Transcript Document

LECTURE PRESENTATIONS
For CAMPBELL BIOLOGY, NINTH EDITION
Jane B. Reece, Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Robert B. Jackson
Chapter 48
Neurons, Synapses, and Signaling
Lectures by
Erin Barley
Kathleen Fitzpatrick
© 2011 Pearson Education, Inc.
Overview: Lines of Communication
• The cone snail kills prey with venom that
disables neurons
• Neurons are nerve cells that transfer
information within the body
• Neurons use two types of signals to
communicate: electrical signals (long-distance)
and chemical signals (short-distance)
© 2011 Pearson Education, Inc.
Figure 48.1
• Interpreting signals in the nervous system
involves sorting a complex set of paths and
connections
• Processing of information takes place in simple
clusters of neurons called ganglia or a more
complex organization of neurons called a brain
© 2011 Pearson Education, Inc.
Concept 48.1: Neuron organization and
structure reflect function in information
transfer
• The squid possesses extremely large nerve cells
and has played a crucial role in the discovery of
how neurons transmit signals
© 2011 Pearson Education, Inc.
Introduction to Information Processing
• Nervous systems process information in three
stages: sensory input, integration, and motor
output
© 2011 Pearson Education, Inc.
Figure 48.2
Nerves
with giant axons
Ganglia
Brain
Arm
Eye
Nerve
Mantle
• Sensors detect external stimuli and internal
conditions and transmit information along
sensory neurons
• Sensory information is sent to the brain or
ganglia, where interneurons integrate the
information
• Motor output leaves the brain or ganglia via
motor neurons, which trigger muscle or gland
activity
© 2011 Pearson Education, Inc.
• Many animals have a complex nervous system
that consists of
– A central nervous system (CNS) where
integration takes place; this includes the brain
and a nerve cord
– A peripheral nervous system (PNS), which
carries information into and out of the CNS
– The neurons of the PNS, when bundled
together, form nerves
© 2011 Pearson Education, Inc.
Figure 48.3
Sensory input
Integration
Sensor
Motor output
Effector
Peripheral nervous
system (PNS)
Central nervous
system (CNS)
Neuron Structure and Function
• Most of a neuron’s organelles are in the cell
body
• Most neurons have dendrites, highly branched
extensions that receive signals from other
neurons
• The axon is typically a much longer extension
that transmits signals to other cells at synapses
• The cone-shaped base of an axon is called the
axon hillock
© 2011 Pearson Education, Inc.
Figure 48.4
Dendrites
Stimulus
Axon hillock
Nucleus
Cell
body
Presynaptic
cell
Axon
Signal
direction
Synapse
Neurotransmitter
Synaptic terminals
Postsynaptic cell
Synaptic
terminals
• The synaptic terminal of one axon passes
information across the synapse in the form of
chemical messengers called neurotransmitters
• A synapse is a junction between an axon and
another cell
© 2011 Pearson Education, Inc.
• Information is transmitted from a presynaptic
cell (a neuron) to a postsynaptic cell (a neuron,
muscle, or gland cell)
• Most neurons are nourished or insulated by cells
called glia
© 2011 Pearson Education, Inc.
Figure 48.5
Dendrites
Axon
Cell
body
Portion
of axon
Sensory neuron
Interneurons
Motor neuron
Figure 48.6
80 m
Glia
Cell bodies of neurons
Concept 48.2: Ion pumps and ion channels
establish the resting potential of a neuron
• Every cell has a voltage (difference in electrical
charge) across its plasma membrane called a
membrane potential
• The resting potential is the membrane potential
of a neuron not sending signals
• Changes in membrane potential act as signals,
transmitting and processing information
© 2011 Pearson Education, Inc.
Formation of the Resting Potential
• In a mammalian neuron at resting potential, the
concentration of K+ is highest inside the cell,
while the concentration of Na+ is highest outside
the cell
• Sodium-potassium pumps use the energy of
ATP to maintain these K+ and Na+ gradients
across the plasma membrane
• These concentration gradients represent
chemical potential energy
© 2011 Pearson Education, Inc.
