three types of muscle tissue 1.skeletal muscle tissue: – attached to bones and skin – striated...
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Three Types of Muscle Tissue
1. Skeletal muscle tissue:– Attached to bones and skin– Striated – Voluntary (i.e., conscious control)– Powerful– Primary topic of this chapter
Three Types of Muscle Tissue
2. Cardiac muscle tissue:– Only in the heart – Striated – Involuntary– More details in Chapter 18
Three Types of Muscle Tissue
3. Smooth muscle tissue:– In the walls of hollow organs, e.g., stomach,
urinary bladder, and airways– Not striated– Involuntary– More details later in this chapter
Figure 9.1
Bone
Perimysium
Endomysium(between individualmuscle fibers)
Muscle fiber
Fascicle(wrapped by perimysium)
Epimysium
Tendon
Epimysium
Muscle fiberin middle ofa fascicle
Blood vessel
Perimysium
Endomysium
Fascicle(a)
(b)
Table 9.1
Table 9.3
Features of a Sarcomere• Thick filaments: run the entire length of an A band• Thin filaments: run the length of the I band and partway
into the A band• Z disc: coin-shaped sheet of proteins that anchors the
thin filaments and connects myofibrils to one another• H zone: lighter midregion where filaments do not
overlap • M line: line of protein myomesin that holds adjacent
thick filaments together
Figure 9.2c, d
I band I bandA bandSarcomere
H zoneThin (actin)filament
Thick (myosin)filament
Z disc Z disc
M line
(c) Small part of one myofibril enlarged to show the myofilamentsresponsible for the banding pattern. Each sarcomere extends fromone Z disc to the next.
Z disc Z discM line
Sarcomere
Thin (actin)filament
Thick(myosin)filament
Elastic (titin)filaments
(d) Enlargement of one sarcomere (sectioned lengthwise). Notice the myosin heads on the thick filaments.
Figure 9.3
Flexible hinge region
Tail
Tropomyosin Troponin Actin
Myosin head
ATP-bindingsite
Heads Active sitesfor myosinattachment
Actinsubunits
Actin-binding sites
Thick filamentEach thick filament consists of manymyosin molecules whose heads protrude at opposite ends of the filament.
Thin filamentA thin filament consists of two strandsof actin subunits twisted into a helix plus two types of regulatory proteins(troponin and tropomyosin).
Thin filamentThick filament
In the center of the sarcomere, the thickfilaments lack myosin heads. Myosin heads are present only in areas of myosin-actin overlap.
Longitudinal section of filamentswithin one sarcomere of a myofibril
Portion of a thick filamentPortion of a thin filament
Myosin molecule Actin subunits
Sarcoplasmic Reticulum (SR)
• Network of smooth endoplasmic reticulum surrounding each myofibril
• Pairs of terminal cisternae form perpendicular cross channels
• Functions in the regulation of intracellular Ca2+ levels
T Tubules
• Continuous with the sarcolemma• Penetrate the cell’s interior at each A band–I
band junction• Associate with the paired terminal cisternae
to form triads that encircle each sarcomere
Triad Relationships
• T tubules conduct impulses deep into muscle fiber
• Integral proteins protrude into the intermembrane space from T tubule and SR cisternae membranes
• T tubule proteins: voltage sensors• SR foot proteins: gated channels that regulate
Ca2+ release from the SR cisternae
Figure 9.5
Myofibril
Myofibrils
Triad:
Tubules ofthe SR
Sarcolemma
Sarcolemma
Mitochondria
I band I bandA band
H zone Z discZ disc
Part of a skeletalmuscle fiber (cell)
• T tubule• Terminal
cisternaeof the SR (2)
M line
Sliding Filament Model of Contraction
• In the relaxed state, thin and thick filaments overlap only slightly
• During contraction, myosin heads bind to actin, detach, and bind again, to propel the thin filaments toward the M line
• As H zones shorten and disappear, sarcomeres shorten, muscle cells shorten, and the whole muscle shortens
Figure 9.6
I
Fully relaxed sarcomere of a muscle fiber
Fully contracted sarcomere of a muscle fiber
IA
Z ZH
I IA
Z Z
1
2
Requirements for Skeletal Muscle Contraction
1. Activation: neural stimulation at aneuromuscular junction
2. Excitation-contraction coupling: – Generation and propagation of an action
potential along the sarcolemma– Final trigger: a brief rise in intracellular Ca2+
levels
Events at the Neuromuscular Junction
• Skeletal muscles are stimulated by somatic motor neurons
• Axons of motor neurons travel from the central nervous system via nerves to skeletal muscles
• Each axon forms several branches as it enters a muscle
• Each axon ending forms a neuromuscular junction with a single muscle fiber
Nucleus
Actionpotential (AP)
