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POWERPOINT PRESENTATION
FOR BIOPSYCHOLOGY,
9TH EDITION
BY JOHN P.J. PINEL
P R E PA R E D B Y J E F F R E Y W. G R I M M
WESTERN WASHINGTON UNIVERSITY
COPYRIGHT © 2014 PEARSON EDUCATION, INC.
ALL RIGHTS RESERVED.
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Chapter 4
Neural Conduction and
Synaptic Transmission
How Neurons Send and Receive
Signals
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Learning Objectives
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LO1: Describe the resting membrane potential and its ionic basis.
LO2: Explain postsynaptic potentials.
LO3: Describe the summation of postsynaptic potentials.
LO4: Explain how an action potential is normally triggered.
LO5: Describe how action potentials are conducted along axons.
LO6: Discuss the structure and variety of synapses.
LO7: Name and explain the classes of neurotransmitters.
LO8: Name and compare different neurotransmitters.
LO9: Discuss 3 examples of how drugs have been used to influence
neurotransmission.
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Resting Membrane Potential
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Recording the Membrane Potential:
Difference in Electrical Charge between
Inside and Outside of Cell
The inside of the neuron is negative with
respect to the outside.
Resting membrane potential is about –
70mV.
Membrane is polarized (carries a charge).
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Ionic Basis of the Resting
Potential
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Factors Contributing to Even Distribution of
Ions (Charged Particles)
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Random motion: particles tend to move down
their concentration gradient
Electrostatic pressure: like repels like; opposites
attract
Factors Contributing to Uneven Distribution
of Ions
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Selective permeability to certain ions
Sodium–potassium pumps
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Ions Contributing to Resting
Potential
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Sodium (Na+)
Chloride (Cl-)
Potassium (K+)
Negatively Charged Proteins (A-)
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Synthesized within the neuron
Found primarily within the neuron
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The Neuron at Rest
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Ions move in and out through ion-specific
channels.
K+ and Cl- pass readily.
There is little movement of Na+.
A- don’t move at all—trapped inside.
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The Neuron at Rest (Con’t)
Equilibrium Potential (Hodgkin-Huxley Model)
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The potential at which there is no net movement of
an ion; the potential it will move to achieve when
allowed to move freely
Na+ = 120mV
K+ = 90mV
Cl- = -70mV (same as resting potential)
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The Neuron at Rest (Con’t)
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Na+ is driven in by both electrostatic
forces and its concentration gradient.
K+ is driven in by electrostatic forces
and out by its concentration gradient.
Cl- is at equilibrium.
Sodium–potassium pump: active (uses
ATP) force that exchanges 3 Na+ inside for
2 K+ outside
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FIGURE 4.1 Three factors that
influence the distribution of Na+ and
K+ ions across the neural membrane.
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Generation and Conduction of
Postsynaptic Potentials (PSPs)
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Neurotransmitters bind at postsynaptic
receptors.
These chemical messengers bind and cause
electrical changes.
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Depolarizations (making the membrane potential
less negative)
Hyperpolarizations (making the membrane
potential more negative)
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FIGURE 4.2 An EPSP, and IPSP, and an
EPSP followed by a typical AP.
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EPSPs and IPSPs
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EPSPs and IPSPs travel passively from
their site of generation.
Decremental (graded)—they get smaller
as they travel.
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Integration of PSPs and
Generation of Action Potentials
(APs)
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One EPSP typically will not suffice to cause a neuron
to “fire” and release neurotransmitter—summation is
needed.
In order to generate an AP (or “fire”), the threshold of
activation must be reached near the axon hillock.
Integration of IPSPs and EPSPs must result in a
potential of about -65mV in order to generate an AP.
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Integration
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Adding or combining a number of
individual signals into one overall signal.
Spatial summation: integration of events
happening at different places
Temporal summation: integration of events
happening at different times
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FIGURE 4.3 The three possible
combinations of spatial summation.
FIGURE 4.4 The two possible
combinations of temporal summation.
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Conduction of APs
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All-or-none: when the threshold is
reached, the neuron “fires” and the action
potential either occurs or it does not.
When the threshold is reached, voltageactivated ion channels are opened.
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FIGURE 4.5 The opening and closing of voltageactivated sodium and potassium channels during the
three phases of the action potential: rising phase,
repolarization, and hyperpolarization.
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Refractory Periods
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Absolute: impossible to initiate another
action potential
Relative: harder to initiate another action
potential
Refractory periods prevent the backwards
movement of APs and limit the rate of
firing.
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PSPs vs. Action Potentials
(APs)
EPSPs/IPSPs
 Decremental
 Fast
 Passive (energy is
not used)
Action Potentials
 Nondecremental
 Conducted more
slowly than PSPs
 Passive and active
(use ATP)
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FIGURE 4.6 The direction of
signals conducted orthodromically
through a typical multipolar neuron.
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Axonal Conduction of APs
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Passive conduction (instant and
decremental) occurs along each myelin
segment to the next node of Ranvier.
A new action potential is generated at
each node.
In myelinated axons, instant conduction
along myelin segments results in faster
conduction than in unmyelinated axons.
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Velocity of Axonal Conduction
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The maximum velocity of conduction in
human motor neurons is about 60 meters
per second.
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Conduction in Neurons
without Axons
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Conduction in interneurons is typically
passive and decremental.
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The Hodgkin-Huxley Model in
Perspective
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This model was based on squid motor
neurons.
