electrode potentials Flashcards

1
Q

membrane potential

A

the potential difference between the inside and outside the cell
-inside -outside
-outside usual;ly define by 0

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2
Q

how to experimentally measure membrane potential

A
  • fill a micro electrode(fine glass pipette) with a conducting solution (KCL)
    -then penetrate the microelectrode into the cell membrane to measure membrane potential
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3
Q

depolarization

A

A decrease in the size of the membrane potential from its normal value. Cell interior becomes less negative e.g. a change from – 70 mV to – 50 m

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4
Q

hyperpolarization

A

An increase in the size of the membrane potential from its normal value. Cell interior becomes more negative e.g. a change from – 70 mV to – 90 mV

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5
Q

what to consider when setting up membrane potentials

A

-concentration gradient(chemical gradient)
-charge gradient (electrical forces)

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6
Q

what is setting up a resting potential dependent on

A
  • concentration gradient the concentration of ions inside and outside of the cell affects the movement of ions
    -sodium-potassium pump is responsible for setting up membrane potential.
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7
Q

equilibrium potential

A

-there is no net movement of ions across a membrane the concentration gradient and charge gradient are equal
-thought of as opposite forces so when the outward diffusion gradient exceeds the inward charge gradient ions move out of the cell

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8
Q

calculating equilibrium potential for K+

A
  • nernest equation, write on cheatsheet
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9
Q

how do we calculate real membrane potentials

A
  • use the GHK equation
    -because real membrane have channels open for more than one type of ion and the contribution of each ion depends on how permeable the membrane is to that ion
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10
Q

excitatory synapses

A
  • Excitatory transmitters open ligand-gated channels that cause membrane depolarization
  • Can be permeable to Na+, Ca2+ or sometimes cations in general
  • The resulting change in membrane potential is called an excitatory post-synaptic potential (EPSP)
    -action potential generated
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11
Q

Inhibitory synapses

A
  • Inhibitory transmitters open ligand-gated channels that cause hyperpolarization
  • Can be permeable to K+ or Cl-
  • The resulting change in membrane potential is called an inhibitory post-synaptic potential (IPSP)
    -no action potential
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12
Q

what are action potentials for?

A
  • passing information along axons causing the release of neurotransmitters or hormones
    -have different thresholds in different body parts
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13
Q

how do we know the direction ions will move in?

A
  • concentration gradient= ions will usually move from an area of high concentration to an area of low concentration
    -electrical charge is also considered to know which side ions will be attracted to and which side repulsion will occur
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14
Q

action potential threshold in axon

A

plus thirty

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15
Q

action potential threshold in skeletal muscle

A

plus forty

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16
Q

action potential threshold in the sino-atrial node

A

plus thirty

17
Q

action potential threshold in cardiac ventricle

A

plus thirty

18
Q

resting potential

A
  • sodium-potassium pump moves 3 sodium ions out and 2 potassium ions in by active transport
    -sodium ion channels are closed and potassium ion channels are open allowing facilitated diffusion
    -therefore, the membrane is more permeable to potassium ions
  • therefore the membrane is polarised.( more positive outside than inside)
    -resting potential= -70
19
Q

how action potential is intiated

A

stimulus causes sodium ion channels to open so sodium ions diffuse into the cell. (membrane is more permeable to sodium)
-when the potential difference reaches -55v, positive feedback occurs so more sodium ion channels open and more sodium ions diffuse into the cell.
-depolarisation occurs (inside more positive than outside). reaches+40v

20
Q

recovery after an action potential

A

-repolarisation = sodium ion channels close and potassium channels open. potassium diffuses out of the cell bringing the potential difference back to more positive than inside.
-there is a potential difference overshoot. making the cell hyperpolarised
-original potential difference is returns and resting potential is maintained by the sodium-potassium pump
- reactionary period= recovery period. after action potential neurones cant be excited straight away