Myelinated axonof motor neuron
Axon terminal ofneuromuscular junction
Sarcolemma ofthe muscle fiber
Ca2+Ca2+
Axon terminalof motor neuron
Synaptic vesiclecontaining ACh
MitochondrionSynapticcleft
Fusing synaptic vesicles
1 Action potential arrives ataxon terminal of motor neuron.
2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.
Figure 9.8
Neuromuscular Junction
• Situated midway along the length of a muscle fiber
• Axon terminal and muscle fiber are separated by a gel-filled space called the synaptic cleft
• Synaptic vesicles of axon terminal contain the neurotransmitter acetylcholine (ACh)
• Junctional folds of the sarcolemma contain ACh receptors
Events at the Neuromuscular Junction
• Nerve impulse arrives at axon terminal• ACh is released and binds with receptors on
the sarcolemma• Electrical events lead to the generation of an
action potential
Figure 9.8
Nucleus
Actionpotential (AP)
Myelinated axonof motor neuron
Axon terminal ofneuromuscular junction
Sarcolemma ofthe muscle fiber
Ca2+Ca2+
Axon terminalof motor neuron
Synaptic vesiclecontaining AChMitochondrionSynapticcleft
Junctionalfolds ofsarcolemma
Fusing synaptic vesicles
ACh
Sarcoplasm ofmuscle fiber
Postsynaptic membraneion channel opens;ions pass.
Na+ K+
Ach–
Na+
K+
Degraded ACh
Acetyl-cholinesterase
Postsynaptic membraneion channel closed;ions cannot pass.
1 Action potential arrives ataxon terminal of motor neuron.
2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.
3 Ca2+ entry causes some synaptic vesicles to release their contents (acetylcholine)by exocytosis.
4 Acetylcholine, aneurotransmitter, diffuses across the synaptic cleft and binds to receptors in the sarcolemma.
5 ACh binding opens ionchannels that allow simultaneous passage of Na+ into the musclefiber and K+ out of the muscle fiber.
6 ACh effects are terminated by its enzymatic breakdown in the synaptic cleft by acetylcholinesterase.
Events in Generation of an Action Potential
1. Local depolarization (end plate potential):– ACh binding opens chemically (ligand) gated ion
channels– Simultaneous diffusion of Na+ (inward) and K+
(outward)– More Na+ diffuses, so the interior of the
sarcolemma becomes less negative– Local depolarization – end plate potential
Events in Generation of an Action Potential
2. Generation and propagation of an action potential:
– End plate potential spreads to adjacent membrane areas
– Voltage-gated Na+ channels open– Na+ influx decreases the membrane voltage
toward a critical threshold– If threshold is reached, an action potential is
generated
Events in Generation of an Action Potential
• Local depolarization wave continues to spread, changing the permeability of the sarcolemma
• Voltage-regulated Na+ channels open in the adjacent patch, causing it to depolarize to threshold
Events in Generation of an Action Potential
3. Repolarization:• Na+ channels close and voltage-gated K+
channels open• K+ efflux rapidly restores the resting polarity• Fiber cannot be stimulated and is in a
refractory period until repolarization is complete
• Ionic conditions of the resting state are restored by the Na+-K+ pump
Events in Generation of an Action Potential
1. Local depolarization (end plate potential):– ACh binding opens chemically (ligand) gated ion
channels– Simultaneous diffusion of Na+ (inward) and K+
(outward)– More Na+ diffuses, so the interior of the
sarcolemma becomes less negative– Local depolarization – end plate potential
Events in Generation of an Action Potential
2. Generation and propagation of an action potential:
– End plate potential spreads to adjacent membrane areas
