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POWERPOINT® LECTURE SLIDE PRESENTATION
by LYNN CIALDELLA, MA, MBA, The University of Texas at Austin
Additional text by J Padilla exclusively for physiology at ECC
UNIT 2
8
PART A
Neurons:
Cellular and Network
Properties
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
DEE UNGLAUB SILVERTHORN
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
FOURTH EDITION
About this Chapter
 Organization of the nervous system
 Electrical signals in neurons
 Cell-to-cell communication in the nervous system
 Integration of neural information transfer
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Nervous System Subdivisions
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Organization of the Nervous System
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Figure 8-1
Model Neuron
Dendrites receive incoming signals; axons carry outgoing information
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Figure 8-2
Cells of Nervous System (NS):
Axons Transport
 Slow axonal transport
 Moves material by axoplasmic flow at 0.2–2.5 mm/day
 Fast axonal transport
 Moves organelles at rates of up to 400 mm/day
 Forward transport: from cell body to axon terminal
 Backward transport: from axon terminal to cell body
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Cells of NS: Glial Cells and Their Function
Glial cells maintain an environment suitable for
proper neuron function
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Figure 8-5 (1 of 2)
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Graded Potential
 The cell body receives
stimulus
 The strength is determined
by how much charge
enters the cell
 The strength of the graded
potential diminishes over
distance due to current
leak and cytoplasmic
resistance
 The amplitude increases
as more sodium enters, the
higher the amplitude, the
further the spread of the
signal
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Electrical Signals: Graded Potentials
Subthreshold and
suprathreshold
graded potentials
in a neuron
If a graded potential
does not go beyond
the treshold at the
trigger zone an action
potential will not be
generated
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Figure 8-8a
Electrical Signals: Graded Potentials
Depolarizing
grading potential
are excitatory
Hyperpolarizing
graded potentials
are inhibitory
Graded potential=
short distance, lose
strength as they
travel, can initate
an action potential
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Figure 8-8b
Electrical Signals: Trigger Zone
 Graded potential enters trigger zone- summation brings it to
a level above threshold
 Voltage-gated Na+ channels open and Na+ enters axon – a
segment of the membrane depolarizes
 Positive charge spreads along adjacent sections of axon by
local current flow – as the signal moves away the currently
stimulated area returns to its resting potential
 Local current flow causes new section of the membrane to
depolarize – this new section is creating a new set of action
potentials that will trigger the next area to be depolarized
 The refractory period prevents backward conduction; loss
of K+ repolarizes the membrane – Once the Na+ close they
will not open in response to backward conduction until they
have reset to their resting position- ensures only one action
potential is initiated at time.
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Electrical Signals: Voltage-Gated Na+ Channels
Na+
channels
have two
gates:
activation
and
inactivation
gates
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Figure 8-10c
Changes in Membrane Potential
Terminology associated with changes in membrane
potential (chpt 5 figure)
PLAY Animation: Nervous I: The Membrane Potential
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Figure 5-37
Electrical Signals: Action Potentials
Cell is
more
positive
outside
than
inside
Rising phase
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Figure 8-9 (1 of 9)
Electrical Signals: Action Potentials
Rising phase
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As ions
move
across the
membrane
the
potential
increases
Figure 8-9 (2 of 9)
Electrical Signals: Action Potentials
Rising phase
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Graded
potentials
have
brought
the
membrane
potential
up to
threshold
Figure 8-9 (3 of 9)
Electrical Signals: Action Potentials
Rising phase
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Beyond
threshold
potential the
sodium gated
channels
allow the ion
to move in,
making the
inside of the
cell more
positive
Figure 8-9 (4 of 9)
Electrical Signals: Action Potentials
Na+ continues to move into the cell until it
reaches electrical equilibrium. At that
point Na+ movement stops
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Figure 8-9 (5 of 9)
Electrical Signals: Action Potentials
Falling phase
K+ moves out of the cell along its
gradient and the inside of the cell
becomes more and more negative
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Figure 8-9 (6 of 9)
Electrical Signals: Action Potentials
Hyperpolarization (undershoot) occurs when
the potential drops below resting; caused by
the continuing movement of K+ out of the cell
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Figure 8-9 (7 of 9)
Electrical Signals: Action Potentials
Leaked Na+ & K+ in cell increases
potential toward resting voltage
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Figure 8-9 (8 of 9)
Electrical Signals: Action Potentials
Returns to its original state where the outside
is more positive than the inside and the
membrane potential is -70mv
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Figure 8-9 (9 of 9)
Electrical Signals: Ion Movement
During an Action Potential
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Figure 8-11
Electrical Signals: Action Potentials
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Figure 8-9
Electrical Signals: Refractory Period
Action potentials will not fire during an absolute refractory period
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Figure 8-12
Action Potential Travel Down Axon
Each region of the
axon experiences a
different phase of the
action potential
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Electrical Signals: Myelinated Axons
Saltatory
conduction- signal
seems to “jump” from
node to node moving
swiftly- compensates
for smaller diameter.