• The opening of ion channels in the plasma
membrane converts chemical potential to electrical
potential
• A neuron at resting potential contains many open
K+ channels and fewer open Na+ channels; K+
diffuses out of the cell
• The resulting buildup of negative charge within the
neuron is the major source of membrane potential
© 2011 Pearson Education, Inc.
Animation: Resting Potential
Right-click slide / select “Play”
© 2011 Pearson Education, Inc.
Table 48.1
Figure 48.7
Key
Na
K
Sodiumpotassium
pump
OUTSIDE
OF CELL
Potassium
channel
Sodium
channel
INSIDE
OF CELL
Modeling the Resting Potential
• Resting potential can be modeled by an artificial
membrane that separates two chambers
– The concentration of KCl is higher in the inner
chamber and lower in the outer chamber
– K+ diffuses down its gradient to the outer
chamber
– Negative charge (Cl–) builds up in the inner
chamber
• At equilibrium, both the electrical and chemical
gradients are balanced
© 2011 Pearson Education, Inc.
Figure 48.8
Inner
chamber
 90 mV
Outer
chamber
140 mM
KCl
5 mM
KCl
Inner
chamber
15 mM
NaCl
 62 mV
Outer
chamber
150 mM
NaCl
Cl
K
Potassium
channel
Cl
Artificial
membrane
(a) Membrane selectively permeable
to K
EK  62 mV
 90 mV
Na
Sodium
channel
(b) Membrane selectively permeable
to Na
ENa  62 mV
 62 mV
• The equilibrium potential (Eion) is the
membrane voltage for a particular ion at
equilibrium and can be calculated using the
Nernst equation
Eion = 62 mV (log[ion]outside/[ion]inside)
• The equilibrium potential of K+ (EK) is negative,
while the equilibrium potential of Na+ (ENa) is
positive
© 2011 Pearson Education, Inc.
• In a resting neuron, the currents of K+ and Na+
are equal and opposite, and the resting potential
across the membrane remains steady
© 2011 Pearson Education, Inc.
Figure 48.8b
Inner
chamber
15 mM
NaCl
62 mV
Outer
chamber
150 mM
NaCl
Cl
Na
Sodium
channel
(b) Membrane selectively permeable
to Na
ENa  62 mV
 62 mV
Concept 48.3: Action potentials are the
signals conducted by axons
• Changes in membrane potential occur because
neurons contain gated ion channels that open
or close in response to stimuli
© 2011 Pearson Education, Inc.
Figure 48.9
TECHNIQUE
Microelectrode
Voltage
recorder
Reference
electrode
Hyperpolarization and Depolarization
• When gated K+ channels open, K+ diffuses out,
making the inside of the cell more negative
• This is hyperpolarization, an increase in
magnitude of the membrane potential
© 2011 Pearson Education, Inc.
Figure 48.10
Stimulus
50
50 Threshold
Resting
potential
Hyperpolarizations
0 1 2 3 4 5
Time (msec)
(a) Graded hyperpolarizations
produced by two stimuli that
increase membrane permeability
to K
50
0
50 Threshold
100
Resting
potential
Depolarizations
0 1 2 3 4 5
Time (msec)
(b) Graded hyperpolarizations
produced by two stimuli that
increase membrane permeability
to Na
Membrane potential (mV)
0
Membrane potential (mV)
Membrane potential (mV)
50
100
Strong depolarizing stimulus
Stimulus
Action
potential
0
50 Threshold
Resting
potential
100
0 1 2 3 4 5 6
Time (msec)
(c) Action potential triggered by a
depolarization that reaches the
threshold
Figure 48.10a
(a) Graded hyperpolarizations
produced by two stimuli
that increase membrane
permeability to K
Stimulus
Membrane potential (mV)
50
0
50 Threshold
100
Resting
potential
Hyperpolarizations
0 1 2 3 4 5
Time (msec)
• Opening other types of ion channels triggers a
depolarization, a reduction in the magnitude of
the membrane potential
• For example, depolarization occurs if gated Na+
channels open and Na+ diffuses into the cell
© 2011 Pearson Education, Inc.