– Voltage-gated Na+ channels open– Na+ influx decreases the membrane voltage
toward a critical threshold– If threshold is reached, an action potential is
generated
Events in Generation of an Action Potential
• Local depolarization wave continues to spread, changing the permeability of the sarcolemma
• Voltage-regulated Na+ channels open in the adjacent patch, causing it to depolarize to threshold
Events in Generation of an Action Potential
3. Repolarization:• Na+ channels close and voltage-gated K+
channels open• K+ efflux rapidly restores the resting polarity• Fiber cannot be stimulated and is in a
refractory period until repolarization is complete
• Ionic conditions of the resting state are restored by the Na+-K+ pump
Figure 9.9
Na+
Na+
Open Na+
Channel
Closed Na+
Channel
Closed K+
Channel
Open K+
Channel
Action potential++++++
+++++
+
Axon terminal
Synapticcleft
ACh
ACh
Sarcoplasm of muscle fiber
K+
2 Generation and propagation ofthe action potential (AP)
3 Repolarization
1 Local depolarization: generation of the end plate potential on the sarcolemma
K+
K+Na+
K+Na+
Wave ofde
po
lari
zatio
n
Figure 9.9, step 1
Na+
Na+
Open Na+
ChannelClosed K+
Channel
K+
Na+ K+Action potential
++++++
+++++
+
Axon terminal
Synapticcleft
ACh
ACh
Sarcoplasm of muscle fiber
K+
1 Local depolarization: generation of the end plate potential on the sarcolemma
1
Wave ofde
po
lari
zatio
n
Figure 9.9, step 2
Na+
Na+
Open Na+
ChannelClosed K+
Channel
K+
Na+ K+Action potential
++++++
+++++
+
Axon terminal
Synapticcleft
ACh
ACh
Sarcoplasm of muscle fiber
K+
Generation and propagation of the action potential (AP)
1 Local depolarization: generation of the end plate potential on the sarcolemma
2
1
Wave ofde
po
lari
zatio
n
Figure 9.9, step 3
Na+
Closed Na+
ChannelOpen K+
Channel
K+
Repolarization3
Figure 9.9
Na+
Na+
Open Na+
ChannelClosed K+
Channel
Action potential++++++
+++++
+
Axon terminal
Synapticcleft
ACh
ACh
Sarcoplasm of muscle fiber
K+
2 Generation and propagation ofthe action potential (AP)
3 Repolarization
1 Local depolarization: generation of the end plate potential on the sarcolemma
K+
K+Na+
K+Na+
Wave ofde
po
lari
zatio
n
Closed Na+
ChannelOpen K+
Channel
Figure 9.10
Na+ channelsclose, K+ channelsopen
K+ channelsclose
Repolarizationdue to K+ exit
Threshold
Na+
channelsopen
Depolarizationdue to Na+ entry
Excitation-Contraction (E-C) Coupling
• Sequence of events by which transmission of an AP along the sarcolemma leads to sliding of the myofilaments
• Latent period:– Time when E-C coupling events occur– Time between AP initiation and the beginning of
contraction
Events of Excitation-Contraction (E-C) Coupling
• AP is propagated along sarcomere to T tubules• Voltage-sensitive proteins stimulate Ca2+
release from SR – Ca2+ is necessary for contraction
Figure 9.11, step 1
Axon terminalof motor neuron
Muscle fiberTriad
One sarcomere
Synaptic cleft
Setting the stage
Sarcolemma
Action potentialis generated
Terminal cisterna of SR ACh
Ca2+
Figure 9.11, step 2
Action potential is propagated alongthe sarcolemma and down the T tubules.
Steps in E-C Coupling:
Troponin Tropomyosinblocking active sites
Myosin
Actin
Active sites exposed and ready for myosin binding
Ca2+
Terminal cisterna of SR
Voltage-sensitivetubule protein
T tubule
Ca2+
releasechannel
Myosincross bridge
Ca2+
Sarcolemma
Calcium ions are released.
Calcium binds to troponin andremoves the blocking action oftropomyosin.
Contraction begins
The aftermath
1
2
3
4
Figure 9.11, step 3
Steps inE-C Coupling:
Terminal cisterna of SR
Voltage-sensitivetubule protein
T tubule
Ca2+
releasechannel
Ca2+
Sarcolemma
Action potential ispropagated along thesarcolemma and downthe T tubules.
