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Physiology PHM > Cellular communication > Flashcards

Cellular communication Flashcards

1
Q

What are the 3 basic types of cell junctions?

A

Anchoring, Communicating, and Occluding

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2
Q

Name 2 types of communicating junctions used to transmit electrical signals from one axon to another.

A
  1. Chemical synapse

2. Gap junction

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3
Q

.Which protein subunits are involved in formation of gap junctions?

A

connexins/connexons

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4
Q

How many connexin subunits make up a gap junction?

A

6

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5
Q

What’s the difference between a gap junction and chemical synapse?

A

Unlike in chemical synapse, materials pass between cells WITHOUT INTERACTING WITH EXTRACELLULAR FLUID

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6
Q

What factors affect the diameter of gap junctions?

A

[Ca2+ ions]
pH
hormones
electrical potential

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7
Q

Define a chemical synapse.

A

The junction between a nerve fiber and non-neuronal cell (ex: muscle) or between 2 nerve fibers, where electrical signals are transmitted

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8
Q

What implications are incurred by mutations of connexin?

A
  1. formation of cataracts in the eyes
  2. deafness
  3. charcot-marie-tooth disease
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9
Q

What does DAG stand for?

A

Diacylglycerol

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10
Q

Name 5 second messsengers.

A
  1. IP3
  2. DAG
  3. Calcium 2+
  4. cAMP
  5. cGMP
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11
Q

How can chemical messengers be classified?

A

based on function and chemical structure

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12
Q

What are the functional classes of chemical messengers and give examples of each.

A
  1. Paracrines (ex: growth factors)
  2. Neurotransmitters (acetylcholine)
  3. Hormones (insulin)
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13
Q

What are the five chemical classes of chemical messengers? Give an example of each.

A
  1. Amino acids (glutamate)
  2. Amines (dopamine, epinephrine, norepinephrine)
  3. Proteins/Polypeptides
  4. Steroids (corticosteroid)
  5. Eicosanoids (prostaglandins, leukotrienes)
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14
Q

Which chemical messenger makes up a majority of all the chemical messengers?

A

Proteins/Peptidtes

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15
Q

Which chemical messengers cannot be stored in vesicles?

A

Steroids and Eicosanoids

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16
Q

What factors affect the magnitude of a target cell’s response?

A
  1. concentration of messenger
  2. number of receptors
  3. affinity of receptors to messengers
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17
Q

Where are receptors of lipophilic messengers usually located?

A

In the cytosol

In the nucleus

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18
Q

How do lipophilic messengers cause a response in the target cell?

A

Once inside the nucleus, they bind to HRE (hormone response element) regions before genes to affect synthesis of proteins

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19
Q

When two hormone receptors are bound to an HRE region, what is the process called?

A

Dimerization

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20
Q

Where are the receptors for lipophobic messengers located?

A

On the plasma membrane

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21
Q

Where does the letter G come from, for the G protein?

A

Its ability to bind guanosine nucleotides

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22
Q

What is the difference between fast ligand-gated and slow ligand-gated channels?

A

Fast ligand-gated channels; receptor and channel are the same protein, effects immediate and brief, ligands can only OPEN the channel, but not close it
Slow ligand-gated channels; receptor and channel are different proteins , effects slow and prolonged, ligands can OPEN and CLOSE the channel

23
Q

G-protein linked receptors are what type of channel?

A

Slow channel-linked (ligand-gated) channel

24
Q

3 ways Calcium is removed from the cytosol

A
  1. Active transport across plasma membrane
  2. Active transport into organelles
  3. Sequestering with proteins in cytosol
25
Q

Location of the G-protein in the G-protein linked receptors.

A

It faces intracellular side of the plasma membrane

26
Q

Function of G-proteins

A

Link RECEPTORS on plasma membrane to EFFECTORS (enzymes and ion channels) in the plasma membrane

27
Q

G protein structure

A

3 subunits

-alpha, beta and gamma

28
Q

Which G protein subunit binds to guanosine?

A

the alpha unit

29
Q

How does G protein deactivate itself?

A

it is an enzyme, so soon after it binds GTP, it hydrolyzes GTP back to GDP and so deactivates itself

30
Q

Functional classes of G-proteins

A
  1. Inhibitory/ Gi - inhibit amplifier enzymes
  2. Stimulatory / Gs - activate amplifier enzymes
  3. Affect ion channels
31
Q

Structural classification of G-proteins

A

Monomeric - one small GTP

Trimeric - the 3 subunit GTP structure

32
Q

How does Vibrio Cholerae affect G-protein action in cells to cause cholera?

