RMP + AP Flashcards

1
Q

what establishes the RMP of a cell?

A

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

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2
Q

which is more concentrated, the cell or extracell? what does this mean for osmotic flow?

A

cell as many proteins + soluble mols, with relatively small cell volume

osmotic pressures cause ions to efflux through CSM

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3
Q

what is the RMP in excitable cells e.g. nerve cells?

A

approx -90mV

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4
Q

what are the ions that contribute to RMP?

A

primarily Na+ and K+
also Cl- and HCO3-

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5
Q

what did the Hodgkin and Katz experiments establish?

A

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+

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6
Q

how much more permeable is the cell to K+ than Na+? what does this mean for membrane potential (Em)?

A

100x

lies closer to equilibrium potential for K+ than Na+

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7
Q

what forces apply to K+ to move in/out of the cell? what is the equilbrium potential?

A

insoluble anions within the cell attract K+, causes influx down ECG

K+ leak out of cell down the osmotic gradient

equilibrate at -93mV

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8
Q

what is the equilibrium potential of Na+?

A

+58mV

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9
Q

what does the membrane potential equilibrate at?

A

-87mV

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10
Q

what equation describes the interactions between the ions that move across the membrane?

A

Goldman

takes into account external and internal conc of each ion, giving RMP

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11
Q

why does K+ have a greater effect on RMP than Na+?

A

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.

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12
Q

what maintains the intra + extracellular ion concs?

A

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

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13
Q

what is some pathology associated with RMPs?

A

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

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14
Q

what causes an action potential?

A

a significant enough depolarisation of the membrane potential

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15
Q

why are neurons excitable?

A

due to voltage-dependent ions in their plasma membranes with ion selectivity

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16
Q

how does positive feedback of Na+ work in an AP?

A

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

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17
Q

do action potentials lose amplitude or velocity along the axon?

A

no

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18
Q

what factors determine conduction velocity?

A

degree of myelination
axon diameter

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19
Q

what is the axon in non-myelinated neurons?

A

region of the axon that is depolarised and +ve compared to the outside

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20
Q

how is a local circuit created in the axon?

A

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

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21
Q

define an action potential

A

a transient electrical impulse in which Em is displaced by up to 100mV, becoming more positive due to ion influx

22
Q

how can you initiate an action potential?

A

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

23
Q

what is the difference between action potential and synaptic potential?

A

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

24
Q

describe the course of an AP

A

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

25
Q

draw a diagram of the profile of an AP

A

do it

26
Q

what are the 2 types of synaptic potentials

A

inhibitory: hyperpolarises post-syn
excitatory: depolarised post-syn

(graded potentials)

27
Q

what NTs are involved in the generation of an IPSP?

A

GABA and glycine

28
Q

what NTs are involved in the generation of an EPSP?

A

ACh and glutamate

29
Q

why are many synaptic potentials needed to trigger an AP?

A

SPs have smaller amplitude
do not have refractory period and degrade quickly as they move away from the synapse

30
Q

what increases conduction speed of an AP?

A

larger diameter = smaller internal resistance = faster rate of conduction

or myelination

decreased capacitance

31
Q

how wide and fast is unmyelinated giant squid axon vs unmyelinated mammalian axon?

A

S = 500 micrometres and 20 m/s
M = 1-2 micrometres and 2 m/s

32
Q

how wide and fast is unmyelinated giant squid axon vs myelinated mammalian axon?

A

US = 500 micrometres and 20 m/s
MM = 1-2 micrometres and 50 m/s

myelination makes the most difference

33
Q

why does myelination increase conduction velocity?

A

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

34
Q

what is a common demyelination disease? what are the symptoms?

A

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

35
Q

how is the action potential propagated?

A

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

36
Q

when have you reached Nernst Potential?

A

when K (IN) = K (OUT)

37
Q

what are the gradients that apply to K+ in the establishment of RMP?

A

In = down electrostatic gradient
out = down conc gradient

38
Q

what are the concentrations of ions inside the cell?

A

K+ = 140mM
Na+ = 15mM
Cl- = ranging (less than extracell)
HCO3- = 10-20mM

39
Q

what are the concentrations of ions outside the cell?

A

K+ = 4mM
Na+ = 140mM
Cl- = 110mM
HCO3- = 25mM

40
Q

what does Nernst potential tell you?

A

that (e.g.) K+ will move out of the cell down its gradient until the inside of the cell becomes -93mV

41
Q

why do we use ‘digital’ APs instead of analogue?

A

axons are very long, would take a long time for ions to diffuse….

42
Q

what voltage do APs reach? why?

A

+30mV

at this point, Na+ channels inactivate

43
Q

what is saltatory conduction?

A

propagation of action potentials along myelinated axons by depolarisation

it is dependent on myelination of axons

44
Q

what creates the myelin sheath?

A

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

45
Q

why does current not pass through the axon in thick axons?

A

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

46
Q

what is myelin composed of?

A

condensed layers of PPLs
therefore powerful electrical insulator

47
Q

how does myelination increase the resistance of the membrane and what does this mean for the path of least resistance?

A

is a powerful electrical insulator

path of LR is not through axon, increases proportion of charge propagated through axon rather than leaking out

48
Q

why do Nodes of Ranvier also increase propagation speed?

A

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

49
Q

why is saltatory conduction and myelination faster?

A

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

50
Q

is myelination faster in very fine axons?

A

no, reduces conduction velocity