1
Figure 9.11, step 4
Steps inE-C Coupling:
Terminal cisterna of SR
Voltage-sensitivetubule protein
T tubule
Ca2+
releasechannel
Ca2+
Sarcolemma
Action potential ispropagated along thesarcolemma and downthe T tubules.
Calciumions arereleased.
1
2
Figure 9.11, step 5
Troponin Tropomyosinblocking active sitesMyosin
Actin
Ca2+
The aftermath
Figure 9.11, step 6
Troponin Tropomyosinblocking active sitesMyosin
Actin
Active sites exposed and ready for myosin binding
Ca2+
Calcium binds totroponin and removesthe blocking action oftropomyosin.
The aftermath
3
Figure 9.11, step 7
Troponin Tropomyosinblocking active sitesMyosin
Actin
Active sites exposed and ready for myosin binding
Ca2+
Myosincross bridge
Calcium binds totroponin and removesthe blocking action oftropomyosin.
Contraction begins
The aftermath
3
4
Figure 9.11, step 8
Action potential is propagated alongthe sarcolemma and down the T tubules.
Steps in E-C Coupling:
Troponin Tropomyosinblocking active sites
Myosin
Actin
Active sites exposed and ready for myosin binding
Ca2+
Terminal cisterna of SR
Voltage-sensitivetubule protein
T tubule
Ca2+
releasechannel
Myosincross bridge
Ca2+
Sarcolemma
Calcium ions are released.
Calcium binds to troponin andremoves the blocking action oftropomyosin.
Contraction begins
The aftermath
1
2
3
4
Role of Calcium (Ca2+) in Contraction
• At low intracellular Ca2+ concentration:– Tropomyosin blocks the active sites on actin– Myosin heads cannot attach to actin– Muscle fiber relaxes
Role of Calcium (Ca2+) in Contraction
• At higher intracellular Ca2+ concentrations:– Ca2+ binds to troponin – Troponin changes shape and moves tropomyosin
away from active sites– Events of the cross bridge cycle occur – When nervous stimulation ceases, Ca2+ is pumped
back into the SR and contraction ends
Cross Bridge Cycle
• Continues as long as the Ca2+ signal and adequate ATP are present
• Cross bridge formation—high-energy myosin head attaches to thin filament
• Working (power) stroke—myosin head pivots and pulls thin filament toward M line
Cross Bridge Cycle
• Cross bridge detachment—ATP attaches to myosin head and the cross bridge detaches
• “Cocking” of the myosin head—energy from hydrolysis of ATP cocks the myosin head into the high-energy state
Figure 9.12
1
Actin
Cross bridge formation.
Cocking of myosin head. The power (working) stroke.
Cross bridge detachment.
Ca2+
Myosincross bridge
Thick filament
Thin filament
ADP
Myosin
Pi
ATPhydrolysis
ATP
ATP
24
3
ADP
Pi
ADPPi
Motor Unit: The Nerve-Muscle Functional Unit
• Motor unit = a motor neuron and all (four to several hundred) muscle fibers it supplies
Figure 9.13a
Spinal cord
Motor neuroncell body
Muscle
Nerve
Motorunit 1
Motorunit 2
Musclefibers
Motorneuronaxon
Axon terminals atneuromuscular junctions
Axons of motor neurons extend from the spinal cord to the muscle. There each axon divides into a number of axon terminals that form neuromuscular junctions with muscle fibers scattered throughout the muscle.
