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Introduction To Pharmacology And Physiology > Signals And Their Receptors > Flashcards

Signals And Their Receptors Flashcards

1
Q

What are the different classifications of signalling molecule?

A

Endogenous-within the body
Exogenous 1-natural plant based
Exogenous 2-synthetic man made

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2
Q

What actually is pharmacology?

A

The study of molecular signallers regulating physiological processes

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3
Q

What do cells need in order to maintain a stable optimised environment?

A

Substrate supply system
Product distribution system
Waste removal system

This allows a controlled physiochemical environment for reactions to occur and responsive control systems that can adjust according to demand

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4
Q

What are the different parts of a negative feedback loop?

A

Environmental change-sensor-system set point comparator-controller-effector-correction signal

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5
Q

What does synergistically and antagonistically mean?

A

Synergistically-turns on a process eg. Sweating

Antagonistically-turns off a process eg insulin decreases amount of blood glucose

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6
Q

Why is our temperature 37 degrees?

A

Proteins engineered by evolution- just right for homeothermic as most proteins operate optimally at this temp
Reduces rate of thermal degradation and denaturation

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7
Q

What is the control centre for temperature regulation?

A

The hypothalamus

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8
Q

What happens above 40 degrees body temperature?

A

Febrile convulsions, coma and loss of temperature regulation at 42 degrees

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9
Q

What is the normal resting range for body temperature?

A

36-38 degrees

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10
Q

What temperature is recognised as mild hyperthermia?

A

38-40 degrees

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11
Q

What temperature is recognised as mild hypothermia?

A

34-36 degrees

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12
Q

What happens to the body below 34 degrees?

A

Impaired temperature regulation

Cardiac fibrillation

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13
Q

What are the 3 major types of signalling molecules in the endocrine system and what are their properties?

A

Hydrophilic 1-amines and amino acid derivatives, these are small charged and hydrophilic. Their receptors are in the plasma membrane. Very short time course of action. Causes change in membrane potential and triggers synthesis of cytosolic second messengers

Hydrophilic 2-peptides to proteins. Receptors in plasma membrane. Minutes to hours time course of action. Triggers synthesis of cytosolic second messengers. Triggers protein kinase activity

Lipophilic-commonly derived from cholesterol
Intracellular receptors. Hours to days time period. Receptor hormone complex controls transcription and stability of mRNA.

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14
Q

What are the major classifications of neurotransmitters?

A

Amino acids, monoamines, peptides. Ach (excitatory at end organ)
Can be excitatory or inhibitory
All are examples of paracrine signalling molecules

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15
Q

What are some examples of local chemical mediators?

A

Cytokines (interleukins, chemolines, interferons, histamine)

Eicosanoids (prostaglandins, leukotrienes)

Also bradykinin, nitric oxide, neuropeptides, platelet activating factors

Local response is rapid focussed and integrated. Not needing to involve whole body resource.

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16
Q

What kind of signalling molecule would growth factor signals be?

A

Autocrine

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17
Q

What is important to remember about using aexogenous signalling molecules?

A

Engineered by humans to carry and transfer the imposter signal
Signal still carried but fit may be suboptimal
Side effects possible

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18
Q

What are the four types of signalling molecule targets?

A

Receptors
Ion channels
Transporters
Enzymes

Except for chemotherapy where target is structural protein or DNA
Distinction is when aiming to selectively kill another organism

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19
Q

What are the different types of receptors?

A

Kinase linked receptors
Ligand gated ion channels
Nuclear/intracellular
G protein coupled receptors (GPCR’s)

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20
Q

What are kinase linked receptors?

A

Mediate signals of wide variety of protein molecules eg growth factors, cytokines, hormones
Act via phosphorylation of specific groups which sets into motion signalling cascade
Can be thought of as molecular switch leading to gene transcription

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21
Q

What do ligand gated ion channels do?

A

When ligand binds gate opens- eg Ach, GABA NMDA
Allow ion currents and voltage change driving or modulating action potential generation in neurones and contraction in muscle

Coupled to Ca2+ signalling

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22
Q

What do nuclear receptors do?

A

Ligands need ot be lipid soluble (steroids)
When bound ligand receptor complex migrates to nucleus then binds to gene transcription factor
This then activates or inactivated a gene
Examples are thyroid hormone, vit D or xenobiotics

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23
Q

What do ion channels do?

