Lecture - Physiol 2 Action Potentials Flashcards
Give a brief overview of this lecture
Cell sets up this resting mem potential by the uneven pumping of ions. They’re held there across it and the permeabiity van be changed to create changes in voltage of the mem. This can happen in passive way where ion channels can open and the potential can deviate up and down from rest. Nothing active happens in membrane - just passive local changes in mem voltage that are used to process information. Ultimately, if net effect of these current changes is great enough, you’ll reach AP. That’s the generation of info in terms of output
Passive/local potentials = even small changes in mem pot can activate the Na or K channels but common way of saying it is ‘passive’ since they havent generated an AP yet.
What are passive potentials?
- caused by
- in response to
- can be what two types
-Local change in membrane potential
-Caused by opening/closing of ion channels
-In response to events external to the membrane
-Can be excitatory, leading to active, regenerative responses in membrane, or
inhibitory, leading to reduced responses or decreased neuronal activity
So a receptor can be activated on surface and that can cause local depol in membrane pot - this is localised (like a Na+ channel can depolarise towards threshold). This is in response to an external stimuli (can be eg a mechanically gated channel like membrane being stretched so it opens)
Now, these can excite the cell - lead to active, regernative response (aka AP) or inhibitory - reduced responses. Excitatory is generally depol towards threshold and an inhibitory isn’t always a hyperpol away from threshold. What it can be is open chloride channels and even if mem pot doesnt change, any other depol - the current will flow and it’ll just get back to where it was aka it inhibits excitatory. This is a nuance that we shall talk about later on
Where do passive (local) potentials occur?
Wherever information is moving into an excitable cell
E.g. at sensory receptors and synapses on dendrites
Like even baroreceptor etc
Local pot brining info to cell so it can be transduced into chem signal to output
Why are they important?
All information processing in the nervous system is based on passive potentials
Info transfer is based on AP passing down axons and into cell bodies but info processing is rather local in perspective on neuron (based on small local changes)
Describe the process of a local potential arising
Rest - tendency of Na to enter bc -ve charges inside and lots of Na outside. Strong conc grad. The Na are open to the extent that Na can leak out and create this negativity so that the exit is balanced by the electrical attraction back in.
- Stimulus
- Sensory input into ending - Open Na channels
- Inital transduction process - Depolarisation
- Crawls up rather than jumps up
- Remains local bc this depol is recovered by exit from K
- Curves up and down, not instantaneous
So Na channels open and that increases driving force for K+ to leave bc cell more positive inside so less negativity to come back. K leaves and brings the mem pot back down again to where it was to start with
What’re the three properties of passive potentials?
- Outlast stimulus:
- Some entering charge is absorbed by capacitance. During depolarisation, charge released from capacitance
- So this yellow dotting = this is where charge being stored.
Capacitance: non conducting membrane and very thin and on either side, we have a conductor. So electircity doesnt pass directly but the charges on either side cna repel or attract. That’s what’s happening here - charges can interact across the mem so the negativity inside cell is most strong collected around inside rim of cell. So all these membrane changes we talk about are really focussed on this barrier between the inside and outside.
When +ve charge comes in, it is opposing some of the stored charge on inside rim aka it’s going there where there is charged area. It crawls up slowly bc it needs to discharge the capacitor before it changes mem potential. Thus the slow time course
During repolarisation, the charge needs to get away in this zone and leave in K ions. So the crawl up and down is like that bc of this stored charge concept - they are slow to let it up and let it go.
- Size reflects stimulus size
- Bigger stimulus = more channels open = bigger depolarisation
- Graded: more channels you open bc more stimulus, so more ions flow in aka more charge so more rapid rise to larger value. More voltage change. - Spread (decremental)
- Poke receptor at one end, some of it gets stored in inner rim, some goes out the ion channels, and this happens along the lenght of membrane. SO when you get out there to the first node of Ranvier (wjere AP generated), there is much less charge coming there than entering cell so they spread over sensory ending but get smaller and smaller the farther you come in
- So you have loss to leakage and capacitance
Passive potentials are good for information process because 4 reasons
- They spread (passive, electrotonic)
- Can put in inputs in different zones of them and if they’re close together, they’ll add up. If they’re spread widely then can’t interact bc too far apart to add together - They outlast the stimulus
- Longer lasting than simulus - Their size reflects the size of the stimulus (they are graded)
- If enough inputs come into dendrite and they’re close enough, big enough then summation = add together (close enough and last long enough and big enough) - They can add together (summation: temporal, spatial)
Passive potentials are not good for carrying information long distances due to what one reason? So how is transmission of information long distances achieved?