Response to Change in Stimulus Strength
• Threshold stimulus: stimulus strength at which the first observable muscle contraction occurs
• Muscle contracts more vigorously as stimulus strength is increased above threshold
• Contraction force is precisely controlled by recruitment (multiple motor unit summation), which brings more and more muscle fibers into action
Figure 9.16
Stimulus strength
Proportion of motor units excited
Strength of muscle contraction
Maximal contraction
Maximalstimulus
Thresholdstimulus
Response to Change in Stimulus Strength
• Size principle: motor units with larger and larger fibers are recruited as stimulus intensity increases
Muscle Tone
• Constant, slightly contracted state of all muscles
• Due to spinal reflexes that activate groups of motor units alternately in response to input from stretch receptors in muscles
• Keeps muscles firm, healthy, and ready to respond
Muscle Metabolism: Energy for Contraction
• ATP is regenerated by:– Direct phosphorylation of ADP by creatine
phosphate (CP) – Anaerobic pathway (glycolysis) – Aerobic respiration
Figure 9.19a
Coupled reaction of creatinephosphate (CP) and ADP
Energy source: CP
(a) Direct phosphorylation
Oxygen use: NoneProducts: 1 ATP per CP, creatineDuration of energy provision:15 seconds
Creatinekinase
ADPCP
Creatine ATP
Figure 9.19b
Energy source: glucose
Glycolysis and lactic acid formation
(b) Anaerobic pathway
Oxygen use: NoneProducts: 2 ATP per glucose, lactic acidDuration of energy provision:60 seconds, or slightly more
Glucose (fromglycogen breakdown ordelivered from blood)
Glycolysisin cytosol
Pyruvic acid
Releasedto blood
net gain
2
Lactic acid
O2
O2ATP
Figure 9.19c
Energy source: glucose; pyruvic acid;free fatty acids from adipose tissue;amino acids from protein catabolism
(c) Aerobic pathway
Aerobic cellular respiration
Oxygen use: RequiredProducts: 32 ATP per glucose, CO2, H2ODuration of energy provision: Hours
Glucose (fromglycogen breakdown ordelivered from blood)
32
O2
O2
H2O
CO2
Pyruvic acidFattyacids
Aminoacids
Aerobic respirationin mitochondriaAerobic respirationin mitochondria
ATP
net gain perglucose
Oxygen Deficit
Extra O2 needed after exercise for:
• Replenishment of– Oxygen reserves – Glycogen stores – ATP and CP reserves
• Conversion of lactic acid to pyruvic acid, glucose, and glycogen
Heat Production During Muscle Activity
• ~ 40% of the energy released in muscle activity is useful as work
• Remaining energy (60%) given off as heat • Dangerous heat levels are prevented by
radiation of heat from the skin and sweating
Force of Muscle Contraction
• The force of contraction is affected by:– Number of muscle fibers stimulated (recruitment)– Relative size of the fibers—hypertrophy of cells
increases strength
Velocity and Duration of Contraction
Influenced by:1. Muscle fiber type2. Load3. Recruitment
Muscle Fiber Type
Classified according to two characteristics:1. Speed of contraction: slow or fast, according
to:– Speed at which myosin ATPases split ATP– Pattern of electrical activity of the motor neurons
Muscle Fiber Type
2. Metabolic pathways for ATP synthesis:– Oxidative fibers—use aerobic pathways– Glycolytic fibers—use anaerobic glycolysis
Muscle Fiber Type
Three types: – Slow oxidative fibers– Fast oxidative fibers– Fast glycolytic fibers
Table 9.2
Effects of Resistance Exercise
• Resistance exercise (typically anaerobic) results in:– Muscle hypertrophy (due to increase in fiber size)– Increased mitochondria, myofilaments, glycogen
stores, and connective tissue
Smooth Muscle
• Found in walls of most hollow organs(except heart)
• Usually in two layers (longitudinal and circular)
Peristalsis
• Alternating contractions and relaxations of smooth muscle layers that mix and squeeze substances through the lumen of hollow organs– Longitudinal layer contracts; organ dilates and
shortens – Circular layer contracts; organ constricts and
elongates
Microscopic Structure
• Spindle-shaped fibers: thin and short compared with skeletal muscle fibers
• Connective tissue: endomysium only• SR: less developed than in skeletal muscle • Pouchlike infoldings (caveolae) of sarcolemma
sequester Ca2+
• No sarcomeres, myofibrils, or T tubules
Myofilaments in Smooth Muscle
• Ratio of thick to thin filaments (1:13) is much lower than in skeletal muscle (1:2)
