Membrane 1 Flashcards
mechanism of facilitated diffusion
- substance binds to carrier protein
- the carrier protein closes and undergoes conformational change
- protein opens on other side and releases the substance
T/F.
Facilitated diffusion is a continuous process
false
it is not continuous because one side of the protein is always closed
Structure of channels
Channels contain:
1. 4-5 protein subunits
2. pore loops
3. central pore
what is important about pore loops in terms of selectivity of molecules
pore loops have physical properties that create a selectivity filter
ligand gated channel
these are important for synaptic transmission
Involves a ligand binding to a receptor which triggers an enzyme activation or opening of a channel
Voltage gated channels
these are sensitive to potential differences and when these differences are detected, a change of conformation will cause the creation of a diffusion pore
How do voltage gated channels detect potential differences?
voltage sensing mechanism in the 4th transmembrane domain of protein- known as the S4 segment
What is the natural position of the s4 segment? why isn’t this always maintained?
The natural position of the segment is upwards, however when the cell is polarized the wings are attracted downwards to the negatively charged inner surface of the membrane
what happens when the cell becomes depolarized?
At -50mV, there is no longer sufficient electrical attraction to hold the s4 wing down- causing it to migrate up
This migration will open the channel, allowing for diffusion
“Kiss and Run” Exocytosis
- the vesicles dock to the membrane- filling up with substances
- the vesicles will move to a specific location on the membrane- kiss it and release some of its contents
- after releasing some of its contents the vesicles will run away and continue the process of kissing and running several times until the vesicle is emptied
Full exocytosis
the vesicle fully fuses to the cell membrane- therefore elongating the membrane
What happens when we elongate the membrane? How is the mechanism counterbalanced?
if we keep adding to the membrane, it will become very lose so there is some type of endocytosis action that cuts off the ends of the membrane to stabilize membrane surface area
Mechanism of Na/K pump
for every ATP molecule broken, 3 Na ions are moved out of cell and 2 K are pumped into cell
Is the inside or outside of the cell more negative?
The inside of the cell is more negative because at rest, the membrane is more permeable to k+ ions, leading to K+ leakage outside of the cell
Why is our resting membrane potential -70mV?
At rest, our membrane is most permeable to potassium, so we have an outward movement of K+ ions making the cell have a net negative charge
The k+ will move outward until there is equilibrium reached- this equilibrium is represented quantitatively by -90mV
This equilibrium is raised slightly by the contributions of Na+ ions which can move Na+ ions inward and this will also create its own equilibrium potential of +60mV-
there is other contributions of Cl- ions however the main driving forces are the Na+ and K+ ions that slightly compete, causing the resting membrane potential to sit at -70mV
Under what conditions can the permeability of Na+ ions outcompete K+ions
When we depolarize the cell (making it slightly more positive) we can open Na+ voltage channels, causing an influx of sodium inside the cell
process of opening Na+ channels
- at -70mV, these channels are closed
- At -55 mV (threshold potential) the channels open
- milliseconds later, inactivation gates imbedded in Na+ channels swing shut- preventing further influx
How do you reopen the inactivation gates?
you must go below the threshold potential
What is the connection between Na+ channels and action potentials?
In order to create an action potential, you need Na+ channels to make the cell excitable.
It is important for the rapid re-upswing of action potentials
What restores the membrane potential?
Na+ channels are quickly inactivated, causing K+ leakage as the main current, restoring the potential
What do you need in order to create an action potential
- voltage gated Na+ channels at high density
- depolarization of cell to -55mV
- potassium leakage channels to restore membrane potential
Is there a difference in magnitude between threshold stimulus and supra threshold stimulus
no, because of the all or nothing principle of action potentials- you either have them or you don’t
How does potassium chloride kill someone?
You can prevent the membrane from producing action potentials by keeping the membrane depolarized.
introduction of potassium chloride kills all potassium gradients, thus preventing the key mechanism that restores the membrane potential below threshold. This keeps the membrane in the absolute refractory period, preventing the generation of an addition action potential (or a heartbeat)
After- Hyperpolarization
This is where we want the K+ channels to act after the inactivation gates have been triggered.
Extra K+ channels with K+ leakage channels cause the cell to be more polarized than usual dropping the potential to around -80mV
Why don’t all cells generate action potentials
because most don’t have voltage gated Na+ channels
Which type of cells are interested in carrying action potentials
Neurons with long axons and muscle cells because they have lots of Na+ voltage gated channels
What are the main parts of the axon
Axon hillock: trigger zone for action potentials
myelin sheath: myelinated axons (taped)
Nodes of ranvier: gaps between myelin sheath that is unmyelinated between two Schwann cells
Synaptic Cleft/ Synapse: at the axon terminal there is a region
presynaptic axon terminal” communicates with a “postsynaptic dendrite” on a postsynaptic neuron
why is it difficult for biological tissue to carry signals
because most biological tissue are poor conductors of electricity and there will be a lot of leakage so by the time you get your signal to the other end, almost all of it would have spilled out
How does increasing diameter improve lambda
there is less internal resistance and therefore less voltage is lost across that resistance as the current travels
How does increasing membrane resistance improve lambda?
the higher the resistance, the less current that is leaked out, forcing the current down the membrane
Multiple sclerosis
this is a disease that is caused from a loss of myelination around axons
Once the AP reaches the end of the axon, it will still generate depolarizing currents. Why can’t this current just go back the other way?