A

Selectively allow ion current to flow across PM
Na, K, Ca, Cl
Regulate voltage signals in excitable cells to maintain membrane potential
Each ion channel family has a range of members variation in structure and function

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24
Q

What is the distribution of the four main cellular ions across the membrane ?

A

More potassium on inside, more sodium, calcium and chloride on outside

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25
Q

How are ion channels regulated?

A

Change in electric field density- this first depends on LGIC current activation
Channel activity can be facilitated or inhibited by phosphorylation of intracellular sites on channels via GPCR- PKA and PKC activation
Activity can also be endogenous allosterically modulated by intracellular signalling molecules- ATP, GTP and ca2+ and signalling proteins
Exogenous channel blockers

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26
Q

What is an agonist molecule?

A

Binds to a receptor and activates it,

Antagonists bind to a receptor and do not activate it (block the effects of agonists)

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27
Q

What can GPCR’s respond to?

A 
Light
Ions
Neurotransmitters
Peptide and non peptide hormones
Large glycoproteins
28
Q

What is the shared common structure of GPCRs?

A

Single polypeptide chain
7 transmembrane spanning regions
Extracellular N terminal
Intracellular C terminal

29
Q

Where can ligands binds to a GPCR?

A

Ligand binding site is formed by the transmembrane domains
Or
The N terminal region

30
Q

What does the GPCR do to the associated G protein?

A

Facilitates exchange of GTP for GDP on G alpha subunit. This causes the GTP alpha subunit to dissociate from the beta gamma subunits which each can then interact with effector proteins which are second messenger generating enzymes or ion channels

31
Q

How is G proteijn signalling terminated?

A

The alpha subunit GTPase hydrolyses the GTP back to GDP. This causes the alpha GDP and beta gamma subunits to recombine to form an inactive heterotrimeric complex

32
Q

What governs Receptor G protein selection?

A

Activated GPCR’s preferentially interact with specific types of G protein, and G alpha subunit is primary determinant.
In turn the G alpha subunits and GBy subunits interact with specific effector proteins

In this way the Galpha subunits can activate or inhibit certain enzymes such as adenylyl cyclase

33
Q

What does pertussis toxin do to G protein function? (PTx)

A

Inhibits exchange of GDP for GTP so subunits not released so effectors not stimulated

34
Q

What does the cholera toxin do to G protein function? (CTx)

A

Inhibits alpha subunit GTPase so subunits cannot reform to heterotrimeric complex

35
Q

What do the activated alpha and beta gamma subunits do?

A

Activate or inactivate effectors-
Can be enzymes eg adenylyl cyclase- forms cyclic AMP (second messenger)

Or ion channels-voltage operated Ca2+ channels

36
Q

What does cyclic AMP do?

A

Activates cyclic AMP-dependent protein kinase (PKA)

This happens by binding to receptor regions which releases catalytic regions

37
Q

What does PKA do?

A

Phosphorylates OH on side chain of targeted proteins

38
Q

What is extracellular calcium?
What is cytoplasmic calcium?
What is ER calcium?

A

1000000nM

100 nM

200000nM

39
Q

How is cytoplasmic calcium concentration increased?

A

Movement of calcium across plasma membrane

Release of calcium from the ER

40
Q

How are increases in cytoplasmic calcium concentration opposed?

A

Relative impermeability of PM to calcium
Pumps and transporters move calcium out of the cytoplasm
Calcium buffer proteins (ca2+ binding proteins)

41
Q

Which two mechanisms maintain low calcium in the cytosol?

A

ATP dependent- Ca2+ ATPases PMCA and SERCA

Transporter mechanisms-Na+, Ca2+ exchanger (NCX)

42
Q

Which mechanisms increase calcium ion concentration in the cytosol?

A

Movement across the membrane (influx)-
Voltage operated Ca2+ channels
Ligand gated ion channels

Movement out of the ER (release)-
Calcium induced calcium release (ryanodine receptors)
IP3 receptors

43
Q

How does an agonist binding to a GPCR cause release of calcium ions from the ER?

