Physiology Flashcards
What is the membrane potential?
Voltage difference across the membrane
- lipid bilayer acts as insulator separating 2 conducting solutions (cytoplasm and extracellular fluid)
Current flows when channels are open
Flow of anions/cations will change membrane potential
Voltage collects AT the membrane
Vm - Vin = Vout
usually equals about -65
what is the membrane potential of glial cells and what are they controlled by?
Dictate by Potassium (only permeable to K+)
Concentration inside 400 mM
outside 20mM
Chemical/concentration gradient rests around -75mV (equilibrium potential where k going out = k being pulled in by negativity)
What is the Nernst Equation?
Used to determine equilibrium potential of an ion
Ex= RT/zF ln (xo)/(xi)
Ex= 58mv/1*log(xo/xi)
why does the ln change to log??
ask jason!
what is the equilibrium potential for na+?
55mv (50mM inside cell, 440mM outside)
what prevents the contiual entry/exit of K+ eliminating concentration gradients?
Sodium Potassium Pump!
-pumping 2 K out
- pumping 3 Na In
Keeps resting membrane potential in tact
what is the equilibrium potential for Cl?
-70, 560mM outside cell, 52mM inside the cell
what is the goldman equation used for?
nernst for all the ions which factors in permeabilities
Vm=RT/F*ln(pKo/pK + pNao/pNai + pClo/pCli)
this gives the -65mV for resting potential
what are relative permeabilities at rest for main 3 ions?
Pk=1
pNa= 0.04
pCl=0.45
What are voltage gated channels?
Help regenerate and mediate signalling
Example: sodium voltage gated channels
i. channel at rest
ii. channels open due to depolarization and na rushes through
iii. channels inactivate: stops further flow of ions through ball and chain mechanism
what are the relative permeabilities for the 3 ions when the na channels have opened?
Pk=1 (unchanged)
Pna=20
pcl= 0.45 (unchanged)
Support the argument “different neurons have different firing patterns because they have different ion channels”
- there are some that fire in bursts, oscillations/rhythms etc
What are some methods for recording action potentials and related activity?
Intracellular electrophysiology
Extracellular electrophysiology (putting it outside/nearby to detect local change)
EEG: clusters of action potentials
Calcium Imaging: fills with fluorescent die only when it binds calcium (which increases during an action potential), recorded as an increase in brightness
fMRI (functional imaging): measures bloodflow in the brain, which increases during activity because they need more nutrients etc. Not super specific, an indirect measure of neuronal activity
How long is the delay from a presynaptic action potential to the excitatory postsynaptic potential?
1ms
How does Calcium relate to the action potential?
Calcium floats outside the cell, so when channels open, calcium rushes into the cell, there are sensors that detect the Ca and cause vesicles to fuse with cell membrane
Postsynaptic receptors bind and become permeable to sodium (EPSP)
Why is mitochondria needed in the cell? Why are so many vesicles needed in the NMJ?
for energy!
to enable it to be repeatedly active
How do we visualize vesicles during synaptic transmission?
Freeze tissues at specific times
How do we know that each receptor ion channel passes a unitary amount of current?
Poke an electrode into a membrane (individual channel- but realistically 3 channels) OR stick it really close then SUCK on the end of the glass to ‘stick’ to the membrane
If you put a bunch of NT in this pipette, you can measure currents as the NT binds the receptor (dont on NMJ)
this shows a specific amount of NT cmoing out. EPSP depends on how many channels are opening.
Each receptor channel is equivalnet,, just the number of them is what matters for summation
increases stepwise function in order of added channels
How do ion channels close?
slowly and irregularly.
You get a decay current and then they come back to zero
Some bind for a long time and others bind quickly
Support the statement “NT is released in unitary vesicles which are additive”
Experiments show that if you stimulate axons a tiny amount (depolarize), you can release about 1-4 vesicles, and determine how much stimulation is needed to cause an EPSP
- this can be variable depending on background activity
- needs to be depolarized 15mV ish
What is Glutamate?
Primary Excitatory NT in the brain!
- Binds to the AMPA receptor (ionotropic)
which physically deforms and allows ions to pass through (cations only- but not selective about which)
What is the AMPA receptor?
glutamate receptor (ionotropic) which physically deforms and allows ions to pass through (cations only- but not selective about which) allow NA to enter and K to exit
reversal potential for ampar is 0mV because na and k act at the same time
what is the difference between reversal potential and equilibrium potential?
reversal is the same as equilibrium EXCEPT that the two ions are always passing and never reach a true equilibirum (like in the AMPA receptor), will always sway to one side or the other.
You will ALWAYS be brought back/trying to reach zero
what causes post synaptic hyper-polarization?
what are some examples of this? what is the effect?
Ionotropic inhibitory NT receptors
- GABA, which activates Cl- receptor channels (GABA a receptors)
[when channels open, chloride rushes into the cell]
Equilibrium potential of Gabaa is -70mV, which doesn’t seem like much, but when paired with an EPSP, this IPSP can prevent reaching threshold! it changes the rate of firing of neurons
SMALL IPSPs can have big effects! only have to depolarize a little bit!
-must act at a very specific window in time in order to silence EPSP
How is information encoded in the stretch reflex circuit? What are the two types of info when converting sensory stimulation into APs?
A stimulus sensitive to stretch is applied, which causes depolarization at the trigger zone, just like an EPSP but no synapse or NT, just morphological change!
1) Strength/magnitude of stim is an increase in spike rate
2) Duration of stimulus is long period of AP firing
As you change amplitude/duration, you get more activity in the neuron and more NT released at the end
what are receptor potentials vs. synaptic potentials?
receptor potentials happen when sending sensory signals from muscle spindles to sensory neurons
synaptic potentials happen between neurons
how are synaptic potentials summed?
Temporal and spatial summation.
Input in dendrites and integration region in the cell body
If another EPSP can happen in the same window as the 1st, before it reaches baseline again, it will push the initial EPSP over the threshold and generate an AP
How are Excitatory and Inhibitoy synapses placed on a cell? Are there other types of synapses mentioned?
Typically inhibitory ones are placed on the cell body or on shaft synapse (axosomatic/axodendritic), and exitatory ones are placed at the end of the dendrites (spines). This allows inhibitory synapses to intercept EPSPs before they reach the soma and generate an action potential
others that modify NT release are placed on axoaxonic synapses
-regulate presynaptic events at the terminal
What is feedforward and feedback inhibition?
Feed Forward: regulates/selects which neurons will fire by activating forward flow to direct the cell to turn off. Direct, a bit faster. Selects which neurons will have activity
Feed Back: constrains activity at physiological levels, allows firing in to some extent, but then that firing ends up activating an inhibitory cell that inhibits ITSELF - keeps things in a range of activity. Can shut off its own circuit and nearby ones from the same circuitry
What is an example of Feed Forward and Feed Back Inhibition?
The reflex circuit!
You want to activate the extensor muscles and inhibit flexor muscles by preventing activity there.
Feedforward: Afferent neurons send signals towards the muscles, and the same circuit that promotes extensor activity, inhibits flexor activity DIRECTLY
In another part of the same circuit, feedback inhibition is working on the extensors when its time for them to turn off, it’s own action inhibits itself by activating an inhibitory neuron in its own circuit
what is convergence and divergence?
convergence: input from presynaptic neurons required to activate the single postsynaptic neuron-common in motor neurons
- neuron will only fire if there is enough activity, won’t cause a behavior if it isn’t sure there is enough stimuli
- allows integration of information
divergence: exemplified in sensory systems (one AP stretches out and activates many neurons)
- allows info to be processed in many different pathways for different purposes
