Exam 3: January 30 - February 3 Flashcards
what are aquaporins?
a protein channel that transports water
water doesn’t diffuse it does osmosis
what is osmosis?
the net diffusion of H2O across a membrane
how does water move during osmosis?
water will move from high to low water concentration
water goes from low solute concentration to high solute concentration
what is osmotic pressure?
the pressure exerted by solutes for water to move across the membrane
what is osmolarity?
total[solutes] in solution
the concentration of solutes is of ALL solutes, there aren’t different osmolarity for different solutes
water goes towards higher osmolarity
what is the osmolarity of 3 mol MgCl2 and 2 mol lc in 1 liter of water
11 mol/1 L
11 Osm
what’s the relationship between [water] and osmolarity?
the bigger the osmolarity means the smaller the amount of water so high osmolarity = low [H2O]
what are the consequences of osmosis?
1) water can move across the membrane through the aquaporins and also slightly through the membrane itself – cholesterol prevents a lot of it but we can still see movement of water
2) change in cell size due to solution: when we put a cell in different osmolarities, we can end up changing how the water is positioned inside of that cell (isotonic and hypertonic and hypotonic solutions)
3) osmotic pressure
what is an isotonic solution?
same concentration of solutes inside and outside of the cell on both sides of the membranes yields no change in volume and there’s no gradient – this only applies for non-penetrating solutes (?) – CO2 and NO2 are penetrative - we want blood to be isotonic with RBC so that our RBC aren’t changing size
what is a hypertonic solution?
there is a higher concentration of np solute outside of the cell than inside the cell: increased [npS] = decreased cell volume because water goes to high osmolarity so the water will leave the cell and the cell will shrink
what’s a hypotonic solution?
there is less solute outside compared to the inside of the cell so the water will go into the cell and the cell will expand
what if the membrane is immobile or if it isn’t semipermeable? what are the consequences in terms of osmotic pressure?
where our membrane is semipermeable (??): some np S – the red balls can’t move across the membrane so the only option we have is to change the volume – water will go towards the higher osmolarity where there’s more solute so we’ll see a shift in water so that the side with higher solute will get bigger so that the two sides match each other now – if the membrane can move to accommodate this, then when this happens there’s no osmotic pressure
what if the membrane is immobile? Then no cell volume change is allowed – now we can’t change the denominator – water still wants to go to higher osmolarity but there isn’t enough space – PV=nRT now comes into play because if we can’t change V but we want to increase n by moving water over to side 2, then there needs to be a larger P – osmotic pressure is when water wants to move to a certain area but there isn’t room for it so there’s a pressure build up that keeps the water back – this only happens when membrane is semipermeable (can’t change the numerator) and when we have an immobile membrane (can’t change the denominator)
what does gating mean?
gating means a channel can either be open or closed
what is carrier mediated transport?
carrier mediated transport are kind of like a revolving door – one side is open and the other is closed –they are not a channel, they’re transporters
our protein will act as a shuttle – the compound that we want to move has to get in there and then you’ll change the shape and get the protein to the other side
will require binding of solute to regulate transport – not the same binding in the chemically gated ion channels where the binding of something else opened to gate but it itself wasn’t what was getting move across
what are the types of carrier mediated transport?
facilitated diffusion and active transport
what is facilitated diffusion?
diffusion with the gradient so no energy cost (figure 3-14)
conformational shape change when it binds causes transport – when you bind something to a protein to ALWAYS get a shape change – you don’t know how big or small the shape change is but nevertheless, there’s a shape change
the transportee regulates the transport
what is specific binding?
only specific things can be transported by specific proteins
what is saturation in terms of facilitated diffusion?
overloading
you can overload these transporters like at na OSU football game - there’s a limit to how fast they can dump things to the other side
what are competitors in terms of facilitated diffusion?
it can be that we’re going to the stadium and there’s a Michigan fan that can’t figure out how to get through the turnstiles – so there can be competitors that get bound there but don’t get moved through and slow the process – an example of this is getting glucose inside of our cells (Glucose transports GLUTs) – there’s more glucose outside than inside so the transporters move it inside your cell
what can you do to hinder facilitated diffusion?
saturation and competitors
what is active transport?
almost always against the gradient - work against diffusion which costs energy because you’re going from high to low concentration
still carrier mediated so still dependent on conformation shape changes caused by transportee binding to the protein and also ATP through the use of equation 1
what are the types of active transport?
primary active transport and secondary active transport
what is primary active transport?
uses ATP directly (ATPase pumps) - ATP is getting broken down comes from “ase” enzyme and they’re making a gradient
one or two things get moved
what’s an example of primary active transport?