Figure 48.10b
(b) Graded depolarizations
produced by two stimuli
that increase membrane
permeability to Na
Stimulus
Membrane potential (mV)
50
0
50 Threshold
100
Resting
potential
Depolarizations
0 1 2 3 4 5
Time (msec)
Graded Potentials and Action Potentials
• Graded potentials are changes in polarization
where the magnitude of the change varies with
the strength of the stimulus
• These are not the nerve signals that travel along
axons, but they do have an effect on the
generation of nerve signals
© 2011 Pearson Education, Inc.
• If a depolarization shifts the membrane potential
sufficiently, it results in a massive change in
membrane voltage called an action potential
• Action potentials have a constant magnitude, are
all-or-none, and transmit signals over long
distances
• They arise because some ion channels are
voltage-gated, opening or closing when the
membrane potential passes a certain level
© 2011 Pearson Education, Inc.
Figure 48.10c
(c) Action potential
triggered by a
depolarization that
reaches the threshold
Strong depolarizing stimulus
Membrane potential (mV)
50
Action
potential
0
50 Threshold
Resting
potential
100
0 1 2 3 4 5 6
Time (msec)
Generation of Action Potentials: A Closer
Look
• An action potential can be considered as a
series of stages
• At resting potential
1. Most voltage-gated sodium (Na+) channels are
closed; most of the voltage-gated potassium
(K+) channels are also closed
© 2011 Pearson Education, Inc.
Figure 48.11-1
Key
Na
K
Membrane potential
(mV)
50
0
Threshold
50
100
OUTSIDE OF CELL
INSIDE OF CELL
Inactivation loop
1 Resting state
Sodium
channel
Potassium
channel
1
Resting potential
Time
• When an action potential is generated
2. Voltage-gated Na+ channels open first and Na+
flows into the cell
3. During the rising phase, the threshold is
crossed, and the membrane potential increases
4. During the falling phase, voltage-gated Na+
channels become inactivated; voltage-gated K+
channels open, and K+ flows out of the cell
© 2011 Pearson Education, Inc.
Figure 48.11-4
Key
Na
K
Membrane potential
(mV)
Action
potential
OUTSIDE OF CELL
INSIDE OF CELL
Inactivation loop
1 Resting state
100
Sodium
channel
Potassium
channel
3
0
50
2 Depolarization
4 Falling phase of the action potential
50
3 Rising phase of the action potential
Threshold
2
4
1
Resting potential
Time
5. During the undershoot, membrane
permeability to K+ is at first higher than at rest,
then voltage-gated K+ channels close and
resting potential is restored
© 2011 Pearson Education, Inc.
Figure 48.11-5
Key
Na
K
Membrane potential
(mV)
Action
potential
OUTSIDE OF CELL
100
Sodium
channel
3
0
50
2 Depolarization
4 Falling phase of the action potential
50
3 Rising phase of the action potential
Threshold
2
1
4
5
Resting potential
Time
Potassium
channel
INSIDE OF CELL
Inactivation loop
1 Resting state
5 Undershoot
1
Figure 48.11a
Membrane potential
(mV)
50
Action
potential
3
0
50
100
2
4
Threshold
1
Resting potential
Time
5
1
• During the refractory period after an action
potential, a second action potential cannot be
initiated
• The refractory period is a result of a temporary
inactivation of the Na+ channels
© 2011 Pearson Education, Inc.
BioFlix: How Neurons Work
© 2011 Pearson Education, Inc.
Animation: Action Potential
Right-click slide / select “Play”
© 2011 Pearson Education, Inc.
Conduction of Action Potentials
• At the site where the action potential is
generated, usually the axon hillock, an electrical
current depolarizes the neighboring region of the
axon membrane
• Action potentials travel in only one direction:
toward the synaptic terminals
© 2011 Pearson Education, Inc.