Cerebral neurons behave in ways that are
not always predicted by the model.
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Snaptic Transmission:
Structure of Synapses
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Axodendritic are most common; axons
synapse onto dendritic spines.
Directed synapse: site of release and
contact are in close proximity
Nondirected synapse: site of release and
contact are separated by some distance
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FIGURE 4.7 The anatomy of a
typical synapse.
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FIGURE 4.8 Presynaptic facilitation
and inhibition.
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FIGURE 4.9 Nondirected neurotransmitter
release. Some neurons release
neurotransmitter molecules diffusely
from varicosities along the axon and its
branches.
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Synthesis, Packaging, and
Transport of Neurotransmitter
Molecules
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Neurotransmitter Molecules
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Small
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Synthesized in the terminal button and packaged
in synaptic vesicles
Large
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Assembled in the cell body, packaged in vesicles,
and then transported to the axon terminal
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Release of Neurotransmitter
(NT) Molecules
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Exocytosis: the process of NT release
The arrival of an AP at the terminal opens
voltage-activated Ca2+ channels.
The entry of Ca2+ causes vesicles to fuse
with the terminal membrane and release
their contents.
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FIGURE 4.10 Schematic and photographic illustrations of exocytosis. (The photomicrograph was
reproduced from J. E. Heuser et al., Journal of Cell Biology, 1979, 81, 275–300, by copyright
permission of The Rockefeller University Press.)
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Activation of Receptors by NT
Molecules
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Released NT molecules produce signals in
postsynaptic neurons by binding to
receptors.
Receptors are specific for a given NT.
Ligand: a molecule that binds to another
An NT is a ligand of its receptor.
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Receptors
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There are multiple receptor types for
a given NT.
Ionotropic receptors: associated with
ligand-activated ion channels
Metabotropic receptors: associated
with signal proteins and G proteins
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Ionotropic Receptors
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NT binds and an associated ion channel
opens or closes, causing a PSP.
If Na+ channels are opened, for example,
an EPSP occurs.
If K+ channels are opened, for example, an
IPSP occurs.
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Metabotropic Receptors
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Effects are slower, longer-lasting, more
diffuse, and more varied.
(1) NT 1st messenger binds. (2) G protein
subunit breaks away. (3) Ion channel
opens/closes OR a 2nd messenger is
synthesized. (3) 2nd messengers may have a
wide variety of effects.
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FIGURE 4.11 Ionotropic and
metabotropic receptors
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Reuptake, Enzymatic
Degradation, and Recycling
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As long as NT is in the synapse, it is
“active”; activity must somehow be
turned off
Reuptake: scoop up and recycle NT
Enzymatic degradation: an NT is
broken down by enzymes
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FIGURE 4.12 The two mechanisms for terminating
neurotransmitter action in the synapse: reuptake
and enzymatic degradation.
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Glial, Gap Junctions, and
Synaptic Transmission
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Astrocytes appear to communicate and to
modulate neuronal activity.
Some communication is through gap
junctions between cells.
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FIGURE 4.13 Gap junctions. Gap junctions connect the cytoplasm of two adjacent cells.
In the mammalian brain, there are many gap junctions between glial cells, between
neurons, and between neurons and glia cells.
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Amino Acid Neurotransmitters
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Usually Found at Fast-Acting Directed
Synapses in the CNS
Glutamate: Most prevalent excitatory
neurotransmitter in the CNS
GABA
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Synthesized from glutamate
Most prevalent inhibitory NT in the CNS
Aspartate and Glycine
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Monoamines
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Effects tend to be diffused.
Catecholamines: synthesized from tyrosine
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Dopamine
Norepinephrine
Epinephrine
Indolamines: synthesized from tryptophan
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Serotonin
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Acetylcholine
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Acetylcholine (Ach)
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Acetyl group + choline
First identified at neuromuscular junction
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Unconventional
Neurotransmitters
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Soluble Gases; Exist Only Briefly
 Nitric oxide and carbon monoxide
 Retrograde transmission; backwards
communication
Endacannabinoids
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Anandamide is one of the two known
endocannabinoids.
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Neuropeptides
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Large Molecules
Example: Endorphins
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“Endogenous opioids”
Produce analgesia (pain suppression)
Receptors were identified before the natural
ligand was.
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FIGURE 4.16 Classes of neurotransmitters and the
particular neurotransmitters that were discussed
(and appeared in boldface) in this section.
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FIGURE 4.17 Seven steps in neurotransmitter action: (1) synthesis, (2) storage in
vesicles, (3) breakdown of any neurotransmitter leaking from the vesicles, (4)
exocytosis, (5) inhibitory feedback via autoreceptors, (6) activation of postsynaptic
receptors, and (7) deactivation.
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Pharmacology of Synaptic
Transmission
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How Drugs Influence Synaptic Activity
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Agonists: increase or facilitate activity
Antagonists: decrease or inhibit activity
A drug may act to alter neurotransmitter activity at
any point in its “life cycle.”
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Behavioral Pharmacology:
Three Influential Lines of
Research
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Drugs selective to specific receptor subtypes
may exert different effects.
 E.g., nicotinic vs. muscarinic acetylcholine
receptors
Discovery of the endogenous opioids provided
insight into brain mechanisms of pleasure and
pain.
Effects of dopamine agonists and antagonists on
psychotic symptoms led to new treatments for
schizophrenia.
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FIGURE 4.18 Some mechanisms of
agonistic and antagonistic drug
effects.
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