RMP + AP Flashcards
what establishes the RMP of a cell?
the presence of large stationary anions within the cell
phosphate groups + amino acids
fixed -ve charge attracts +ve ions from extracellular material, establishes inflow of charge
which is more concentrated, the cell or extracell? what does this mean for osmotic flow?
cell as many proteins + soluble mols, with relatively small cell volume
osmotic pressures cause ions to efflux through CSM
what is the RMP in excitable cells e.g. nerve cells?
approx -90mV
what are the ions that contribute to RMP?
primarily Na+ and K+
also Cl- and HCO3-
what did the Hodgkin and Katz experiments establish?
1ry ion influencing RMP is K+
experimentally altered conc of K+ inside/outside cell and when the gradient across the membrane for K+ was 0, the RMP became approx 0mV
membrane is most permeable to K+
how much more permeable is the cell to K+ than Na+? what does this mean for membrane potential (Em)?
100x
lies closer to equilibrium potential for K+ than Na+
what forces apply to K+ to move in/out of the cell? what is the equilbrium potential?
insoluble anions within the cell attract K+, causes influx down ECG
K+ leak out of cell down the osmotic gradient
equilibrate at -93mV
what is the equilibrium potential of Na+?
+58mV
what does the membrane potential equilibrate at?
-87mV
what equation describes the interactions between the ions that move across the membrane?
Goldman
takes into account external and internal conc of each ion, giving RMP
why does K+ have a greater effect on RMP than Na+?
more K+ leak channels
membrane 100x more permeable to K+
Na+ can enter cell down its conc grad but there are less channels, so less influence.
what maintains the intra + extracellular ion concs?
Na/K ATPase
pumps 3 Na+ out and 2 K+ in using energy from hydrolysis of ATP
ions stay on the side they were pumped to unless there is a leak channel, bc membrane is impermeable to them, maintaining conc grad
what is some pathology associated with RMPs?
in anorexia, when refeeding, can develop hypokalemia
as during fasts, intracellular K+ used to maintain serum K+ levels, refeeding can cause rapid uptake of K+ leaving insufficient K+ in blood + ECF
hyperpolarisation of neurons = muscle weakness + hyporeflexia
what causes an action potential?
a significant enough depolarisation of the membrane potential
why are neurons excitable?
due to voltage-dependent ions in their plasma membranes with ion selectivity
how does positive feedback of Na+ work in an AP?
if neuron sufficiently depolarises to threshold potential, Na+ channels change shape allowing ions to flow into neuron down ECG
local influx causes depolarisation which drives other channels to open
+ve feedback in Na+ permeability
do action potentials lose amplitude or velocity along the axon?
no
what factors determine conduction velocity?
degree of myelination
axon diameter
what is the axon in non-myelinated neurons?
region of the axon that is depolarised and +ve compared to the outside
how is a local circuit created in the axon?
ahead of the active zone the cell has a negative potential, creating potential difference along the axon and local circuit currents which flow between the portions of the axon
define an action potential
a transient electrical impulse in which Em is displaced by up to 100mV, becoming more positive due to ion influx
how can you initiate an action potential?
ACh binding to and opening ligand-gated Na+ channels on post-syn membrane
if enough ACh excreted, enough ligand-gated ion channels open to depol the membrane past threshold potential -55mV
once past threshold, Na+ v.g. channels are activated and they start to initiate AP
what is the difference between action potential and synaptic potential?
SP: the electrical potential difference across the post-synaptic membrane
AP: occurs as a result of summation of many synaptic potentials across the membrane of a neuron
describe the course of an AP
stimulus occurs, if it causes membrane to depolarise to threshold i.e.
enough of a sensory change e.g. in stretch channels to open enough channels to let enough Na+ in to reach threshold
then v.g. Na+ channels open, depol occurs, Na+ slowly close, K+ are slowly opening the whole time
Na+ shut, become inactivated, K+ floods in, repols the cell towards Ek, absolute refractory period, Na+ channels stop being inactivated.
then hyperpolarises, K+ channels shut, relative refractory period: AP can be initiated but large stimulus is needed, Na/K returns cell to RMP
draw a diagram of the profile of an AP
do it
what are the 2 types of synaptic potentials
inhibitory: hyperpolarises post-syn
excitatory: depolarised post-syn
(graded potentials)
what NTs are involved in the generation of an IPSP?