Na/K ATPase pump
there’s “naturally” more K inside the cell than outside but how did that happen
pump moves Na against its gradient from inside to outside the cell and puts K into the cell
what are the steps of the Na/K ATPase pump?
1) 3 Na bind
2) shape change
3) ATP breaks down into Pi and energy and ADP
4) energy reorients carrier to the extracellular fluid which also causes us to not be able to hold onto Na anymore
5) 3 Na released into ECF
6) 2 K from ECF bind and there’s a shape change which releases the bound phosphate on the inside of the cell which releases energy and causes us to shape change back to the ICF
7) 2 K released into the inside of the cell
8) Repeat
what is secondary active transport?
uses ATP indirectly
relies of primary facilitated diffusion just like how Krebs cycle relies on ETC
always moves at least two compounds - one of the compounds will always be going with its gradient and the other will be going against it’s gradient so one gradient will be getting bigger and the other will be getting smaller
what’s an example of secondary active transport?
Na/K glucose pump
what are the steps of the Na/K glucose pump?
1) Na binds to transporter in ECF which causes a shape change (Na from diet)
2) shape change allows glucose to bind
3) second binding of glucose causes a shape change the reorients our protein to the ICF and it’ll dump out the Na and glucose (Na i going with its gradient and glucose is going against)
4) after the release, the protein will reorient back to ECF
5) repeat
under what conditions will the Na/K glucose pump work?
will only happen if Na gradient is still there with more Na outside the cell than inside – you’ll only have the sodium gradient if the Na/K ATPase pump is working to create the Na/K gradient
what is cotransport?
both to ECF or both to ICF (Na/glucose transport)
what is counter transport?
one to ECF and the other to ICF
what is vesicle formation?
moves large compounds - not limited by movement through a protein
requires ATP
plasma membrane needs cholesterol associated with it to make vesicles because it provides stiffness and creates bends in PM that have a distinct shape – can’t be fluid or shape won’t form
how are vesicles formed/destroyed?
endocytosis vs exocytosis
intake vs. export
what is endocytosis?
creating a vesicle
endocytosis makes the plasma membrane smaller
intakes things
what is exocytosis?
taking an existing vesicle and being able to release things
adds to the PM
export
what could we need to export from the cell?
paracrines, nerve transmitters, endocrines
what is a signal?
extracellular chemicals that are messengers aka ligands
what’s a receptor?
protein that binds ligand and receive the message
what is activation? what’s it based on?
ligand bound receptor
based on shape and charge - ligand has to appropriately bind to that receptor so must match and fit in the position - they must be complimentary and opposite
what is the relationship between binding and specificity and specifcity and affinity?
only if we have binding can we say that we have specificity – it’s either yes or no on if you have specificity, there’s no in between
what’s the affinity? How well are they binding? This is a range. You can have really good binding all the way down to really weak – even the weakest affinity still has specificity – you can’t have affinity without specificity
what is saturation?
% bound
what percent of the receptors are bound to a ligand? Saturation will be higher for high affinity compounds because they bind really well and stay attached well – you need specificity to talk about saturation
what is the relationship between competitors and specificity? what’s an agonist vs. antagonist?
there can be specificity with more than one ligand for the same specific receptor – what level of competition there is determined by their different affinities
you can have an agonist which means there’s a shape change that gets us the same thing as the natural ligand binding and you get the same response as if you had the natural ligand binding
there’s also antagonist which means competitor binds but there isn’t the same shape change in the protein that will give us the same response so you slow the pathway
what is signal transduction?
Turning the signal into a response in the cell – signal transformed into response by target cell
what are the different changes in the cell that can happen as a response to a signal?