Demyelination slows
down signal
conduction because
the current leaks.
Sometimes
conduction does not
reach the next node
and dies out.
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Electrical Signals: Speed of action potential
 Speed of action potential in
neurons is influenced by:
 Diameter of axon
 Larger axons are faster- less
resistance to ion flow due to the
larger diameter. Large diameter
axons are only found in animals
with small less complex nervous
systems.
 Resistance of axon membrane to ion
leakage out of the cell
 Myelinated axons are faster – the
myelin sheath insulates the
membrane allowing the action
potential to pass along myelinated
are sustaining conduction without
slowing down by ion channels
opening.
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Electrical Signals: Coding for Stimulus Intensity
Since all action potentials are identical, the strength
of a stimulus is indicated by the defrequency of
action potentials. Neurotransmitter amounts
released are directly propertional to frequency as
long as a sufficient supply is available
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Figure 8-13b
POWERPOINT® LECTURE SLIDE PRESENTATION
by LYNN CIALDELLA, MA, MBA, The University of Texas at Austin
Additional text by J Padilla exclusively for physiology at ECC
UNIT 2
5
PART A
Membrane Dynamics
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
DEE UNGLAUB SILVERTHORN
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
FOURTH EDITION
Electricity Review
 Law of conservation of electrical charges- the net
amount of electrical charge produced in any process
is zero.
 Opposite charges attract; like charges repel each
other- happens with protons & electrons
 Separating positive charges from negative charges
requires energy – membrane pumps use active
transport so separate ions
 Conductor versus insulator – a conductor allows
the charges to move towards each other and an
insulator keeps them separate- does not carry current.
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Separation of Electrical Charges
Resting membrane potential is
the electrical gradient
between ECF and ICF
Inside of the cell is
more negative than
the outside
Electrical gradient
create the ability to
do work just like
concentration
gradients
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Figure 5-32b
Separation of Electrical Charges
Resting membrane potential is the electrical gradient
between ECF and ICF. Resting membrane potential
is due mostly to potassium- it is the equilibrium
potential of K+
A relative scale
shifts the charge
to a -2
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Figure 5-32c
Potassium Equilibrium Potential
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Sodium Equilibrium Potential
Can be calculated using the
Nernst Equation
Concentration
gradient is
opposed by
membrane
potential
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Figure 5-35
Electrical Signals: Nernst Equation
 Predicts membrane potential for single ionmembrane potentials result from an uneven
distribution of ions across a membrane.
 Membrane potential is influenced by :
 Concentration gradient of ions – Na+, Cl-, & Ca2+
have higher [extracellular] and K+ has a higher
[intracellular]
 Membrane permeability to those ions - only K+ is
allowed to move in so this ion contributes to the
resting potential
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Electrical Signals: GHK Equation
 Predicts membrane potential using multiple ionsresting membrane potential= the contribution of all
ions that cross the membrane X membrane
permeability values. Ion contribution is proportional
to membrane permeability for that ion. Potentials
will be affected if ion concentrations change.
