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CEP > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What are hormones

A

Substances that are secreted directly into the blood by specialised cells, only present in minute concentrations in blood and bind to specific receptors in target cells to influence cellular reactions

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2
Q

What is endocrine signalling

A

Secretory cell releases substance (hormone) into blood stream, hormone diffuses to the target cell. Relatively slow process

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3
Q

Paracrine signalling

A

Secretory cell releases substance which diffuses short distance to an adjacent target cell. Local mediators

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4
Q

What is paracrine signalling important for

A

During development e.g. spinal cord development

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5
Q

When is paracrine signalling not effective

A

For large complex organisms

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6
Q

What is autocrine signalling

A

Cell releases substance that acts on the same cell. Target sites on the same cell. Local effect

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7
Q

When is autocrine signalling most effective

A

When performed simultaneously by neighbouring cells of same type

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8
Q

What is autocrine signalling used for

A

Important during development. Thought to play key role in metastasis, so cancer cells often use this.

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9
Q

Synaptic transmission

A

An example of paracrine signalling. Electrical impulse (neurotransmitters) transferred from axon on presynaptic neurone to receptors on post synaptic neurone. Fast

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10
Q

What is a receptor

A

A specific protein located either on plasma membrane or within target cell which receive a signal and transduce it into a biological response

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11
Q

How are effects of first messengers (hormones, neurotransmitters etc) mediated

A

By binding to specific receptors

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12
Q

What was the Otto Loewi experiment

A

He used two frog hearts and put them in chambers of saline. One heart attached to vagus nerve, vagus nerve was stimulated to slow heart down. First heart slowed down then after a delay the second heart slowed down. Now know this chemical as Ach

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13
Q

What is an agonist

A

Compounds that will produce the same effects as neurotransmitter

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14
Q

What is an antagonist

A

Fit into active site but has no response. It blocks the effect of the native neurotransmitter, no response

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15
Q

Nicotinic effects of AChRs (Acetylcholine receptors)

A

Agonist= Nicotine- bind to and activates nAChRs (ion channels) at NMJ, causes Na+ influx- results in muscle contraction
Antagonist= curare (arrow poison)- binds to active site of nAChR at NMJ (blocking effect of ACh) causing skeletal muscle paralysis
Muscle contraction, synaptic transmission (autonomic ganglia, parasympathetic postganglionic, CNS)
— nAChRs (ion channels)

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16
Q

Muscarinic effects

A

Agonist= Muscarine (Amanita muscaria) fly agaric -activates M1-5 receptors GPCRs
Antagonist= Atropa Belladonna alkaloids, blocks effects
Atropine, scopolamine etc
Too much can cause Bradycardia (low heart rate), salivation, bronchospasm, midriasis (dilated pupils)
M1-5 GPCRs

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17
Q

What is Kd

A

Dissociation constant. Parameter. Concentration at which 50% of receptors occupied by a ligand, measure of affinity

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18
Q

What are ligands

A

The signalling molecule used by the body for various cells to communicate with other cells

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19
Q

What are the four main receptor types

A

Ligand gated ion channels (ionotropic receptors)
G-protein coupled receptors (metabotropic) GPCRs
Kinase linked receptors
Nuclear receptors

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20
Q

Ligand gated ion channels (ionotropic receptors)

A

Rapid effects. Ligand binding creates a change in the shape of the receptor that allows specific ions to pass. Hyperpolarisation or depolarisation —> cellular effects
E.g. nicotinic ACh receptor

21
Q

GPCRs

A

Transmembrane proteins made up of a single polypeptide chain and span seven times through plasma membrane
Each receptor has a n-terminal extracellular domain and a c terminal intracellular domain
Slower, Largest family of membrane receptors in genome. Mediate effects of many hormones and neurotransmitters
E.g. Muscarinic ACh receptor

22
Q

How do GPCRs work

A

Receptor has ligand binding site on outside of plasma membrane and has a transmembrane portion that can bind to a G-protein in the intracellular space

23
Q

How GPCRs work 2

A

Agonist binds to receptor, G protein coupling and GDP is exchanged to GTP in alpha region of G protein. G protein is active and changes shape. subunits regulate effector proteins. GTP hydrolysis changes to GDP inactivation of Galpha protein. Reassembly of heterotrimeric G protein.

