Flashcards in 11/5 Graded Potentials Deck (47)
The basic outline of nyelinated neuron signal transduction:
signal in the dendrites, computed from many different inputs then output through the cell body, to the axon hillock (where if there is a great enough net signal then...) down the axon, to the next neuron where a synapse releases neurotransmitters, that conduct the signal (which may be stored long term and or inform many other cells) to the dendrites of the next cell.
what is ion pore selectivity
the central pore will only allow a specific type of ion to flow through.
what are gating properties of ion channels
they open and close in respone to things such aas membrane potential, ions, hormones, etc.
channesl that open and close due to changes in membrane potential
voltage gated channels
compare the rate of movement in transporters and channels
they channels are fast and the transporters are complex and slow
what is the action of the Na-K pump?
the movement of 2 potassium ions into the cell and three sodium ions out of the cell.
what are the two passive driving forces to move ions?
they are the electrical gradient and the concentration gradient (electrochemical gradient)
why would a normal resting cell tend to pull sodium into itself and expel chlorine ions?
Cations tend to have a force vector into the cell and anions tend to have a force vector out of the cell. (intracellular about -85mv)
what sets the resting potential of a cell?
the Potasium concentrations with a little adjustment by the sodium leak
how to calculate the Vk for a cell?
Vk= 60 log ([Kout]/[Kin])
conceptual interpretation of Vk?
the volatage that must exist across the cell inorder for that concentration difference of K to exist.
why would the action potential go positive when the Na ion channels are opened?
The cell is permiable to K usually and so sets the potential with its equilibrium value, and then when AP is triggered then permeable to Na and so resets the membrane potential to Na equilibrium value (positive value).
What if the cell did not have any open K+ channels -- and then I changed the external potasium concentration by half?
it wouldn't change the resting Vm!
Oh, no I have a membrane that is permeable to multiple ions at the same time, ho do lI find the resting potential?
use the relative membrane permeabilities: and the nernst equation would be modified with the out/in conc. of each ion that is permiable with each conc. multiplied by the ions permiablility!
hmmm,my membrane just became much more permeable to sodium, how will this change my membrane potential?
it will swing the potential towards sodium! this is how we get a action and/or graded potential.
contrast Action potentials moving through a system and graded potentials moving through a system.
Action potentials have a voltage threshold, refractory period and conduct without decrement. Graded potentials have no threshold ror refractory period, have variable amplitude and duration and conduct decrementally, they are depolarizing or hyperpolarizing
contrast the purpose of action potentials and graded potentials:
action potentials relay a signal, such as in the heart or in a nerve axon, graded potentials relay a stimulus that may or may not cause a reaction!
a graded mpotential that leas to action potential are?
synaptic potentials (post-synaptic neurons); Generator potentials/receptor potentials (sensory cells); end plate potentials (skeletal muscle cells)
how did this graded potential originate in my cell?!
external stimuli and neurotransmitters activate ion channels!!
what are some external sitmulus that can cause a graded potential?
pain, light, stretch, temperature, sound etc.
what are some neurotransmitters that can cause a graded potential?
ACh, NE, dopamine, serotonin, glutmate, GABA, glycine, etc.
wait....how can a graded potential be either a depolarizing or a hyperpolarizing stimulus?
let either positive (Na+) or negative (Cl-) ion channels open
great, a graded potential has been created from multiple stimuli and depolarized my cell, how do I know if it will cause an AP?
the AP and the number of AP will depend onthe graded potential causing the cell to depolarize Vm to the AP threshold and the magnitude above the threshold will coorilate to the number of APs!
hmm...graded potential stimuli can be either depolarizing or hyperpolarizing, so what?!
depolarizing stimuli cause Excitatiory postsynaptic potentials, and hyperpolarizing stimuli cuase inhibitory postsynaptic potentials -- EPSPs bring the membrane potential closer to threshold and to firing an action potential. IPSPs bring the membrane farther from it!
what are some Excitatory Postsynaptic portetials (EPSP signals)?
ACh, norepinephrine, epinephrine, dopamine, glutamate, and serotonin.
what are some inhibitory postsynaptic potential (IPSP) signals
Gama-aminobutric acid (GABA) and glycine.
what channels cause a Excitatory ostsynaptic potential?
open Na+ and K+ channels (postive to depolarize and drive potential to about zero, or half between the Na and K nernst potentials)
what channels cause an Inhibitory postsynaptic potential?
Cl- that will drive the potential towards the Vcl of -90mV!
how can graded potentials act as a little computational center in the neuon cell body?
the cell wil recieve multiple IPSP and EPSP that will be graded over space and time through local circuit currents etc. in the cell and sum together to give a net post-synaptic potential (PSP) in the initial segment that can reach a INa threshold to trigger an action potential(s) that will be large, constant and fast with a refractory period etc. as it travels down the axon.
contrast spatial summation and temporal summation in a nerve cell
spatial summation is the summation of multiple pre-synaptic axons giving a signal to the cell. Temporal is the same axon giving a signal in rapid succession; either can lead to a larger graded potential and therefore can cause the PSP to reach the threshold and cause action potential(s)
Action potentials are some uniform, how can they ever cary as much information as the graded potential originally did?
they will vary (and code info) by the average rate of firing, the total number of potentials, and the temporal pattern. (or a combination of signals)
In summary how do we depolarize and repolarize a cell in an action potential?
threshold is reached Na channel opens, sodium postive ion flow in depolarizes the cell, the channel blocks and refractory period, K channels allow K positive ion flow out that will repolarize the cell. the Na channels reset! in sum: outward ionic currents repolarize Vm and inward ionic urrnets depolarize Vm.
How could I slow the rate of rise of the cation potential...hypothetically speaking of course!
by having sodium channel blockers partially inhibit the sodium current.
how could I prolong the duration of an action potential (just sayin')
could slow the sodium channel innactivation!
what if I don't like sodium...what other ion could I use to depolarize and action potential (looking at you cardiac muscle)
what if I just have a little potasium channel blocker thrown in on those cells...?
then it will prolong the action potential by preventing the rapid repolarization of the cell!
how is the cardiac action potential so different (heart alwasy has to be special!0
it is much longer and relies on a calcium current to creat that duration! the refractory period will also be longer (refractory periods are about as long as the AP)
What is the one spot(s) along an axon where the AP can be continued by the presence of a sodium current due to sodium channels (i.e. where are the sodium channels)
at the nodes of Ranvier!
How can I prevent my local circuit currents from excaping from my axon and diminishing before it can cause the next AP down the axon?
by myelinating the axon!!
The horrible disease that attacks the myelination of neruons
man, it is a good thing that the nodes of ranvier are space where they are...why?
the local circuit currents can only propigate a depolarization of the cell so far, even with mylination and so the nodes need to be somewhat close, but the signal is fast!
the hopping of action potential form node of ranvier to node of ranvier
What is the primary cause of the change in membrane potential during an action potential (inital depolarization)
the movement of Na out of the cell due to the opening of Na+ channels.
what is primary responsible for the nerve AP repolarization?
the opening of K+ channels and the influx of potasium into the cell.
What type of ion signal would be an inhibitory post synaptic potential?
opeing of ligand gated chloride channels and omvement of clorid ionsinto the clel leads to hyperpolariztion of the membrane!
how are signals transmitted from the dendrite to the soma of a neouron