1) change in membrane
2) change in metabolism
3) change in contractile activity
4) secrete product
5) change in proliferation rate
6) change in differentiation
what is a change in the membrane?
change how discriminatory the plasma membrane barrier is being
what is a change in metabolism?
it could be telling the cell we’re not going to have enough oxygen so you need to run glycolysis anerobically – or telling the krebs cycle we’re running low on sugar so start breaking down fats and proteins and feeding them into the krebs cycle – or it could be the immune system to get the ETC to make more free radicals
what is a change in contractile activity?
muscle cells contract and change their shape
what is secreting a product?
maybe you want the second cell to release something
what is change in proliferation rate?
maybe you’re telling the cell to make more cells just like ti
what is a change in differentiaion?
it could be telling the cell to become a liver cell or heart cell
what does the receptor location depend on?
receptor location dependent on the ligand’s polarity
what are the two places a receptor can be located?
nonpolar location: cytosol or nucleus - intracellular receptors which isn’t a problem because ligand is non polar and can get through the PM and can get to it
polar location: need an integral protein that’s a membrane bound receptor where ligand can bind and get its message across
what are intracellular receptors?
nonpolar ligands because they’re the only ones that can get through PM and get inside the cell to be able to interact with the receptor
receptor will be in the cytosol or nucleus
what is the pathway that the ligand uses to get to an intracellular receptor?
before you called them ligands you called them neurotransmitters, paracrines and endocrines
pararines and neurotransmitters travel short distances through interstitial fluid which is polar and ligand is nonpolar which is bad but since the distance is short then it’s fine
however, with the endocrine it travels long distances and spends a lot of time in our polar plasma and since it’s nonpolar that’s bad so to resolve this we give the nonpolar endocrines a amphipathic plasma binding protein which will carry the nonpolar ligand through the polar interstitial fluid – outside part of PBP is polar so it can interact with plasma while inside is nonpolar so it can carry the endocrine
what does the plasma binding protein/nonpolar ligand complex do?
once inside the cell, it ALWAYS increases or decreases transcription
what’s a plasma binding protein?
helps non polar endocrine cells which travel long distances in polar ECF reach intracellular receptor
they’re amphipathic - outside part is polar so it can interact with plasma while inside is non polar so it can carry the endocrine
what is a membrane bound receptor?
has a polar ligand
ligand cannot enter the cell because plasma membrane is a barrier to polar items
use the receptor to pass the message on, NOT to enter the cell
it’s a relay system so it’s only the 1st messenger - relay requires 2nd messengers before you finally see the response in the cell
is there a pathway problem with membrane bound receptors?
no
interstitial fluid is polar and plasma is polar and ligand is polar so there’s no issue
what are the different types of membrane bound receptors based on the receptor?
1) receptor = chemically gated channel which causes a change in charge distribution because it’s an ion channel - this is how most neurotransmitters work
2) receptor = enzyme - it’s not a channel, it’s an enzyme like tyrosine kinase
receptor is receiving the ligand and getting us a response in the cell
what does a kinase do?
a kinase phosphorylates and does our equation 1 and breaks down ATP to ADP
enzyme will cause a cascade of phosphorylations
what are the types of membrane bound receptors based on the receptor being coupled?
1) receptor associated with JAK/STAT enzyme
2) G-protein coupled receptor
what’s a JAK/STAT enzyme coupled receptor?
a type of membrane bound receptor
the second protein is a JAK kinase which is our equation 1 happening and our phosphate is getting broken down and moved from compound to compound = cascade of phosphorylation
we got there by our receptor doing it indirectly since the JAK kinase is what actually did it
this is a big thing because it’s how our immune system does its communication through immune system cytokines – 2 proteins: JAK and kinase
what is a g-protein coupled receptor?
receptor gets ligand to bind to it and then passing the message on to another protein which is the G protein
there’s actually three proteins involved: the receptor which binds the ligand in the interstitial fluid and the ligand can’t come in the cell because it’s polar, our g protein which doesn’t get us our response directly but it passed on the message to our third protein called our effector – this is our most typical system
what is the g protein?
a heterotrimeric protein aka a three part protein made of alpha, beta and gamma subunit
how does the g-protein coupled receptor pathway work?
