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MCDB 3650 Class 3
Website: http://mcdb.colorado.edu/courses/3650
Recap from last class
Neurons conduct electricity. They do so because they are
differently permeable to different ions, and thus have an
electrical potential across their cell membrane.
Membrane potential is caused by:
1.  concentration gradients of ions
2.  charge (voltage) gradient
Res%ng Poten%al: The state at which the concentra.on and voltage gradient are equal across the neuronal membrane: net flux of ions is equal! The “equilibrium potential” is defined as:
a.  When there is no ion flow across the membrane
b.  When the concentration gradient and electrical
gradient are counterbalanced for a single ion
c.  When the concentration of all ions are equal on both
sides
When the concentration gradient for an ion is known, the
equilibrium potentials can be calculated using the Nernst
Equation. For a typical neuron:
EQUIL. POT.
K+
-90 mV
Na+ +60 mV
Cl-70 mV
•  Resting membrane potential
–  two forces act on ions to produce net
passive diffusion across a membrane
•  the concentration gradient for each ion
•  electrical gradient for each ion.
•  When two forces on ONE ion are equal
and opposite, this is called the
“equilibrium potential”
What happens to the resting membrane potential of the
neurons in Tomekia’s body when exposed to TTX?
You said (mostly): nothing
TTX blocks the Na+ channel
What happens to K+?
K+ continues to flow out, leaving the inside more
negative than usual: resting membrane is more negative
This also affects the repolarization rate (falling phase)
—speeding it up since no Na is countering K
Touching an Amazon jungle bird causes
numbness and an extended positive
membrane potential in neurons.
What else besides blocking K+ channel
could cause this?
Prevents closing of Na+ channels
Synaptic Transmission
Learning Goals:
1.  Connect the flow of neurotransmitters through an axon to the
mechanism of its potential effect on another neuron
2.  Outine the steps in chemical synaptic transmission and predict
changes in the efficacy of transmission when the system is
perturbed (e.g. changes in ion concentrations or addition of
drugs).
3.  Explain the role of the neurotransmitter receptor in
determining a neurotransmitter’s effect on the post-synaptic
cell.
4.  Compare the mechanisms of action and output of different
neurotransmitters
Propagation of information
How does an incoming action potential
travel down the axon and ultimately
affect another cell (neuron, muscle, etc)
Passive movement of current
continues to trigger
depolarization of each
section of axon
But, because current can
also leak out of the axon,
this propagation could be
quite slow, or even stop.
3.12 Action potential conduction requires both active and passive current flow. (Part 1)
Propagation down the axon
The electrical change in the membrane allows Na channels
nearby to open, carrying the action potential down the axon
Why can’t the action potential flow the other way?
K channels reopen and K+ flows out. Na channels take time to reopen after they shut so the membrane is in a refractory period
An axon with a larger diameter will conduct an action
potential
a.  Faster than a small diameter axon because of
lower internal resistance
b.  Faster than a small diameter axon because of
higher internal resistance
c.  Slower than a small diameter axon because of
higher internal resistance
d.  Slower than a small diameter axon because of
lower internal resistance
Myelination: insulation
glial cells called oligodendrocytes wrap around the axon
Different axons have different amounts of myelination,
and different diameters
These two factors together determine speed of
conduction
Myelination: insulation
Myelination decreases the internal resistance to passive current flow
(under the myelin sheath, no ions can leak out)
This allows the action potential to “hop” from node to node
Myelination speeds up conduction from ~10 meters/sec to ~150 meters/
sec!
Loss of myelination has severe consequences: e.g. multiple sclerosis
Communication between neurons
What is transmitted between a
neuron and its target?
5.4 Loewi’s experiment demonstrating chemical neurotransmission. (Part 1)
Otto Loewi, 1926
Stimulation of the vagus nerve slows heart rate
Vagus nerve was releasing a chemical that was flowing through the heart:
Acetylcholine
5.1 Electrical and chemical synapses differ fundamentally in their transmission mechanisms.
Which is more
common in human
nervous system?
a.  Electrical
synapses
b.  Chemical
synapses
Not very common: Hormone secreting
neurons within hypothalamus
Most synapses!
5.3 Sequence of events involved in transmission at a typical chemical synapse.
Label the steps of
transmission
on your diagram
What triggers
vesicle fusion and
transmitter
release?
What causes
response in postsynaptic cell?
How can synaptic transmission be affected at the
neuromuscular junction?
1.  Each group: look up the toxin on the index card at your
table:
Sarin, Latrotoxin, Botulinum, Tetanun, Curare, Fampridine
2.  What’s the mechanism of action? Indicate on the
drawing of the synapse where this toxin acts.
3.  How will it affect individual action potentials and
muscular contraction? (Draw effects on other side of
handout)
4.  Agree as a table and transfer a sketch of the neuron and
the trace (action potential and muscle response) to a
white board to share with class