Transcript Human Physiology - Maryville University

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Chapter 7
The Nervous System:
Neurons and Synapses
7-1
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Chapter 7 Outline
Structure
of NS
Neurons
Supporting/Glial Cells
Membrane Potential
Action Potential
Axonal Conduction
Synaptic Transmission
Neurotransmitters
Synaptic Integration
7-2
Structure of Nervous System
7-3
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Nervous System (NS)
Is
divided into:
Central nervous system (CNS)
= brain & spinal cord
Peripheral nervous system (PNS)
 = cranial & spinal nerves
7-4
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Nervous System (NS) continued
Consists
of 2 kinds of cells:
Neurons & supporting cells (= glial cells)
Neurons are functional units of NS
Supporting cells maintain homeostasis
 Are 5X more common than neurons
7-5
Neurons
7-6
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Neurons
Gather
& transmit information by:
Responding to stimuli
Sending electrochemical impulses
Releasing chemical messages
7-7
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Neurons continued
Have
a cell body, dendrites, & axon
Cell body contains nucleus
Fig 7.1
7-8
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Neurons continued
Cell
body makes macromolecules
Groups of cell bodies in CNS are called nuclei; in PNS
are called ganglia
Fig 7.1
7-9
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Neurons continued
Dendrites
receive information, convey it to cell body
Axons conduct impulses away from cell body
Fig 7.1
7-10
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Neurons continued
Axon
length necessitates special transport systems:
Axoplasmic flow moves soluble compounds toward
nerve endings
Via rhythmic contractions of axon
Axonal transport moves large & insoluble
compounds bidirectionally
Along microtubules; very fast
Viruses & toxins enter CNS this way
7-11
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Functional Classification of Neurons
 Sensory/Afferent
neurons conduct
impulses into CNS
 Motor/Efferent neurons
carry impulses out of
CNS
 Association/
Interneurons integrate
NS activity
 Located entirely
inside CNS
Fig 7.3
7-12
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Structural Classification of Neurons
 Pseudounipolar:
 Cell
body sits along side
of single process
 e.g. sensory neurons
 Bipolar:
 Dendrite & axon arise
from opposite ends of cell
body
 e.g. retinal neurons
 Multipolar:
 Have many dendrites &
one axon
 e.g. motor neurons
Fig 7.4
7-13
Supporting/Glial Cells
7-14
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Supporting/Glial Cells
PNS
has Schwann & satellite cells
Schwann cells myelinate PNS axons
Fig 7.2
7-15
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Supporting/Glial Cells continued
CNS
has oligodendrocytes, microglia, astrocytes, &
ependymal cells
Fig 7.5
7-16
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Supporting/Glial Cells continued
Each
oligodendrocyte
myelinates several
CNS axons
Ependymal cells are
neural stem cells
Other glial cells are
involved in NS
maintenance
Fig 7.8
7-17
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Myelination
In
PNS each Schwann
cell myelinates 1mm of
1 axon by wrapping
round & round axon
Electrically insulates
axon
Fig 7.6
7-18
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Myelination continued
Uninsulated
gap between adjacent Schwann cells is
called node of Ranvier
Fig 7.2
7-19
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Nerve Regeneration
Occurs
much more readily in PNS than CNS
Oligodendrocytes produce proteins that inhibit
regrowth
7-20
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Nerve Regeneration continued
 When
axon in PNS is
severed:
 Distal part of axon
degenerates
 Schwann cells survive;
form regeneration tube
 Tube releases
chemicals that
attract growing
axon
 Tube guides
regrowing axon to
synaptic site
Fig 7.9
7-21
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Neurotrophins
Promote
fetal nerve growth
Required for survival of many adult neurons
Important in regeneration
7-22
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Astrocytes
 Most
common glial cell
 Involved in:
 Inducing capillaries to
form blood-brain barrier
 Buffering K+ levels
 Recycling
neurotransmitters
 Regulating adult
neurogenesis
Fig 7.10
7-23
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Blood-Brain Barrier
Allows
only certain compounds to enter brain
Formed by capillary specializations in brain
Capillaries are not as leaky as those in body
Do not have gaps between adjacent cells
 Closed by tight junctions
7-24
Membrane Potential
7-25
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Resting Membrane Potential (RMP)
At
rest, all cells have a negative internal charge &
unequal distribution of ions:
Results from:
Large cations being trapped inside cell
Na+/K+ pump & limited permeability keep Na+
high outside cell
K+ is very permeable & is high inside cell
 Attracted by negative charges inside
7-26
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Excitability
Excitable
cells can discharge their RMP quickly
By rapid changes in permeability to ions
Neurons & muscles do this to generate & conduct
impulses
7-27
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Membrane Potential (MP) Changes
 Measured
by placing 1
electrode inside cell & 1
outside
Fig 7.11
 Depolarization occurs when
MP becomes more positive
 Hyperpolarization: MP
becomes more negative than