1) when the receptor is bound by the ligand, the receptor becomes activated which changes the shape of the receptor - the g protein is bound to the receptor so it also changes shape
2) GDP leaves and GTP binds to the alpha subunit which then activates it and causes it to separate from the beta and gamma subunit
3) now the alpha subunit moves to activate the plasma membrane effector protein which is what starts the response in the cell
what can the protein membrane effector protein be?
it’s either an enzyme or an ion channel
if it’s a channel it opens up and you get a change in electrical distribution across the membrane
if it’s an enzyme it starts doing its chemical reaction
what’s an example of a plasma membrane effector protein?
adenylyl cyclase
what does adenylyl cyclase do?
PMEP
the enzyme causes us to use our ATP and convert it into a cyclic form called cAMyou’re activating an enzyme which causes amplification processes
this system is impacted by phosphatases which takes away the phosphate of the cAMP – phosphatases do the opposite of kinases because phosphatases take away energy associated with phosphate bonds
what is amplification?
– one ligand binds to our one receptor which activates one GTP which activates our one PMEP but this gets us hundreds of cAMP made which then goes and activates other enzymes like when a video goes viral – we see changes in the membrane, products being secreted, changes in cell metabolism, proliferation and differentiation happening and the sixth change too aka all responses happen
how can you decrease activation?
1) go after the ligand itself 2) remove the receptor
3) change the affinity of the receptor
4) endocytose the receptor
5) inactivate secondary messenger
how can you alter the ligand to decrease activation?
if you breakdown the ligand before it can bind to the receptor – like in our nervous system you can destroy your neurotransmitters
how can you change the receptor to decrease activation?
you can also change things about the receptor itself – you can break down the receptor – if the receptor isn’t there then it can’t be activated by the ligand – this is one of the ways we break down intracellular receptors when we don’t want that activation pathway to happen
how can you change the affinity of the receptor to decrease activation?
if you change the shape or charge of the receptor you change the affinity and there’s a less likelihood of activation since they won’t match up as well
how does endocytosing a receptor decrease activation?
if you endocytose the receptor and bring it inside the cell then you’ve hidden it behind 2 membranes and a ligand can’t get through a membrane, let alone 2 – this is a cost saving mechanism because you could catabolize the receptor but by bringing them in with a vesicle you can later exocytose them back out to the surface without having to rebuild the receptor
how can you increase activation?
1) focus on the receiving cell
2) make more receptors
3) exocytose the receptor
how can you alter the receiving cell to increase activation?
he only thing that the receiving cell can control is the receptor that’s on it but it doesn’t have control of the ligands that are coming to it
how can you make more receptors to increase activation?
anabolize – you see this in the intracellular case because you lower the pathway by destroying so the only way to get it back up is to make more
how does exocytosing the receptors increase activation?
exocytose the receptors back up to the surface – this works ONLY for membrane bound receptors; doesn’t work for intracellular receptors
what are the two parts of the nervous system?
central nervous system
peripheral nervous system
what does the CNS do? what are the parts of the CNS?
brain and spinal cord
our CNS in terms of our reflex arc is our integrator which means that we need to have something sending it information and we also need to send out information to the body
what is the peripheral nervous system? what are the parts of the PNS?
does the intake and outtake part of the template reflex act to and from the CNS
afferent and efferent peripheral nervous system
what do the afferent and efferent parts of the PNS do?
afferent: sensory - brings information in
efferent: action - outgoing side that tells us we need to do something and get us some sort of response
what are the functions of the nervous system?
1) communication
2) processing and control
how does the CNS help our body communicate?
It works by electrical impulses covering long distances in your body
Neurotransmitters travel short distances but the messages that tell the neurotransmitters to be released are electrical and can travel long distances
It’s about neurotransmitters being told to pass the message to the next cell through the interstitial fluid through a synapse
Limited by connections
Fast and quick in duration gets us quick responses
how does our CNS help us with processing and control?
it acts as our integrator in our reflex template
key for controlling homeostasis