 P=permeability value
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Electrical Signals: Ion Movement
 Resting membrane potential determined by
 K+ concentration gradient
 Cell’s resting permeability to K+, Na+, and Cl–
 Gated channels control ion permeability
 Mechanically gated – respond to physical forces
(pressure)
 Chemical gated - respond to ligands (neurotransmitter)
 Voltage gated - respond to membrane potential
changes
 Threshold voltage varies from one channel type to
another – the minimum stimulus required and the
response speed varies for each type
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Cell-to-Cell: Postsynaptic Response
Fast and slow responses in postsynaptic cells involve
ion channels and G-protein receptor
Presynaptic axon
terminal
Rapid, short-acting
fast synaptic potential
Neurotransmitter
Chemically
gated ion channel
Slow synaptic potentials
and long-term effects
G protein–
coupled
receptor
R
G
Inactive
pathway
Postsynaptic
cell
Alters open
state of
ion channels
Ion channels open
More
Na+ in
EPSP =
excitatory
depolarization
More K+
out or
Cl– in
Ion channels close
Less
Na+ in
IPSP =
inhibitory
hyperpolarization
Activated second
messenger pathway
Modifies existing
proteins or regulates
synthesis of new
proteins
Less K+
out
EPSP =
excitatory
depolarization
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Coordinated
intracellular
response
Figure 8-23
Cell-to-Cell: Chemical Synapse
Chemical synapses use neurotransmitters;
electrical synapses pass electrical signals.
Chemical
synapses are most
common.
Electrical
synapses are
found in the CNS
and other cells
that use electrical
signals (heart)
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Figure 8-20
Cell-to-Cell: Calcium
 Events at the synapse
1 An action potential depolarizes
the axon terminal.
Action
potential
2 The depolarization opens voltagegated Ca2+ channels and Ca2+
enters the cell.
Axon
terminal
3 Calcium entry triggers exocytosis
of synaptic vesicle contents.
Synaptic
vesicle
4 Neurotransmitter diffuses across
the synaptic cleft and binds with
receptors on the postsynaptic cell.
1
Ca2+
Voltage-gated
Ca2+ channel
2
Ca2+
Postsynaptic
cell
Docking
protein
3
5 Neurotransmitter binding initiates
a response in the postsynaptic
cell.
4
Receptor
5
Cell
response
 Exocytosis: Classic versus kiss-and-run
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Figure 8-21
Cell-to-Cell: Acetylcholine
Synthesis and recycling of acetylcholine at a synapse
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Figure 8-22
Integration: Long-Term Potentiation
Long-term potentiation- mechanism used in learning and
memory using Glutaminergic Receptors.
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Figure 8-30
Cell-to-Cell: Inactivation of Neurotransmitters
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Figure 8-24
Cell-to-Cell: Neurocrines
 Seven classes by structure  Acetylcholine –(Ach) neurotransmitter composed of choline and
coenzyme A (acetyl CoA), binds to cholinergic receptors
 Amines – neurotransmitter, derived from a single amino acid:
Dopamine, Norepinephrine, Epinephrine, Serotonin, Histamine
 Amino acids – an amino acid that functions as a neurotransmitter:
Glutamate, Aspartate, Gamma-aminobutyric, Glycine
 Purines –made from adenine
 Gases – act as neurotransmitter, half-life of 2-30 sec.
 Peptides -neurohoromones, neurotransmitters, and neuromodulator,
 Lipids – eicosanoids
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Cell-to-Cell: Amine
 Derived from single amino acid
 Tyrosine
 Dopamine -neurotransmitter/neurhormone
 Norepinephrine -tyrosine ,
neurotransmitter/neurhormone, secreted by
noradrenogenic neurons,
 Epinephrine - neurotransmitter/neurhormone, also
called adrenaline, secreted by adrenogenic neurons
 Others
 Serotonin – neurotransmitter, is made from tryptophan
 Histamine – neurotransmitter, is made from histadine
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Cell-to-Cell: Amino Acids
 Glutamate: primary excitatory  CNS
 Aspartate: primary excitatory  brain (select regions)
 Gamma-aminobutyric(GABA): Inhibitory  brain
 Glycine
 Inhibitory  spinal cord
 May also be excitatory
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Cell-to-Cell: Neurocrines
 Peptides -involved in pain and pain relieve pathways
 Substance P and opioid peptides
 Purines- bind purinergic receptors
 AMP and ATP
 Gases- produced inside the body, function and
mechanisms not totally understood
 NO and CO
 Lipids -bind cannabinoid receptors in brain and
immune system cells
 Eicosanoids
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Cell-to-Cell: Receptors
 Cholinergic receptors
 Nicotinic on skeletal muscle, in PNS and CNS
 Monovalent cation channels  Na+ and K+
 Muscarinic in CNS and PNS
 Linked to G proteins
 Adrenergic Receptors
  and - two classes
 Linked to G proteins- initiate second messenger
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Integration: Injury to Neurons
If the cell body is not damaged the neuron will
most likely survive. Axon healing is similar to
growth cone of a developing axon.
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Figure 8-32

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