Communication, Integration, Homeostasis Flashcards

1
Q

Cell to cell communication(short distance)

A

Gap junctions, juxtacrine (contact dependant), autocrine and paracrine

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2
Q

2 key control systems

A

Endocrine and Nervous

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3
Q

Gap juctions

A

channels that produce a direct pathway between cytoplasm of one and another cell, for electrical or chemical signals
- Direct cytoplasmic transfer

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4
Q

Contact dependant

A

Juxtacrine: one end is stuck in the membrane of one cell and receptor is stuck in another cells membrane. They have to come in contact with receiving cell.
- cell to cell dependant

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5
Q

Autocrine

A

Cell is signaling itself, same cell releases signal and bind to receptor on the same cell
- release signal

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6
Q

Paracrine

A

Release signal to neighboring cell and binds

- release signal

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7
Q

communication via long distance: hormone

A

hormone: endocrine cells
released by endocrine cells and travels through the blood to target cells. Target cells need to have correct receptors to be activated

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8
Q

communication via long and short distance: neurons

A

use local and long distance. Neurons secrete signals = neurocrines
1- neurohormone: transported like hormone, through the blood
2- neurotransmitter: something secreted by neuron into neighboring cell
3- neuromodulator: substances released by neurons, modifies how neuron responds to normal primary signal

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9
Q

Electrical signaling

A

Excitable cells use e- signals for communication
ex; nerves, muscles, some endocrine cells.
- due to changes in membrane potential. [ difference in charge is only along the membrane]

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10
Q

Membrane potential

A

All cells have it
electrical potential difference = Vm = voltage = stored energy
** reported inside relative to outside. Use absolute value when determining the largest potential difference

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11
Q

How do membrane potentials arise?

A

1- unequal distribution of ions

2- selective membrane permiablity

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12
Q

Chemical (diffusional ) forces

A

Concentration of gradient principle, ECF vs ICF

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13
Q

Electrical force

A

ionic charge vs membrane charge

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14
Q

electrochemical equilibrium

A

= no net electrochemical force

- 2 forces(chemical and electrical) are equal but opposite = equilibrium potential.

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15
Q

Nerst equation, what you need to know

A
Nerst = Eion = 61/z *( [ion]out/[ion]in)
Z= valence electrons, if anion use a (-)
log(#>1)= +
log(1)= 0
log(#<1)= -
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16
Q

Ex of different Ions

A
k+ = -90mv
Na = +60 mV
Cl- = -63 mV
Ca+ = +240
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17
Q

Membrane potentials influenced by equilibrium potentials

A

due to multiple ions
reality of how much charge is unequally distributed.
unequeal distributions give us ion equilibrium potentials(Ex).

18
Q

Equilibrium potentials

A

each ions desired value.

- ions want to move Vm towards ions Ex to be at equilibrium.

19
Q

What is the driving force?

A

Membrane potential - Equilibrium potential = driving force

(Vm-Ex) = determines ion flow in/out of a cell

20
Q

Membranes permeability to certain ions

A

Leakage (open), but a small drop in the ocean

K+>Cl->Na+, K+ has more votes

21
Q

Resting membrane potential equation

A
Vm = pK(Ek)+ pNa(Ena) + pCl(Ecl)
Px = permeability
22
Q

How are concentration gradients maintained over time?

A

Active transporters, Like the Na+/K+ ATPase. 3 Na for 2K, always running and controls the “leak” of potassium

23
Q

types of gated channels

A
chemically  gated: 
1- ligand(lock and key)
2- ATP channel (Na/K)
Voltage: activated by depolarization
Mechanically gated: Activated with stretch or pressure
24
Q

How can changes to a membrane’s permeability depolarize or hyperpolarize a cell?

A

ion channels display specificity and allow rapid flow of ions
- ions flow to change membrane potential of cell (Vm) towards their equilibrium potential(Ex)

25
Q

Depolarize vs repolarize vs hyperpolarize

A

Depolarize; making more positive(|Vm decreases|)
Repolarization; returning, making more negative
hyperpolarization; too negative, pass the threshold.
|Vm increases|

26
Q

What does chemical signaling rely on?

A

ligand- receptor interactions
ligand- ex, insulin
receptor: have binding sites for ligand (specificity, competition, saturation)

27
Q

intracellular vs vs membrane receptors

A

intracellular: lipophilic, hydrophobic
membrane: lipophobic, hydrophilic,

28
Q

Lipophobic receptors:

A

receptor channels: simplest, most rapid (neurotransmitter) ** confused based on the learning goals

29
Q

GPCR

A

Most signal transduction uses GPCR

  • membrane-spanning protein
  • extracellular binding sites
  • cytoplasmic tail linked G protein (3 parts to it)
  • when activated, they can open ion channels, or alter enzyme activity inside cell [ protein kinase/phosphatases (amplifier enzymes).]
30
Q

What is amplification?

A

allows a small amount of signal to have a large effect.
2 most common amplifier enzymes:
-adenylylcyclase
- phospholipase C

31
Q

Step one of cAMP

A
ligand (1st messenger) binds to GPCR.
- G-protein activated -> exchanges GDP for GTP.
functions like molecular switch
-GTP = active
- GDP = inactive
32
Q

step 2 of the cAMP

A

activated G Protein activates adenylyl cyclase

- adnyl cyclase converts ATP => cyclic amp(secondary messenger)

33
Q

step 3 of cAMP

A

cAMP activates protein kinase A and then that has multiple functions

34
Q

What does protein kinase A do?

A

cAMP dependant, can influence many factors, including opening ion channels and regulating gene transcription.

35
Q

What stops the cAMP pathway?

A

G protein: GTPase: converts GTP back to GDP
cAMP:phosphodiesterase: breaks down cAMP
Protein kinase A:phosphatases, unphosphorylated things

36
Q

Phospholipase C pathway

A
  • instead of adenylyl cyclase there is phospholipase C.
  • instead of cAMP, there is DAG and IP3
  • -> DAG is made from membrane phospholipids and then continues to protein kinase C on the membrane
  • -> IP3 activates Ca+ storage
37
Q

can receptors have more than one ligand?

A

yes;

ex; adrenergic receptors bind to both epinephrine and norepinephrine, ligands compete

38
Q

endogenous

A

into, from within. something that is provided from within the body

39
Q

exogenous

A

drugs, come from the outside that can also bind to receptors. They block activity.

40
Q

upregulation vs down regulation

A

upregulation: mechanism to increase cell response, increase # of receptors
downregulation: mechanism to decrease cell response
decrease # of receptors or binding affinity or receptors

41
Q

Antagonistic vs tonic control

A

antagonistic is faster, both branches(S7P) are active

tonic = volume dial

42
Q

how is a signaling molecule turned off?

A
  • degrade/inactive signal (1st or 2nd messenger): GTPase or phosphodiesterase
  • remove signal: 1st or second mess, by transporting it, ex; pumping Ca+ back into ER
  • endocytosis of receptor-ligand complex.