• Thick filaments have heads along their entire length
• No troponin complex; protein calmodulin binds Ca2+
Role of Calcium Ions
• Ca2+ binds to and activates calmodulin • Activated calmodulin activates myosin (light
chain) kinase• Activated kinase phosphorylates and activates
myosin • Cross bridges interact with actin
Special Features of Smooth Muscle Contraction
Hyperplasia:– Smooth muscle cells can divide and increase their
numbers– Example:
• estrogen effects on uterus at puberty and during pregnancy
Functions of the Nervous System
1. Sensory input– Information gathered by sensory receptors about
internal and external changes
2. Integration– Interpretation of sensory input
3. Motor output– Activation of effector organs (muscles and
glands) produces a response
Peripheral Nervous System (PNS)
• Two functional divisions1. Sensory (afferent) division
• Somatic afferent fibers — convey impulses from skin, skeletal muscles, and joints
• Visceral afferent fibers — convey impulses from visceral organs
2. Motor (efferent) division • Transmits impulses from the CNS to effector organs
Motor Division of PNS
1. Somatic (voluntary) nervous system– Conscious control of skeletal muscles
Motor Division of PNS
2. Autonomic (involuntary) nervous system (ANS); “ a law unto itself”
– Visceral motor nerve fibers– Regulates smooth muscle, cardiac muscle, and
glands– Two functional subdivisions
• Sympathetic• Parasympathetic
Histology of Nervous Tissue
• Two principal cell types1. Neurons — excitable cells that transmit electrical
signals
Histology of Nervous Tissue
2. Neuroglia (glial cells)—supporting cells:• Astrocytes (CNS)• Microglia (CNS)• Ependymal cells (CNS)• Oligodendrocytes (CNS)• Satellite cells (PNS)• Schwann cells (PNS)
Astrocytes
• Most abundant, versatile, and highly branched glial cells
• Cling to neurons, synaptic endings, and capillaries
• Support and brace neurons
Astrocytes
• Help determine capillary permeability• Guide migration of young neurons• Control the chemical environment• Participate in information processing in the
brain
Microglia
• Small, ovoid cells with thorny processes• Migrate toward injured neurons• Phagocytize microorganisms and neuronal
debris
Ependymal Cells
• Range in shape from squamous to columnar• May be ciliated
– Line the central cavities of the brain (ventricles) and spinal column
– Separate the CNS interstitial fluid from the cerebrospinal fluid in the cavities
– Circulates CSF
Oligodendrocytes
• Branched cells• Processes wrap CNS nerve fibers, forming
insulating myelin sheaths
Satellite Cells and Schwann Cells
• Satellite cells– Surround neuron cell bodies in the PNS
• Schwann cells (neurolemmocytes)– Surround peripheral nerve fibers and form myelin
sheaths– Vital to regeneration of damaged peripheral
nerve fibers
Neurons (Nerve Cells)
• Special characteristics:– Long-lived ( 100 years or more)– Amitotic—with few exceptions– High metabolic rate—depends on continuous
supply of oxygen and glucose– Plasma membrane functions in:
• Electrical signaling • Cell-to-cell interactions during development
Cell Body (Perikaryon or Soma)
• Biosynthetic center of a neuron• Spherical nucleus with nucleolus• Well-developed Golgi apparatus• Rough ER called Nissl bodies (chromatophilic
substance)
Cell Body (Perikaryon or Soma)
• Network of neurofibrils (neurofilaments) • Axon hillock — cone-shaped area from which
axon arises• Clusters of cell bodies are called nuclei in the
CNS, ganglia in the PNS
Processes
• Dendrites and axons• Bundles of processes are called
– Tracts in the CNS– Nerves in the PNS
Dendrites
• Short, tapering, and diffusely branched • Receptive (input) region of a neuron• Convey electrical signals toward the cell body
as graded potentials
The Axon• One axon per cell arising from the axon
hillock• Long axons (nerve fibers)• Occasional branches (axon collaterals)
The Axon
• Numerous terminal branches (telodendria)• Knoblike axon terminals (synaptic knobs or
boutons) – Secretory region of neuron– Release neurotransmitters to excite or inhibit
other cells
Axons: Function
• Conducting region of a neuron• Generates and transmits nerve impulses
(action potentials) away from the cell body
Myelin Sheath
• Segmented protein-lipoid sheath around most long or large-diameter axons