A

The bacterium releases a toxin that binds to the G-protein coupled receptor, causing constant activation of G protein. G protein then overstimulates production of adenylate cyclase = excess cAMP –> constant activation of protein kinases that affect Chlorine channels (CFTR; cystic fibrosis transmembrane conductance regulator) causing excess chlorine to be pumped out = high intestinal concentration of chlorine and water to leave cell via osmosis to higher concentration leading to diarrhea

33
Q

The two major categories of intercellular communication

A

Electrical/Synaptic

Hormonal/Chemical

34
Q

The four types of chemical intercellular communication

A

*MNEMONIC: PAJE armstrong
Paracrine (same tissue)
Autocrine (cell communicates with itself)
Juxtacrine (between adjacent cells)
Endocrine (cells in another distant location)

35
Q

3 stages of cell signalling

A
  1. reception
  2. transduction
  3. response
36
Q

How much greater is the concentration of Calcium outside the cell than inside?

A

10,000x

37
Q

The 3 proteins calcium binds to

A
  1. Troponin - for muscle contraction
  2. Calmodulin - smooth muscle contraction, apoptosis
  3. Calbindin - absorption of Calcium from intestines, promotes reabsorption of calcium for bone
38
Q

In the JAK-STAT pathway. JAK stands for? STAT stands for?

A

JAK - JAnus Kinase

STAT - signal transducer and activator of transcription

39
Q

True or false: STAT proteins activate JAK

A

FALSE; JAK activates STAT

40
Q

In each STAT dimer, they bind to the __________ of the other STAT.

A

Phosphotyrosine

41
Q

Explain the JAK-STAT pathway.

A

Ligand binds to JAK receptor
2 JAK receptors brought together to form a dimer
JAKs are close enough to activate each other
Receptors also get activated (phosphorylated in the process)
STAT binds and also gets activated and form a STAT dimer (active transcription factor) each binding to the other’s phosphotyrosine domain
STAT dimer enters nucleus and binds to specific DNA sequence at promoter region to activate gene transcription

42
Q

How is the JAK-STAT pathway shut down?

A

dephosphorylation of other proteins involved in the pathway

43
Q

Two hormones that bind to JAK receptors and their effects.

A

Leptin - regulation of body weight

Growth hormone - stimulate growth

44
Q

3 paracrines/cytokines that bind to JAK-linked receptors and their effects

A

Interleukin 2 –> lympocyte proliferation during immune response
IFN-gamma/Type 2 IFN —> activation of macrophages
IFN-beta and alpha –> induce antiviral state

45
Q

2 ways drugs targeting JAK-STAT pathway work.

A
  1. Blocking ligand receptors (Injection)

2. Inhibit kinase activity of JAK (Drug)

46
Q

STUDY BREAK

Drugs targeting the JAK-STAT pathway are used to turn down the immune response.

A

ex: Tofacitinib (rheumatoid arthritis treatment) and Baxiliximab (prevent transplant rejection)

47
Q

Presynaptic dense bodies

A

Also called active zones, the area where neurotransmitter release occurs

48
Q

The protein that binds vesicles to actin, microtubule, and spectrin filaments.

A

Synapsin 1

49
Q

Describe the mechanism of neurotransmitter release

A
  1. When voltage changes due to action potential transmission, Calcium voltage gated channels open
  2. Influx of calcium at active zone
  3. Calcium binds to calmodulin to form Calcium-calmodulin complex
  4. Calcium calmodulin complex activates CaM kinase 2 (calmodulin dependent protein kinase 2)
  5. CaM kinase 2 phosphorylates synapsin 1
  6. synapsin 1 relases the vesicle which is now free to go for exocytosis
50
Q

Proteins involved in guiding free vesicles to active zones

A

Rab 3a and Rab 3b on the vesicle membrane

51
Q

Which proteins are involved in vesicles binding to the plasma membrane for exocytosis?

A

Synaptobrevin on vesicle membrane binds to syntaxin on plasma membrane

52
Q

3 examples of G-protein coupled receptors

A
  1. Beta adrenergic receptors in cardiac muscle bind epinephrine
  2. Rhodopsin receptors bind to retinal
  3. Prostaglandin E2 (PGE2) receptors bind prostaglandin
53
Q

Classification of receptors

A

Plasma membrane receptors (on/in cell membrane); include 1. G-protein coupled 2. Enzyme-coupled 3. Ion channels

Intracellular receptors (are for hormones and other fat-soluble ligands); include 1. Nuclear receptors 2. Cystoplasmic receptors

Physiology PHM (19 decks)

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