24
Q

How many main types of alpha subunit

A

5

25
Q

Kinase linked receptors

A

Receptors carry enzymatic activity, kinase transfers phosphate group so leads to protein phosphorylation leading to gene transcription then protein synthesis then cellular effects. Slow
E.g. RTKs cytokine receptors

26
Q

Nuclear receptors

A

Receptors inside nucleus leads to gene transcription to protein synthesis to cellular effects. Slow
E.g. Oestrogen receptor

27
Q

Protein kinase

A

adds phosphate

28
Q

Protein phosphatase

A

Removes phosphate

29
Q

What are the three main groups of hormones

A

Protein/peptide
Steroid
Amine

30
Q

How to measure hormones

A

Bioassays (higher conc the darker)
Mass spectrometry

31
Q

What is the endocrine system

A

A system of ductless glands and cells that secrete hormones

32
Q

Anterior pituitary hormones

A

ACTH (regulation of adrenal cortex)
TSH (thyroid hormone regulation)
GH (growth metabolism)
LH/FSH (reproductive control)
PRL (breast milk production)

33
Q

Posterior pituitary hormones

A

ADH water regulation
Oxytocin breast milk expression

34
Q

Grave’s disease (autoimmune hyperthyroidism)

A

Auto-antibody binds to TSH receptors producing too much thyroid hormones.
Tachycardia, restlessness, weight loss

35
Q

Cushing’s disease/ syndrome

A

Glucocorticoid excess, ACTH excess (i.e. pituitary adenoma) . Adrenocortical tumour, latrogenic (long term steroid medication)
High BP, thin arms and legs, pendulous abdomen, red straition, red cheeks, fat pads, thin skin, poor wound healing, bruising, osteoporosis compressed vertebrae

36
Q

Acromegaly

A

Growth hormone and IGF-1 in excess (insulin- like growth factor 1) which mediates effects of GH, important role in childhood growth has anabolic effects in adults
Typical features: large hands and feet, prognathism (protruding jaw), thick and greasy skin, interdental spacing, weight gain, goitre , gradual changes in facial features- large prominent facial features- nose getting larger, deepening voice,

37
Q

Severe hypothyroidism

A

Lethargy/tiredness, feeling cold, weight gain, dry skin/myxoedema, hair loss

38
Q

Affect of cholera toxin on G protein

A

Acts as a classical A-B type toxin, leads to ADP-ribosylation of G protein, and constitutive activation of AC (adenylate cyclase), thereby giving rise to increased levels of cyclic AMP within host cell
It inhibits GTPase of Gs but not Gi

39
Q

What binds to N-terminal extracellular domain GPCRs

A

Ligands (hormones) which can’t pass through cell membrane bind to extracellular domain and trigger intracellular signalling cascades which mediate the functions of that specific ligand

40
Q

What are G-proteins

A

A group of membrane resident proteins which recognise activated GPCRs and relay their messages in order to elicit the cellular effects of the ligand.
G proteins consist of three subunits alpha, beta and gamma
The gamma subunit is anchored to the plasma membrane via a fatty acid chain

41
Q

Resting state G-protein

A

G protein exists as the alpha beta gamma trimer, which may or may not be pre coupled to receptor
And in resting state GDP is bound to alpha subunit

42
Q

Activated G protein

A

When an agonist molecule binds with the receptor a conformational change occurs, this causes interaction of the receptor with the G protein
GDP dissociates from alpha subunit and GTP binds this causes activation of G protein and release of alpha GTP fragment and beta and gamma dimer from each other, these are the active forms of G protein

43
Q

Alpha GTP fragment

A

Can bind with effector enzymes like adenylyl cyclase and phospholipase C

44
Q

Beta gamma dimer

A

Mainly binds to ion channels or kinases and activate them

45
Q

4 types of G proteins

A

Gs (stimulatory), Gi (inhibitory), Go (node), Gq

46
Q

Adenylyl cyclase pathway

A

Adenylyl cyclase (AC) is a membrane bound enzyme
Activated by Gs proteins and inhibited by Gi proteins
When activated it catalyses conversion of ATP into cyclic AMP which activates cAMP-dependent protein kinases and these kinases cause phosphorylation of certain enzymes according to agonist molecule bound to receptor

47
Q

Phospholipase C pathway

A

When Agonist binds with receptor it activates a Gq protein
Activated Gq protein then activates phospholipase C which catalyses cleavage of phosphatidylinositol bi phosphate into diacylglycerol DAG and IP3
The IP3 receptor which is a ligand gated calcium channel is located on membrane of endoplasmic reticulum, binding of IP3 with receptor causes release of calcium ion into cytoplasm
Main goal of IP3 is to increase cytosolic calcium ion concentration, Ca2+ aid in muscle contraction and enzyme activation
DAG causes increase in protein kinases C levels within cell, PKC causes phosphorylation of enzymes &protein

48
Q

How were biological effects measured of drug on muscle contraction

A

Using a muscle stripe put into a force transducer which was linked to a pen that was recording contraction over time (before and after drug was applied)

CEP (10 decks)

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