RMP
 Repolarization: MP returns to
RMP
7-28
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Membrane Ion Channels
MP
changes occur by ion flow through membrane
channels
Some channels are normally open; some closed
Closed channels have molecular gates that can be
opened
Voltage-gated (VG) channels are opened by
depolarization
1 type of K+ channel is always open; other type is
VG & is closed in resting cell
Na+ channels are VG; closed in resting cells
7-29
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Model of a Voltage-gated Ion Channel
)
Fig 7.12
7-30
Action Potential
7-31
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The Action Potential (AP)
Fig 7.13
 Is
a wave of MP change
that sweeps along the axon
from soma to synapse
 Wave is formed by rapid
depolarization of the
membrane by Na+ influx;
followed by rapid
repolarization by K+ efflux
7-32
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Mechanism of Action Potential
Depolarization:
threshold, VG Na+ channels open
Na+ driven inward by its electrochemical gradient
This adds to depolarization, opens more channels
Termed a positive feedback loop
Causes a rapid change in MP from –70 to +30 mV
At
7-33
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Mechanism of Action Potential continued
Repolarization:
Na+ channels close; VG K+ channels open
Electrochemical gradient drives K+ outward
Repolarizes axon back to RMP
VG
7-34
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Mechanism of Action Potential continued
Depolarization
& repolarization occur via diffusion
Do not require active transport
After an AP, Na+/K+ pump extrudes Na+, recovers K+
7-35
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APs Are All-or-None
When
MP reaches threshold, an AP is irreversibly fired
Because positive feedback opens more & more Na+
channels
Shortly after opening, Na+ channels close
& become inactivated until repolarization
7-36
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How Stimulus Intensity is Coded
Increased
stimulus intensity causes more APs to be
fired
Size of APs remains constant
7-37
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Refractory Periods
 Absolute
refractory period:
 Membrane cannot
produce another AP
because Na+ channels
are inactivated
 Relative refractory period
occurs when VG K+
channels are open, making
it harder to depolarize to
threshold
Fig 7.16
7-38
Axonal Conduction
7-39
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Cable Properties
Refers
to ability of axon to conduct current
Axon cable properties are poor because:
Cytoplasm has high resistance
Though resistance decreases as axon diameter
increases
Current leaks out through ion channels
7-40
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Conduction in an Unmyelinated Axon
 After
axon hillock reaches
threshold & fires AP, its
Na+ influx depolarizes
adjacent regions to
threshold
 Generating a new AP
 Process repeats all
along axon
 So AP amplitude is
always same
 Conduction is slow
Fig 7.18
7-41
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Conduction in Myelinated Axon
 Ions
can't flow across
myelinated membrane
 Thus no APs occur
under myelin
 & no current leaks
 Increases current
spread
Fig 7.19
7-42
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Conduction in Myelinated Axon continued
 Gaps
in myelin are
called Nodes of Ranvier
 APs occur only at
nodes
 Current from AP at 1
node can depolarize
next node to
threshold
 Fast because APs
skip from node to
node
 Called Saltatory
conduction
Fig 7.19
7-43
Synaptic Transmission
7-44
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Synapse
Is
a functional connection between a neuron
(presynaptic) & another cell (postsynaptic)
There are chemical & electrical synapses
Synaptic transmission in chemicals is via
neurotransmitters (NT)
Electricals are rare in NS
7-45
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Electrical Synapse
 Depolarization
flows from
presynaptic into
postsynaptic cell through
channels called gap
junctions
 Formed by connexin
proteins
 Found in smooth &
cardiac muscles,
brain, and glial cells
Fig 7.20
7-46
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Chemical Synapse
Fig 7.22
 Synaptic
cleft separates
terminal bouton of
presynaptic from
postsynaptic cell
 NTs are in synaptic
vesicles
 Vesicles fuse with bouton
membrane; release NT by
exocytosis
 Amount of NT released
depends upon frequency of
APs
7-47
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Synaptic Transmission
APs
travel down axon to depolarize bouton
Open VG Ca2+ channels in bouton
Ca2+ driven in by electrochemical gradient
Triggers exocytosis of vesicles; release of NTs
7-48
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Neurotransmitter Release
Is
rapid because vesicles are already docked at
release sites on bouton before APs arrive
Docked vesicles are part of fusion complex
Ca2+ triggers exocytosis of vesicles
7-49
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Synaptic Transmission continued
NT
(ligand) diffuses across cleft
Binds to receptor proteins on postsynaptic
membrane
Chemically-regulated ion channels open
Depolarizing channels cause EPSPs (excitatory
postsynaptic potentials)
Hyperpolarizing channels cause IPSPs (inhibitory
postsynaptic potentials)
These affect VG channels in postsynaptic cell
7-50
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Synaptic Transmission continued
EPSPs
& IPSPs
summate
If MP in
postsynaptic cell
reaches threshold,
a new AP is
generated
Fig 7.23
7-51