• It functions to:– Protect and electrically insulate the axon– Increase speed of nerve impulse transmission
Myelin Sheaths in the PNS
• Schwann cells wraps many times around the axon – Myelin sheath — concentric layers of Schwann
cell membrane
• Neurilemma — peripheral bulge of Schwann cell cytoplasm
Myelin Sheaths in the PNS
• Nodes of Ranvier – Myelin sheath gaps between adjacent Schwann
cells– Sites where axon collaterals can emerge
Myelin Sheaths in the CNS
• Formed by processes of oligodendrocytes, not the whole cells
• Nodes of Ranvier are present• No neurilemma• Thinnest fibers are unmyelinated
Functional Classification of Neurons
• Three types: 1. Sensory (afferent)
• Transmit impulses from sensory receptors toward the CNS
2. Motor (efferent)• Carry impulses from the CNS to effectors
Functional Classification of Neurons
3. Interneurons (association neurons)• Shuttle signals through CNS pathways; most are
entirely within the CNS
Neuron Function
• Neurons are highly irritable• Respond to adequate stimulus by generating
an action potential (nerve impulse) • Impulse is always the same regardless of
stimulus
Role of Membrane Ion Channels
• Proteins serve as membrane ion channels• Two main types of ion channels
1. Leakage (nongated) channels—always open
Role of Membrane Ion Channels
2. Gated channels (three types):– Chemically gated (ligand-gated) channels—open with binding
of a specific neurotransmitter– Voltage-gated channels—open and close in response to
changes in membrane potential– Mechanically gated channels—open and close in response to
physical deformation of receptors
Gated Channels
• When gated channels are open:– Ions diffuse quickly across the membrane along
their electrochemical gradients• Along chemical concentration gradients from higher
concentration to lower concentration• Along electrical gradients toward opposite electrical
charge– Ion flow creates an electrical current and voltage
changes across the membrane
Resting Membrane Potential (Vr)
• Potential difference across the membrane of a resting cell– Approximately –70 mV in neurons (cytoplasmic
side of membrane is negatively charged relative to outside)
• Generated by:– Differences in ionic makeup of ICF and ECF – Differential permeability of the plasma membrane
Resting Membrane Potential
• Differences in ionic makeup– ICF has lower concentration of Na+ and Cl– than
ECF– ICF has higher concentration of K+ and negatively
charged proteins (A–) than ECF
Resting Membrane Potential
• Differential permeability of membrane– Impermeable to A–
– Slightly permeable to Na+ (through leakage channels)
– 75 times more permeable to K+ (more leakage channels)
– Freely permeable to Cl–
Resting Membrane Potential
• Negative interior of the cell is due to much greater diffusion of K+ out of the cell than Na+ diffusion into the cell
• Sodium-potassium pump stabilizes the resting membrane potential by maintaining the concentration gradients for Na+ and K+
Membrane Potentials That Act as Signals
• Two types of signals– Graded potentials
• Incoming short-distance signals
– Action potentials • Long-distance signals of axons
Changes in Membrane Potential
• Depolarization– A reduction in membrane potential (toward zero)– Inside of the membrane becomes less negative
than the resting potential– Increases the probability of producing a nerve
impulse
Figure 11.9a
Depolarizing stimulus
Time (ms)
Insidepositive
Insidenegative
Restingpotential
Depolarization
(a) Depolarization: The membrane potentialmoves toward 0 mV, the inside becoming less negative (more positive).
Changes in Membrane Potential
• Hyperpolarization– An increase in membrane potential (away from
zero)– Inside of the membrane becomes more negative
than the resting potential– Reduces the probability of producing a nerve
impulse
Figure 11.9b
Hyperpolarizing stimulus
Time (ms)
Restingpotential
Hyper-polarization
(b) Hyperpolarization: The membranepotential increases, the inside becomingmore negative.
Graded Potentials
• Short-lived, localized changes in membrane potential
• Depolarizations or hyperpolarizations• Graded potential spreads as local currents
change the membrane potential of adjacent regions
Figure 11.10b
(b) Spread of depolarization: The local currents (black arrows) that are created depolarize adjacent membrane areas and allow the wave of depolarization to spread.