They get smaller as they spread (and will have faded completely some distance away)
-Action Potentials
____ _____, and ______ maintain electrochemical gradients, and resting potential,
Inputs are processed as _______ _______, signals are transmitted as ______ ______
Ion pumps, and channels maintain electrochemical gradients, and resting potential,
Inputs are processed as local potentials, signals are transmitted as action potentials
What is temporal vs spatial summation?
-Have to arise close enough in time else they’ll fade away and can’t add up (temporal summation)
Spatial = need to be close enough together bc if too far apart, they’ll be too faded when they finally meet
AP Pre-potential:
- Action potentials happen when?
- in nerve axons, what channels give rise to AP? - What are three properties of vg Na channel?
- Action potentials happen when passive potentials arrive at membranes that contain voltage gated channels
- In nerve axons, voltage gated Na+ channels give rise to AP
- Basically, add up these depol inputs which operate the channels and if have enough then get output and these Na+ gated channels give rise to it - Three properties:
- Open probability increases with depolarisation. At rest, random channels can open or close (Na+ channels) - it’s a porbability thing. There is a possibility it can even open during hyperpolarisation.
- After opening, inactivate; non-permeable state so can’t add AP on top of another (each of these AP are transient and can’t stack one on top of another)
- Require repolarisation to become active again so have absolute refractory period (hyperpolarise the potential a little - come back down to rest to do anything again (need to recover the channels) )
AP Threshold:
- As ions arrive from passive potential, what starts to happen?
- Entry of ions is offset by what? Reducing the effect on membrane potential
- However, what happens at a certain membrane potential so you can’t offer further depol from Na+ entry?
- This equals what?
- What does it mean when it says AP is ‘regenerative’?
- As ions arrive from passive potential, v.g. Na+ channels start to open
- Entry of ions is offset by increased leakage, reducing effect on membrane potential
- However, at a certain membrane potential,‘resting’ leakage is saturated - cannot offset further depol.
from Na+ entry - = Threshold, as any additional entry of ions will have large effect on membrane potential and will
(usually) trigger AP. So much current coming in that not enough leaking out to recover. Once reached, all or none event - same AP - AP is “regenerative”. Na+ channels open, current flows, membrane depolarizes, more channels open,
more current flows………
AP: Depolarising phase
- What’s the positive feedback all about?
- Unlike local potentials, APs aren’t graded - what does that mean?
- So what does the membrane potential reach?
- Further depolarisation increases open probability
for remaining vg Na channels = More channels open = More depolarisation = go back to start - Unlike local potentials, APs are not graded, but are all or none events, that do not fade away, but regenerate.
- Note that membrane potential passes through zero (inside becomes +ve c/f outside). +20mV reached. Equil pot for Na higher than that but it appraches it
AP: Clinical note
- What does TTX (tetreodoxin) do?
- How do local anaesthetics work?
- TTX selectively enters v.g. Na+ channels,
binds there, blocks pore, prevents upstroke.
No AP possible. Deadly! Similar toxins in shellfish following algal blooms, ‘red tide - Local anaesthetics (eg lidocaine) also block v.g. Na channels, but are short acting. Use-dependent block, especially of (TTX-resistant)
Na channels in small diameter pain fibres
AP: Repolarization
- With the peak, what is the upstroke limited by? So size of AP depends on what?
- What happens during repolarisation in terms of channels?
- What is the absolute refractory period?
- What’s special about K channels?
- Upstroke is limited by Ena, and opposing K currents (doesn’t quite get there bc always some K leaving to being cell back down). Size of AP depends on biophysical properties of cell, not size of stimulus
- K start to open such that mem pot will start to repolarise. So you’ve got Na not conudcting since inactivated and K open to potential comes back down again towards rest bc K leaving
- You have inactivated Na+ channels and so it is impossible to evoke a superimposed AP, no matter how strong the stimulus is.
- During this time, the Na channels are inactive and K channels open so you can’t possiibly get to threshold value again bc sodium channels can’t do the positive feed back in inactive phase - K channels can’t open as fast as Na channels so they respond over same voltage range, be opened by same depolarsations but they are delayed so this AP can reach this positive value befroe they are open to bring it back down again