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Acetylcholine (ACh)
Most
widely used NT
NT at all neuromuscular junctions
Used in brain
Used in ANS
Where can be excitatory or inhibitory
 Depending on receptor subtype
 Nicotinic or muscarinic
7-52
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Ligand-Operated Channels
Ion
channel runs through receptor
Opens when ligand (NT) binds
7-53
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Nicotinic ACh Channel
 Formed
by 5 polypeptide
subunits
 2 subunits contain ACh
binding sites
 Opens when 2 AChs
bind
 Permits diffusion of Na+
into and K+ out of
postsynaptic cell
 Inward flow of Na+
dominates
 Produces EPSPs
Fig 7.24
7-54
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G Protein-Operated Channels
Receptor
is not part of the ion channel
Is a 1 subunit membrane polypeptide
Activates channel indirectly through G-proteins
7-55
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Muscarinic ACh Channel
Binding
of 1 ACh activates G-protein cascade
Opens some K+ channels, causing hyperpolarization
Closes others, causing depolarization
Fig 7.25
7-56
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Acetylcholinesterase (AChE)
Inactivates ACh,
terminating its action; located in cleft
Fig 7.26
7-57
Neurotransmitters
7-58
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Neuromuscular Junction (NMJ)
Cholinergic
neurons use acetylcholine as NT
The large synapses on skeletal muscle are termed end
plates or neuromuscular junctions
Produce large EPSPs called end-plate potentials
Open VG channels beneath end plate
Cause muscle contraction
Curare blocks ACh action at NMJ
7-59
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Monoamine NTs
Receptors
channels
activate G-protein cascade to affect ion
Fig 7.29
7-60
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Monoamine NTs continued
Include
serotonin, norepinephrine, & dopamine,
Serotonin is derived from tryptophan
Norepi & dopamine are derived from tyrosine
Called catecholamines
7-61
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Monoamine NTs continued
 After
release, are mostly
inactivated by:
 Presynaptic reuptake
 & breakdown by
monoamine oxidase
(MAO)
 MAO inhibitors are
antidepressants
Fig 7.28
7-62
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Serotonin
Involved
in regulation of mood, behavior, appetite, &
cerebral circulation
LSD is structurally similar
SSRIs (serotonin-specific reuptake inhibitors) include
antidepressants
Prozac, Zolof, Paxil, Luvox
Block reuptake of serotonin, prolonging its action
7-63
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Dopamine
Involved
in motor control & emotional reward
Degeneration of dopamine motor system neurons
causes Parkinson's disease
Reward system is involved in addiction
Schizophrenia treated by anti-dopamine drugs
7-64
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Norepinephrine (NE)
Used
in PNS & CNS
In PNS is a sympathetic NT
 In CNS affects general level of arousal
Amphetamines stimulate NE pathways
7-65
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Amino Acids NTs
Glutamic
acid & aspartic acid are major CNS excitatory
NTs
Glycine is an inhibitory NT
Opens Cl- channels which hyperpolarize
Strychnine blocks glycine receptors
GABA (gamma-aminobutyric acid) is most common NT
in brain
Inhibitory, opens Cl- channels
7-66
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Polypeptide NTs (neuropeptides)
Cause
wide range of effects
Not thought to open ion channels
Many are neuromodulators
Involved in learning & neural plasticity
Most neurons can release a classical & polypeptide NT
7-67
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Polypeptide NTs (neuropeptides)
CCK
promotes satiety following meals
Substance P is a pain NT
Endorphins, enkephalins, & dynorphin are analgesics
Effects are blocked by naloxone, an opiate
antagonist
7-68
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Polypeptide NTs (neuropeptides)
Neuropeptide
Y is most common neuropeptide
Inhibits glutamate in hippocampus
Powerful stimulator of appetite
Endocannabinoids - similar to THC in marijuana
Only lipid NTs
Have analgesic effects
NO & CO are gaseous NTs
Act through cGMP second messenger system
NO causes smooth muscle relaxation
Viagra increases NO
7-69
Synaptic Integration
7-70
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EPSPs
Graded
in
magnitude
Have no threshold
Cause
depolarization
Summate
Have no refractory
period
Fig 7.27
7-71
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Spatial Summation
Cable
properties
cause EPSPs to fade
quickly over time &
distance
Spatial summation
takes place when
EPSPs from different
synapses occur in
postsynaptic cell at
same time
Fig 7.31
7-72
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Temporal Summation
Temporal
summation occurs because EPSPs that
occur closely in time can sum before they fade
7-73
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Synaptic Plasticity
Repeated
use of a synapse can increase or decrease
its ease of transmission
= synaptic facilitation or synaptic depression
High frequency stimulation often causes enhanced
excitability
Called long-term potentiation
 Believed to underlie learning
7-74
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Synaptic Inhibition
 Postsynaptic
inhibition
 GABA & glycine
produce IPSPs
 IPSPs dampen EPSPs
 Making it harder to
reach threshold
 Presynaptic inhibition:
 Occurs when 1 neuron
synapses onto axon or
bouton of another
neuron, inhibiting
release of its NT
Fig 7.32
7-75