21
Q

basic structure of NA+ channels

A

-complex arrangement of proteins that forms a transmembrane pore through which sodium ions can pass in response to changes in the cell membrane potential.
-primary structural component is the alpha subunit, which is responsible for ion conduction and gating.
-It consists of four homologous domains (I to IV), and each domain has six transmembrane segments (S1 to S6).
-Voltage sensors are present in the S4 segment of each domain and play a crucial role in responding to changes in the membrane potential

22
Q

basic structure of K+ channels

A

-have a tetrameric structure, consisting of four alpha subunits.
-Each subunit consists of six transmembrane segments (S1 to S6).
-S1 to S4 form the voltage-sensing domain, and S5 and S6 form the pore-forming domain

23
Q

comparison of K+ channels and Na+ channels

A
  • Na+ channels alpha subunits are linked whereas in K+ they are four separate units
24
Q

how does the action potential propagate along the axon

A
  • can only travel in one direction from the cell body down the axon
    -travels without a loss in amplitude
25
Q

local current

A
26
Q

length constant

A
  • the distance it takes for the potential to fall to thity7% of its original value
  • influences how efficiently the action potential is propagated down the axon.
    -Neurons with longer length constants can propagate action potentials more effectively over longer distances without significant loss of the depolarizing signal
27
Q

saltatory conduction

A

-The membrane is only depolarised at the nodes of Ranvier
-creates a longer localised circuit;
-increases the rate of impulse transmission;
-occurs in myelinated neurones

28
Q

neuromuscular junction

A
  • the synapse between a nerve and a skeletal muscle fibre
    -called a chemical synapse
29
Q

actions at the neuromuscular junction

A

-An action potential travels down the axon of a motor neuron
-When the action potential reaches the axon terminals at the neuromuscular junction, it triggers the opening of voltage-gated calcium channels in the presynaptic neurone
-there is an influx of calcium ions
-calcium ions bind to synaptotagmin
-the snare complex makes vesicles containing ACh to fuse with the presynaptic membrane
-Acetylcholine is released into the synaptic cleft (
-Acetylcholine diffuses across the synaptic cleft and binds to acetylcholine receptors on the postsynaptic membrane (motor end plate) of the muscle fibre.
The binding of acetylcholine to its receptors causes the opening of these ion channels, allowing an influx of sodium ions into the muscle fibre.
-This influx results in a local depolarization which causes an action potential triggering muscle contraction

30
Q

nicotinic receptor

A
  • ACh binding site
    ACh binds to each alpha subunit causing a conformational change leading to the opening of the pore
31
Q

competitive blockof ACh by d-tubocurarine

A
  • competes with ACh for the binding site on the nicotinic receptor
    -prevents a conformational change from occurring therefore inactivation of the receptor
32
Q

block of ACh by succinylcholine

A

-succinylcholine functions as a depolarizing neuromuscular blocker, leading to a prolonged activation of the nicotinic receptors
-Succinylcholine initially acts as an agonist at the nicotinic receptors. It binds to the receptor sites on the postsynaptic membrane at the neuromuscular junction.
-Unlike acetylcholine, which is rapidly broken down by acetylcholinesterase after binding to the receptor, succinylcholine is more resistant to enzymatic degradation.
As a result, succinylcholine induces a persistent depolarization of the postsynaptic membrane.
-Succinylcholine keeps the nicotinic receptors activated for a more extended period compared to acetylcholine.
-This prolonged depolarization prevents the muscle fibre from responding to subsequent nerve impulses and leads to temporary paralysis.

33
Q

clinical use of neuromuscular blockers

A

= They are added in combination with general anaesthetic to cause temporary paralysis during surgery

34
Q

difference between ACh binding to nicotinic and muscarinic receptors

A

-nicotinic receptors produce a fast depolarisation because it is a ligand-gated ion channel
-muscarinic receptor produces a slower response because they are G =-protein =s which trigger a cascade of events in the cell