for amplification of signal?

A

As hormones in very minute amounts are able to control processes occurring in cells through this cascade of chemical reactions; because the message is amplified.

62
Q

Provide atleast 2 examples of hormones who’s action is regulated by the mechanism of cAMP.

A
  1. PTH - acts on bone causing reabsorption.

2. ADH - acts on kidneys causing water reabsorption.

63
Q

State the general extracellular [Ca+2].

A

10^-3 M.

64
Q

State the general intracellular [Ca+2].

A

10^-7 M.

65
Q

How is calcium removed from the cytosol?

A

Ca-ATPases (active).

66
Q

How is Ca+2 similar to cAMP?

A

Both cAMP and Ca+2 are important intracellular regulators (or secondary messengers; depending how you look at it).

67
Q

State what cell surface receptors may be coupled to. (2)

A
  1. Adenylate cyclase molecues.

2. Calcium channels.

68
Q

What may cause permeability to Ca+2 changes?

A

Extracellular, electrical signal.

69
Q

Explain the steps involved with signalling via Ca+2.

A
  1. Depolarisation arrives at cell, activating voltage gated Ca+2 channels.
  2. Ca+2 influx into cell.
  3. Ca+2 binds to calmodulin.
  4. Calmodulin undergoes conformational change.
  5. Conformational change causes increased affinity of calmodulin-binding proteins (enzymes) to calmodulin, thus activating them and bringing about a cellular response.
    (note: this basically means enzymes which are inactive at low [Ca+2] become active by high [Ca+2]; the middle linkage is calmodulin)
70
Q

How many binding spots does calmodulin have for Ca+2?

A

4.

71
Q

Expand the following acronym:

InsP3.

A

Inositol triphosphate.

72
Q

Expand the following acronym:

PI.

A

Phosphatidyl inositol.

73
Q

How is InsP3 formed and released?

A
  1. 2 phosphate groups are added to PI.
  2. This forms PIP2.
  3. PIP2 is hydrolysed by phopholipase C.
  4. This forms InsP3 and DAG.
  5. InsP3 is released into the cytoplasm, DAG is membrane bound.
74
Q

Is DAG released into the cytoplasm?

A

No, DAG is membrane bound.

75
Q

Insp3 and DAG are both examples of what?

A

Secondary messengers.

76
Q

How do G-proteins tie into the production of Insp3 and DAG?

A

G-proteins activate phospholipase C, which converts PIP2 to InsP3 and DAG.

77
Q

State general effect of InsP3.

A

InsP3 triggers release of Ca+2 from intracellular stores. Then, calcium exerts its effects by binding to calmodulin; the Ca+2-calmodulin complex has that increased affinity for calmodulin-binding proteins and voala! Enzymes get to doing their bizzzz.

78
Q

State the general effect of DAG.

A

DAG activates protein kinase C.

79
Q

Explain atleast 3 cell functions which are regulated by Insp3 and DAG.

A
  1. Thrombin - acts on platelets activating them.
  2. ACh - acts on smooth muscle causing contraction.
  3. ACh - acts on pancreas causing insulin secretion.

Physiological concepts (12 decks)

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