A

Binding of agonist causes change in conformation of GPCR which causes exchange of GDP for GTP on alpha subunit. This separates and activates an enzyme called phospholipase C. This breaks PIP2 apart into DAG and IP3. DAG activates PKC which starts to phosphorylate things. IP3 binds to IP3 receptors on the ER membrane

44
Q

How does adrenaline cause inotropy in the heart? (Increase in force of contraction)

A

Binding of adrenaline has agonist effect. Alpha S subunit released. This activates adenylyl cyclase which forms cyclic AMP which activates cyclic AMP dependent protein kinase. This phosphorylates VOCC- voltage operated calcium channels which increases their activity to more calcium ions diffuse in when stimulated so stronger contraction.
The effect is the same with noradrenaline and M3 muscarinic receptors in smooth muscle

45
Q

How is neurotransmitter release controlled?

A

In both the CNS and PNS neurotransmitter release is controlled by presynaptic G protein coupled receptors- the beta gamma subunit released binds to VOCC and stops calcium entry

46
Q

What is a semi permeable membrane

A

A layer through which only allowed substances can pass

47
Q

What two things is passive transport dependent on?

A

Permeability and concentration gradient

48
Q

Does active transport have a positive or negative delta G value?

A

Positive- things are being moved against their concentration gradient so becoming more ordered

49
Q

How does delta G increase with concentration ratio and membrane potential

A

Graph is straight line- directly proportional

50
Q

What does uniport mean?

A

Only one molecule transported at a time

51
Q

What does symport mean?

A

Two or more molecules transported at the same time- a type of cotransport

52
Q

What is anti port?

A

When a molecule is moved one way across a membrane as another is moved in the opposite direction

53
Q

What kind of ATPase is NaKATPase and what does it do?

A

P type, it actively transports 3 na ions out for every 2 K ions that it pumps in.

54
Q

Where is the NaK pump phosphorylated?

A

On an aspartate residue

55
Q

What does the B subunit glycoprotein do in the NaK pump?

A

Directs the pump to the cell surface.

56
Q

Where is the ouabain binding site on the NaK pump?

A

On the alpha subunit

57
Q

What is mainly responsible for the resting membrane potential?

A

The potassium diffusion through channels.

58
Q

What is wrong with the membrane transporters in cystic fibrosis?

A

Chloride ion channel protein to pump chloride ions into alveolar space not working. Therefore water is retained in lung epithelial cells so mucus is more viscous and clogs airways.

59
Q

What are sodium and potassium gradients necessary for?

A

Electrical excitability
Contributes a small amount to resting membrane potential
Drives secondary active transport-control of pH regulation of cell volume and calcium concentration
Absorption of sodium in epithelia
Nutrient uptake eg glucose

60
Q

Why is calcium toxic to cells?

A

If calcium ions meet phosphate they will precipitate to make hydroxyapatite crystals

61
Q

What role does the NCX have?

A

Role in expelling intracellular calcium ions during cell recovery
Exchanges 3 na for 1 ca
Electrogenic- flows in direction of Na gradient
Possible role in cell toxicity during ischemia

62
Q

When will the direction of the NCX change?

A

When membrane is depolarised

63
Q

How is the sodium calcium exchanger affected in ischaemia?

A

When ATP is depleted due to poor perfusion sodium ions accumulate in cell-depolarised
NCX reverses, calcium ions moved in-toxic-kills cell

64
Q

How is cell pH controlled?

A

Acid extruders-sodium H+ exchanger NHE

Base extruders-Cl-/HCO3- exchanger (anion exchanger)
Sodium dependent Cl-/HCO3- exchanger (sodium bicarbonate cotransporter)

65
Q

What is the NHE and how is it controlled?

A 
Exchanges na and H+
Electroneutral exchange
Regulates pH
Regulates cell volume
Activated by growth factors and inhibited by amiloride(potassium sparing diuretic)
66
Q

What is different about brain and liver glucose uptake compared to adipose and muscle glucose uptake?

A

Brain and liver use GLUT 3-facilitated diffusion, adipose and muscle use GLUT 4- also facilitated diffusion but insulin sensitive

67
Q

What prevents efflux of glucose from cells in adipose and skeletal muscle when circulating glucose concentration falls to resting levels in post absorptive period after a meal?

A

Glucose is converted into triglycerides or glycogen which are insoluble so cannot diffuse across the phospholipid bilayer

Introduction To Pharmacology And Physiology (3 decks)

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