• Inactivated Na+ channels behind the zone of
depolarization prevent the action potential from
traveling backwards
© 2011 Pearson Education, Inc.
Figure 48.12-3
Axon
Plasma
membrane
Action
potential
1
Na
K
2
Cytosol
Action
potential
Na
K
K
3
Action
potential
Na
K
Evolutionary Adaptation of Axon Structure
• The speed of an action potential increases with
the axon’s diameter
• In vertebrates, axons are insulated by a myelin
sheath, which causes an action potential’s
speed to increase
• Myelin sheaths are made by glia—
oligodendrocytes in the CNS and Schwann
cells in the PNS
© 2011 Pearson Education, Inc.
Figure 48.13
Node of Ranvier
Layers of myelin
Axon
Schwann
cell
Axon
Myelin sheath
Nodes of
Ranvier
Schwann
cell
Nucleus of
Schwann cell
0.1 m
• Action potentials are formed only at nodes of
Ranvier, gaps in the myelin sheath where
voltage-gated Na+ channels are found
• Action potentials in myelinated axons jump
between the nodes of Ranvier in a process
called saltatory conduction
© 2011 Pearson Education, Inc.
Figure 48.14
Schwann cell
Depolarized region
(node of Ranvier)
Cell body
Myelin
sheath
Axon
Concept 48.4: Neurons communicate with
other cells at synapses
• At electrical synapses, the electrical current
flows from one neuron to another
• At chemical synapses, a chemical
neurotransmitter carries information across the
gap junction
• Most synapses are chemical synapses
© 2011 Pearson Education, Inc.
• The presynaptic neuron synthesizes and
packages the neurotransmitter in synaptic
vesicles located in the synaptic terminal
• The action potential causes the release of the
neurotransmitter
• The neurotransmitter diffuses across the
synaptic cleft and is received by the
postsynaptic cell
© 2011 Pearson Education, Inc.
Animation: Synapse
Right-click slide / select “Play”
© 2011 Pearson Education, Inc.
Figure 48.15
Presynaptic
cell
Postsynaptic cell
Axon
Synaptic vesicle
containing
neurotransmitter
1
Postsynaptic
membrane
Synaptic
cleft
Presynaptic
membrane
3
K
Ca2 2
Voltage-gated
Ca2 channel
Ligand-gated
ion channels
4
Na
Generation of Postsynaptic Potentials
• Direct synaptic transmission involves binding of
neurotransmitters to ligand-gated ion channels
in the postsynaptic cell
• Neurotransmitter binding causes ion channels to
open, generating a postsynaptic potential
© 2011 Pearson Education, Inc.
• Postsynaptic potentials fall into two categories
– Excitatory postsynaptic potentials (EPSPs)
are depolarizations that bring the membrane
potential toward threshold
– Inhibitory postsynaptic potentials (IPSPs) are
hyperpolarizations that move the membrane
potential farther from threshold
© 2011 Pearson Education, Inc.
• After release, the neurotransmitter
– May diffuse out of the synaptic cleft
– May be taken up by surrounding cells
– May be degraded by enzymes
© 2011 Pearson Education, Inc.
Summation of Postsynaptic Potentials
• Most neurons have many synapses on their
dendrites and cell body
• A single EPSP is usually too small to trigger an
action potential in a postsynaptic neuron
© 2011 Pearson Education, Inc.
Figure 48.16
Synaptic
terminals
of presynaptic
neurons
5 m
Postsynaptic
neuron
Figure 48.17
Terminal branch
of presynaptic
neuron
E1
E2
E1
E2
Postsynaptic
neuron
Membrane potential (mV)
E1
E1
E2
E2
Axon
hillock
I
I
I
I
0
Action
potential
Threshold of axon of
postsynaptic neuron
Action
potential
Resting
potential
70
E1
E1
(a) Subthreshold, no
summation
E1 E1
(b) Temporal summation
E1  E2
(c) Spatial summation
E1
I
E1  I
(d) Spatial summation
of EPSP and IPSP
• If two EPSPs are produced in rapid succession,
an effect called temporal summation occurs
© 2011 Pearson Education, Inc.
