Action Potential

 A brief increase in the

permeability of the cell
membrane to Na+(allow
ions to rush into the cell),
immediately followed by
the transient increase in
the permeability of the
membrane to K+ (allow
them to rush out of the
cell)
 1. Depolarization 2. Repolarization
phase phase

Threshold potential

Resting potential
3. Hyperpolarization phase
 https://www.youtube.com/watch?
v=ifD1YG07fB8
Two important types of ion channels:
1.) Na+ voltage gated channels
2.) K+ voltage gated channels

How voltage-gated channels work

At the resting potential, voltage- Conformational changes open

gated Na+ channels are closed. voltage-gated channels when
the membrane is depolarized.
Resting Potential - Both voltage gated Na+ and K+ channels are
closed.
Initial Depolarization - Some Na+ channels open. If enough Na+
channels (voltage dependent ion channels) open, then the threshold
is surpassed and an action potential is initiated.
The influx of positively charged sodium ions -------- rapid change in
membrane potential from -70mv to +40mv
Na+ channels open quickly. K+ channels are still closed ( as they
are less sensitive than voltage dependent sodium channels) .
Require greater level of depolarization to open. Will open later
than sodium channels.
PNa+ > PK+
AP reaches at its peak in about 1 msec. Na+ channels self-inactivate (become
refractory) become blocked, No more Na+ entered into the cell. Then K+
channels are open ( move freely through the membrane). Inside is positively
charge at this time. K+ driven out of the cell by FOD and FOEP. Outflow of
cations------- MP to normal value. K+ channels become to close again
PK+ >> PNa+
MP become normal. K+ channels closed. No more K+ leaves the cell. Na+
channels reset so that another depolarization cause them to open again
Emembrane ≈ E K+
PK+ > PK+ at resting state
 Membrane overshoot
(hyperpolarized) its resting value (-
70mv) gradually returns to normal.
Accumulation of K+ ions outside
the membrane are responsible for
this temporary Hyper pol.
 Extra K+ ions diffused away
 MP returns to -70mv
 SP transporters remove the Na+
ions that leaked in and retrieve the
K+ ions that leaked out.
Resting Potential - Both Na+ and K+ channels are closed.
 Axonal Conduction: All or none law
This law states that an action
potential either occurs of does not
occur and once triggered it will be
transmitted down to the end of the
axon
AP remains same in size
All or none law is supplementary
by rate law (a high rate of firing/
production of AP cause a strong
muscle contraction, and a strong
stimulus (bright light) causes a high
rate of firing in axons.
PROPAGATION OF ACTION POTENTIAL

Axon
Neuron

1. Na+ enters axon.

2. Charge spreads;
membrane
“downstream”
depolarizes.

Depolarization at
next ion channel

3. Voltage-gated
channel opens in
response to
depolarization.
 3 4

2 6
1 5

Review of Process:
Why does the membrane potential increase during stage 3 of the action potential?

A. Both the voltage-gated Na+ channels and voltage gated K+ channels are open.

B. All of the K+ channels (both leak and voltage gated) are open.

C. The voltage gated Na+ channels are open, but the voltage gated K+ channels have
not opened yet.

D. The voltage gated Na+ channels are open, but the K+ channels (both voltage gated
Action potentials jump down axon.
Action potential jumps
from node to node

Nodes of Ranvier Axon

Schwann cells (glia)
wrap around axon,
forming myelin sheath
Schwann cell membrane
wrapped around axon
Babies need lots of fat – not only for energy storage but also to myelinate their neurons.
 Disease results in damage to
myelin and impairs electrical
signaling.

 Muscles weaken and coordination

decreases.
Communication
Between
Neurons
These chemicals are
 Neurotransmitters Hormones
released by terminal
buttons (short distance)
 Neuromodulators
released by terminal
buttons (long distance,
travel further, dispersed
more widely than
neurotransmitters,
modulate the activity of
many neurons in
particular brain areas)
composed of protein like
(peptides)
 Synapse
 Binding site: chemical exert
their effect by attaching to a
particular region of a receptor
called BS
 Ligand: A chemical that
attaches to a binding site is
called ligand
 Neurotransmitters ,neuro-
modulators and hormones are
natural ligands
 Presynaptic
membrane:

 Location of synapses
On dendrites (axodendritic)
On soma (axosomatic) Post synaptic
On other axon (axoaxonic) membrane:
located on the
neuron that
received message
 Synaptic cleft:
The two membranes(pre and post)
face each other across synaptic cleft
A gap that varies from synapse to
synapse (about 20 nm wide)
SC contain extracellular fluid in which
the NT diffused
Presynaptic

Postsynaptic
 neurotransmitter

Synaptic vesicle
Neurotransmitter
transporter Axon Terminal
Voltage- (pre-synapse)
gated
Ca++
channel Neurotransmitter
Receptor
Don’t worry Synapse
about this
Dendrite
(post-synapse)
ACTION POTENTIAL TRIGGERS RELEASE OF
NEUROTRANSMITTER

Na+ and K+ 1. Action potential arrives;

channels Action triggers entry of Ca2+.
potentials
Presynaptic 2. In response to Ca2+, synaptic
vesicles fuse with presynaptic
membrane
membrane, then release
(axon)
neurotransmitter.

3. Ion channels open when

Postsynaptic neurotransmitter binds; ion
flows cause change in
membrane
postsynaptic cell potential.
(dendrite or
cell body)
4. Ion channels will close as
neurotransmitter is broken
down or taken back up by
presynaptic cell (not shown).
 Excitatory synapses cause the post-
synaptic cell to become less
negative triggering an excitatory
post-synaptic potential (EPSP)
 Increases the likelihood of firing an action
potential

 Inhibitory synapses cause the post-

synaptic cell potential to become
negative triggering an inhibitory
post-synaptic potential
 Decreases the likelihood of firing an
action potential
 Four types of NT dependent ion
channels found in the PSM
 Sodium (Na+)----- depolarization---
EPSP
 Potassium (K+)----
hyperpolarization----IPSP
 Chloride (Cl-)---- neutralize EPSP
 Calcium (Ca2+)-----depolarize----
EPSP