Communication, Integration, Homeostasis Flashcards by John Maldonado

Cell to cell communication(short distance)

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

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2 key control systems

Endocrine and Nervous

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Gap juctions

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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Contact dependant

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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Autocrine

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

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Paracrine

Release signal to neighboring cell and binds

- release signal

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communication via long distance: hormone

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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communication via long and short distance: neurons

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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Electrical signaling

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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Membrane potential

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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How do membrane potentials arise?

1- unequal distribution of ions

2- selective membrane permiablity

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Chemical (diffusional ) forces

Concentration of gradient principle, ECF vs ICF

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Electrical force

ionic charge vs membrane charge

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electrochemical equilibrium

= no net electrochemical force

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

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Nerst equation, what you need to know

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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Ex of different Ions

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

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Membrane potentials influenced by equilibrium potentials

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

Equilibrium potentials

each ions desired value.

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

What is the driving force?

Membrane potential - Equilibrium potential = driving force

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

Membranes permeability to certain ions

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

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

Resting membrane potential equation

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

How are concentration gradients maintained over time?

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

types of gated channels

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

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

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

Depolarize vs repolarize vs hyperpolarize

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

What does chemical signaling rely on?

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

intracellular vs vs membrane receptors

intracellular: lipophilic, hydrophobic membrane: lipophobic, hydrophilic,

Lipophobic receptors:

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

GPCR

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).]

What is amplification?

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

Step one of cAMP

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

step 2 of the cAMP

activated G Protein activates adenylyl cyclase | - adnyl cyclase converts ATP => cyclic amp(secondary messenger)

step 3 of cAMP

cAMP activates protein kinase A and then that has multiple functions

What does protein kinase A do?

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

What stops the cAMP pathway?

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

Phospholipase C pathway

- 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

can receptors have more than one ligand?

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

endogenous

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

exogenous

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

upregulation vs down regulation

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

Antagonistic vs tonic control

antagonistic is faster, both branches(S7P) are active | tonic = volume dial

how is a signaling molecule turned off?

- 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.