Figure 48.17a
Terminal branch
of presynaptic
neuron
E1
E2
E2
Postsynaptic
neuron
Membrane potential (mV)
E1
Axon
hillock
I
I
0
Action
potential
Threshold of axon of
postsynaptic neuron
Resting
potential
70
E1
E1
(a) Subthreshold, no
summation
E1 E1
(b) Temporal summation
• In spatial summation, EPSPs produced nearly
simultaneously by different synapses on the
same postsynaptic neuron add together
• The combination of EPSPs through spatial and
temporal summation can trigger an action
potential
© 2011 Pearson Education, Inc.
Figure 48.17b
E1
E1
E2
E2
I
I
Action
potential
E1  E2
(c) Spatial summation
E1
I
E1  I
(d) Spatial summation
of EPSP and IPSP
• Through summation, an IPSP can counter the
effect of an EPSP
• The summed effect of EPSPs and IPSPs
determines whether an axon hillock will reach
threshold and generate an action potential
© 2011 Pearson Education, Inc.
Modulated Signaling at Synapses
• In some synapses, a neurotransmitter binds to a
receptor that is metabotropic
• In this case, movement of ions through a
channel depends on one or more metabolic
steps
© 2011 Pearson Education, Inc.
• Binding of a neurotransmitter to a metabotropic
receptor activates a signal transduction pathway
in the postsynaptic cell involving a second
messenger
• Compared to ligand-gated channels, the effects
of second-messenger systems have a slower
onset but last longer
© 2011 Pearson Education, Inc.
Neurotransmitters
• There are more than 100 neurotransmitters,
belonging to five groups: acetylcholine, biogenic
amines, amino acids, neuropeptides, and gases
• A single neurotransmitter may have more than a
dozen different receptors
© 2011 Pearson Education, Inc.
Table 48.2
Acetylcholine
• Acetylcholine is a common neurotransmitter in
vertebrates and invertebrates
• It is involved in muscle stimulation, memory
formation, and learning
• Vertebrates have two major classes of
acetylcholine receptor, one that is ligand gated
and one that is metabotropic
© 2011 Pearson Education, Inc.
Amino Acids
• Amino acid neurotransmitters are active in the
CNS and PNS
• Known to function in the CNS are
– Glutamate
– Gamma-aminobutyric acid (GABA)
– Glycine
© 2011 Pearson Education, Inc.
Biogenic Amines
• Biogenic amines include
– Epinephrine
– Norepinephrine
– Dopamine
– Serotonin
• They are active in the CNS and PNS
© 2011 Pearson Education, Inc.
Neuropeptides
• Several neuropeptides, relatively short chains of
amino acids, also function as neurotransmitters
• Neuropeptides include substance P and
endorphins, which both affect our perception of
pain
• Opiates bind to the same receptors as
endorphins and can be used as painkillers
© 2011 Pearson Education, Inc.
Figure 48.18
EXPERIMENT
Radioactive
naloxone
1 Radioactive naloxone and
a test drug are incubated
with a protein mixture.
Drug
Protein
mixture
2 Proteins are trapped on a filter.
Bound naloxone is detected
by measuring radioactivity.
RESULTS
Drug
Opiate
Concentration That Blocked
Naloxone Binding
Morphine
Yes
6  109 M
Methadone
Yes
2  108 M
Levorphanol
Yes
2  109 M
Phenobarbital
No
No effect at 104 M
Atropine
No
No effect at 104 M
Serotonin
No
No effect at 104 M
Gases
• Gases such as nitric oxide and carbon monoxide
are local regulators in the PNS
© 2011 Pearson Education, Inc.
Figure 48.UN01
Action potential
Membrane potential (mV)
50
Falling
phase
0
Rising
phase
Threshold (55)
50
100
Resting
potential
70
Depolarization
0 1 2 3 4 5 6
Time (msec)
Undershoot
Figure 48.UN03
LECTURE PRESENTATIONS
For CAMPBELL BIOLOGY, NINTH EDITION
Jane B. Reece, Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Robert B. Jackson
Chapter 48
Neurons, Synapses, and
Signaling
Questions prepared by
Christopher Gregg
Louisiana State University
Lectures
by
John Lepri
Erin
Barley
University of North Carolina,
Greensboro
Kathleen Fitzpatrick
© 2011 Pearson Education, Inc.