GABA and glycine
what NTs are involved in the generation of an EPSP?
ACh and glutamate
why are many synaptic potentials needed to trigger an AP?
SPs have smaller amplitude
do not have refractory period and degrade quickly as they move away from the synapse
what increases conduction speed of an AP?
larger diameter = smaller internal resistance = faster rate of conduction
or myelination
decreased capacitance
how wide and fast is unmyelinated giant squid axon vs unmyelinated mammalian axon?
S = 500 micrometres and 20 m/s
M = 1-2 micrometres and 2 m/s
how wide and fast is unmyelinated giant squid axon vs myelinated mammalian axon?
US = 500 micrometres and 20 m/s
MM = 1-2 micrometres and 50 m/s
myelination makes the most difference
why does myelination increase conduction velocity?
depolarisation travels further in each movement to reach the channels which are only present in the Nodes of Ranvier
also reduces CM as layers of insulation can behave as capacitors
what is a common demyelination disease? what are the symptoms?
Multiple Sclerosis
autoimmune: myelin sheath targeted
if severe, AP may decay before reaches Na+ channels at the next Node = propagation failure since there are no Na+ channels inbetween
= numbness + weakness in limbs
how is the action potential propagated?
depol caused by one Na+ channel is able to aid activation of next, helps propagate p.d.
as flow of charge in the membrane is a current, induces a magnetic field causing flow of charge through the axon
when have you reached Nernst Potential?
when K (IN) = K (OUT)
what are the gradients that apply to K+ in the establishment of RMP?
In = down electrostatic gradient
out = down conc gradient
what are the concentrations of ions inside the cell?
K+ = 140mM
Na+ = 15mM
Cl- = ranging (less than extracell)
HCO3- = 10-20mM
what are the concentrations of ions outside the cell?
K+ = 4mM
Na+ = 140mM
Cl- = 110mM
HCO3- = 25mM
what does Nernst potential tell you?
that (e.g.) K+ will move out of the cell down its gradient until the inside of the cell becomes -93mV
why do we use ‘digital’ APs instead of analogue?
axons are very long, would take a long time for ions to diffuse….
what voltage do APs reach? why?
+30mV
at this point, Na+ channels inactivate
what is saltatory conduction?
propagation of action potentials along myelinated axons by depolarisation
it is dependent on myelination of axons
what creates the myelin sheath?
PNS: schwann cells create insulating layered membrane called myelin that surrounds axon, leaving gaps rich in K+ and Na+ channels (NoR)
CNS: oligodendrocytes insulate entire neurons
why does current not pass through the axon in thick axons?
it takes the path of least resistance, which is out through the membrane and along the outside
thus the AP decays too quick in the axon and cannot be propagated through there
what is myelin composed of?
condensed layers of PPLs
therefore powerful electrical insulator
how does myelination increase the resistance of the membrane and what does this mean for the path of least resistance?
is a powerful electrical insulator
path of LR is not through axon, increases proportion of charge propagated through axon rather than leaking out
why do Nodes of Ranvier also increase propagation speed?
have high conc of v.g. Na+ channels in close proximity: depol can activate them all at once, rapidly increasing membrane’s permeability to Na+ ions
causes large influx of +ve charge, inducing strong magnetic field
but neighbouring axon is insulated and cannot be depol, therefore mag field induces currents in the insulated region of the axon and depols next node
distance travelled depends on strength of induced mag field
why is saltatory conduction and myelination faster?
without myelination, whole axon needs to be depol
myelin also decreases membrane capacitance: smaller influx of charge can depol the membrane compared to unmyelinated axon
is myelination faster in very fine axons?
no, reduces conduction velocity
