BMS1052 Lecture Notes - Lecture 3: Sodium-Calcium Exchanger, Tetrodotoxin, Local Anesthetic
30 May 2018
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Week 2. Action potentials II, synaptic transmission and
integration
ACTION POTENTIALS II – PROPOGATION
• An electrical signal is a change in voltage that deviates from the resting membrane potential
• Signal can move via:
1. Passive diffusion of ions through the cytosol
-slow and breaks down over long distances (concentration gradients become smaller)
2. Active- action potentials
-propagates but requires energy
• An action potential is a spike that results in a brief change in the membrane potential
-> neurons hae a stereotpial shape for AP’s hih a e eplaied hages i hael
permeability and ionic concentrations
• The rate ad tiig of AP’s is ho iforatio is oeed.
• Stages of an AP
Depolarisation: becomes more positive
Repolarisation: becomes negative after depolarisation
Hyperpolarisation: becomes more negative than resting potential
1. Depolarisation to threshold
o Depolarisation past the threshold allows voltage
gated Na+ channels to open
o If threshold is not reached -> no AP
o Membrane becomes more permeable to Na than K
-> heads towards Na equilibrium potential
o Initial depolarisation is caused by:
1. physically gated Na+ channels opening
2. may be inherited from elsewhere in neuron
(summation of depolarisations)
2. Voltage gated Na+ channels open
-rapid depolarisation
o When voltage gated Na+ channels open (~1ms)
-> Pna >>Pk
o As Na enter cell, membrane continues to depolarise,
more Na channels open (positive feedback)
3. Voltage gated Na+ channels close
-repolarisation
o Channels close and inactivate
o Na does not reach equilibrium instead as Na
channels close we return to Pna < Pk
(going towards K equilibrium)
o Higher K permeability due to K2P channels ->
repolarisation
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4. Kv delayed rectifier K channels open
-hyperpolarisation
o Delayed rectifier channels open
(K2P leak channels stay open)
o Open at high voltages but opening is delayed
o Now Pna << Pk -> membrane potential approaches K
equilibrium
5. Na+ channels inactivate
-absolute refractory period
o Na channels remain inactive until membrane
potential is hyperpolarised
o Cannot get a second AP for at least 1 ms
o Prevents subsequent AP
o Places limit on information transmitted
6. K+ channels close
-relative refractory period
o Delayed rectifier channels take time to close
o This prolongs hyperpolarisation and makes it more
difficult to initiate further AP (however not
impossible -> if get sufficient Na channels to open,
can initiate another AP)
• Channel openings are stochastic (random)
• Getting to the threshold = spike initiation zone:
o Initial depolarisation by:
1. physically gated Na+ channels opening
2. may be inherited from elsewhere in neuron
(summation of depolarisations)
o Only axons have high density of Na channels
o In most interneurons, there is spike-initiating zone.
o Each time a signal comes in to a dendrite at a synapse, there is a small depolarisation.
These have to diffuse to the cell body and the spike initiation zone. If they add together
and cross threshold, we get a spike.
• Propagation of action potential:
o AP usually propagates away from spike initiating zone (towards axon terminal)
o Self-generated
o Na+ entry causes adjacent membrane to depolarise -> trigger AP
o Inactivated Na channels prevent back flow
o Travels in only one direction however if artificially stimulated in the middle of an axon ->
get AP traellig i oth diretios eause Na haels are’t alread iatiated
• Myelination (Oligodendrocytes and Schwann cells) provides insulation and prevents ion crossing
the membrane
-no AP under myelin
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find more resources at oneclass.com
• Ion channels are concentrated in the Nodes of Ranvier
->AP jump node to node = Saltatory conduction
-diffusion acts quickly over short distances within axon
-separation of nodes is limited by diffusion distance
• Conduction velocity is affected by:
o Thickness
o Temperature
o Myelination
• In Japan, fugu, or certain species of pufferfish, are sold as a delicacy. Preparation is carefully
controlled by law. TTX, or tetrodotoxin is a sodium channel blocker, but it does not cross the
blood-brain barrier. It binds to the voltage-gated sodium channels, preventing them from
opening. Prevents action potentials in peripheral nerves. Remain conscious, but lose electrical
communication in peripheral nerves – i.e. respiratio, peripheral sesatio. Does’t diretl
affect heart.
Lidocaine also blocks sodium channels -> acts as local anaesthetic
find more resources at oneclass.com
find more resources at oneclass.com