Choose the correct pathway of information flow
through neurons while taking a test, starting with
reading a question and ending with marking an
answer.
a) interneurons  motor neurons  sensory neurons 
effectors
b) effectors  sensory neurons  interneurons  motor
neurons
c) sensory neurons  interneurons  motor neurons 
effectors
d) interneurons  sensory neurons  motor neurons 
effectors
Adding a poison that specifically disables
the Na+/K+ pumps to a culture of neurons
will cause
a) the resting membrane potential to drop to 0
mV.
b) the inside of the neuron to become more
negative relative to the outside.
c) the inside of the neuron to become positively
charged relative to the outside.
d) sodium to diffuse out of the cell and potassium
to diffuse into the cell.
For a nerve cell at its resting potential, the
forces acting on potassium ions (K+) are
a) none: K+ ions do not move at the resting potential.
b) an electrical gradient, pulling K+ inward, and a
chemical gradient, pushing K+ outward.
c) an electrical gradient, pushing K+ outward, and a
chemical gradient, pulling K+ inward.
d) an electrical gradient, pulling K+ inward, and a
chemical gradient, pushing K+ outward.
e) an electrical gradient, pushing K+ outward, and a
chemical gradient, pushing K+ outward.
A(n) ___ in Na+ permeability and/or
a(n) ___ in K+ permeability across a
neuron’s plasma membrane could shift
membrane potential from −70 mV to
−80 mV.
a)
b)
c)
d)
increase; increase
increase; decrease
decrease; increase
decrease; decrease
At time ZERO msec on the graph, it is
likely that there was
a) a localized opening of
K+ channels.
b) a localized opening of
some Na+ channels.
c) a rapid opening of
most K+ channels.
d) a rapid opening of
most Na+ channels.
At step four in the graph, it is
likely that
a) most Cl− channels
closed.
b) most Na+ channels
opened.
c) most K+ channels
closed.
d) most K+ channels
opened.
e) Na/K pumps were
inactivated.
Of the following choices, the slowest
conduction velocity for moving action
potentials is likely seen in
a)
b)
c)
d)
a large-diameter, nonmyelinated axon.
a small-diameter, nonmyelinated axon.
A myelinated axon.
any of the above, as all neurons conduct
action potentials at the same speed.
Injecting ethylene glycol tetraacetic acid (EGTA), a
chelating agent that prevents calcium ions from
moving across membranes, to a synaptic region
would likely
a) increase the release of neurotransmitters by the
presynaptic neuron.
b) decrease the release of neurotransmitters by the
presynaptic neuron.
c) result in neurotransmitters being released, but could
not bind to its receptors on the post synaptic neuron.
d) result in the lack of calcium ions keeping the ligandgated ion channels open on the post synaptic neurons.
The use of organophosphate pesticides that inhibit
acetylcholinesterase, an enzyme that breaks down
acetylcholine, could cause skeletal muscle cells to
a) undergo more graded depolarizations, because
acetylcholine would remain in the synaptic cleft longer.
b) undergo more graded hyperpolarizations, because
acetylcholine would remain in the synaptic cleft longer.
c) undergo more graded depolarizations, because
acetylcholine would prevent ligand-gated ion channels
from opening.
d) undergo more graded hyperpolarizations, because
excess acetylcholine opens Cl− channels.
Adderall, an amphetamine stimulant,
works on the CNS by
a) increasing the release of GABA and
decreasing its catabolism/reuptake.
b) increasing the release of serotonin and
decreasing its catabolism/reuptake.
c) increasing the release of endorphins and
decreasing their catabolism/reuptake.
d) increasing the release of dopamine and
norepinephrine and decreasing their
catabolism/reuptake.