Cannot turn around because of refractory periods and inactivated Na+. At the end of the axon the action potential dies out.
Explain the process of chemical synapse
- once the AP reaches the axon terminal, the presynaptic surface will release vesicle containing neurotransmitter to the postsynaptic membrane (containing specific protein receptors that binds to the transmitter after transmitter is released)
Explain the structure of axon terminal
axon terminal contains the synapse
the synapse contains presynaptic surface (bouton containing vesicles) and the postsynaptic membrane, the membrane of the adjacent neuron
as well as the synaptic cleft, the space between the bouton and the membrane
What triggers the exocytosis of neurotransmitters
- the action potential that reaches the axon terminal will depolarize terminal
- this depolarization triggers calcium channels to open- calcium enters cell
- the entry of calcium triggers exocytosis of synaptic vesicle content
- neurotransmitter diffuses across synaptic cleft and binds to receptors on postsynaptic cell
- neurotransmitter binding initiates a response in the postsynaptic cell that will cause a change in shape of the receptor protein
Types of post-synaptic receptors
Ionotropic: directly opens channels
Metabotropic: initiates a metabolistic cascade to activate enzymes
Specific ligands for inotropic receptors
acetylcholine
glutamate
GABA
Glycine
**keep in mind that these can also bind to metabotropic receptors
Which ligand is common IPSP
GABA, this decreases excitability, benzodiazepines are GABA inducers used commonly for anxiety
How do metabotropic receptors work
the binding of a ligand to a metabotropic receptor will cause the activation or destruction of second messengers
second messengers are either cAMP, cGMP, or Inp3
if second messengers are activated this can cause the activation of other enzymes- these enzymes could be phosphokinases
what happens when you phosphorylate membrane proteins
results in opening of ion currents
Why is metabotropic effects slower that ionotropic
Ionotropic effects are immediate because they directly open channels
Metabotropic effects must first go through all the enzyme activity before influencing ion channels
how do PSPs travel to the initial segment of the axon
By passive conduction through the membrane
How do you get signal degradation as the potential travels from dendrite to trigger zone?
Signal degradation occurs if the distance between the trigger zone and PSP is too far, if this is the case then once the signal reaches the zone, it will not be intense enough to set off an action potential
how does spatial summation work?
- 3 separate EPSPs are generated, each with a potential below the threshold
- they arrive at the trigger zone at the same time and the sum of each of their potentials create a suprathreshold signal
- action potential is generated
How does temporal summation work?
graded potentials die out, so before they have a chance to do this the frequency of another potential is added to the dying one boosting the frequency in order to reach threshold
strategic advantage of IPSPs
they can shut down depolarizing EPSP currents out of cell by making the membrane more negative
How exactly does IPSPs make the membrane more negative?
- IPSPs contain Cl channels with an equilibrium potential around -70 mV
- When the cell becomes depolarized, the Cl channels open quickly bringing the membrane back down to -70 mV
- Cl channels clamp the membrane potential- preventing excitation
How do you generate Spike Train?
- depolarize membrane to reach threshold potential- this causes Na+ channels to inactivate and lead to a refractory period
- Quickly bring the potential below threshold in order to generate a secondary AP (hyperpolarization
What are the possibilities for the receptor protein once it changes shape?
- Directly open ion channels
- Enzyme is activated via G protein coupling
What is amplification in terms of sensory proteins binding to metabotropic receptors
Amplification refers to the production of lots of 2nd messengers by one stimulus molecule
Stages of amplification
- G protein can activate a number of different enzyme molecules
- Each of these enzyme molecules produce lots of 2nd messenger (cAMP)
Taste receptor
- Chemical stimulus binds to tongue and mucous layer
- This binding produces depolarizing current
- This depolarizing current causes the release of transmitters by opening calcium channels
Rapid adaptation
This is when the receptor potential goes to zero if the stimulus is constant
Slow Adaptation
This is explaining that some receptors cannot adapt well to stimulus so they will always have some potential as long as a stimulus is present
Habituation
This is where we have successive identical stimuli that will elicit weaker and weaker responses
What is the connection between the depolarization and hyperpolarization for a spike train
The greater the depolarization the faster the membrane will be brought from hyperpolarization
There will be a ceiling due to refractory period, what do you do if you want to code above this ceiling
You have to recruit higher threshold sensory neurons
Higher threshold sensory neurons
Require greater stimulus before generating any receptor potential