Graded Potentials
• Occur when a stimulus causes gated ion channels to open– E.g., receptor potentials, generator potentials,
postsynaptic potentials (IPSP, EPSP)• Magnitude varies directly (graded) with
stimulus strength • Decrease in magnitude with distance as ions
flow and diffuse through leakage channels• Short-distance signals
Action Potential (AP)
• Brief reversal of membrane potential with a total amplitude of ~100 mV
• Occurs in muscle cells and axons of neurons• Does not decrease in magnitude over
distance• Principal means of long-distance neural
communication
Actionpotential
1 2 3
4
Resting state Depolarization Repolarization
Hyperpolarization
The big picture
1 1
2
3
4
Time (ms)
ThresholdMem
bra
ne p
ote
nti
al (m
V)
Figure 11.11 (1 of 5)
Generation of an Action Potential
• Resting state– Only leakage channels for Na+ and K+ are open– All gated Na+ and K+ channels are closed
Depolarizing Phase
• Depolarizing local currents open voltage-gated Na+ channels
• Na+ influx causes more depolarization• At threshold (–55 to –50 mV) positive
feedback leads to opening of all Na+ channels, and a reversal of membrane polarity to +30mV (spike of action potential)
Repolarizing Phase
• Repolarizing phase– Na+ channel slow inactivation gates close– Membrane permeability to Na+ declines to
resting levels– Slow voltage-sensitive K+ gates open– K+ exits the cell and internal negativity is restored
Hyperpolarization
• Hyperpolarization– Some K+ channels remain open, allowing excessive
K+ efflux – This causes hyperpolarization of the membrane
(undershoot)
Propagation of an Action Potential
• Na+ influx causes a patch of the axonal membrane to depolarize
• Local currents occur• Na+ channels toward the point of origin are
inactivated and not affected by the local currents
Propagation of an Action Potential
• Local currents affect adjacent areas in the forward direction
• Depolarization opens voltage-gated channels and triggers an AP
• Repolarization wave follows the depolarization wave
• (Fig. 11.12 shows the propagation process in unmyelinated axons.)
Threshold
• At threshold:– Membrane is depolarized by 15 to 20 mV – Na+ permeability increases– Na influx exceeds K+ efflux– The positive feedback cycle begins
Threshold
• Subthreshold stimulus—weak local depolarization that does not reach threshold
• Threshold stimulus—strong enough to push the membrane potential toward and beyond threshold
• AP is an all-or-none phenomenon — action potentials either happen completely, or not at all
Coding for Stimulus Intensity
• All action potentials are alike and are independent of stimulus intensity– How does the CNS tell the difference between a
weak stimulus and a strong one?
• Strong stimuli can generate action potentials more often than weaker stimuli
• The CNS determines stimulus intensity by the frequency of impulses
Figure 11.13
Threshold
Actionpotentials
Stimulus
Time (ms)
Figure 11.14
Stimulus
Absolute refractoryperiod
Relative refractoryperiod
Time (ms)
Depolarization(Na+ enters)
Repolarization(K+ leaves)
After-hyperpolarization
Conduction Velocity
• Conduction velocities of neurons vary widely • Effect of axon diameter
– Larger diameter fibers have less resistance to local current flow and have faster impulse conduction
• Effect of myelination– Continuous conduction in unmyelinated axons is
slower than saltatory conduction in myelinated axons
Conduction Velocity
• Effects of myelination– Myelin sheaths insulate and prevent leakage of
charge– Saltatory conduction in myelinated axons is about
30 times faster• Voltage-gated Na+ channels are located at the nodes• APs appear to jump rapidly from node to node
Electrical Synapses
• Less common than chemical synapses– Neurons are electrically coupled (joined by gap
junctions)– Communication is very rapid, and may be
unidirectional or bidirectional– Are important in:
• Embryonic nervous tissue• Some brain regions
Chemical Synapses
• Specialized for the release and reception of neurotransmitters
• Typically composed of two parts – Axon terminal of the presynaptic neuron, which
contains synaptic vesicles – Receptor region on the postsynaptic neuron
Synaptic Cleft
• Fluid-filled space separating the presynaptic and postsynaptic neurons
• Prevents nerve impulses from directly passing from one neuron to the next
Synaptic Cleft
• Transmission across the synaptic cleft: – Is a chemical event (as opposed to an electrical
one)– Involves release, diffusion, and binding of
neurotransmitters– Ensures unidirectional communication between
neurons
Information Transfer
• AP arrives at axon terminal of the presynaptic neuron and opens voltage-gated Ca2+ channels
• Synaptotagmin protein binds Ca2+ and promotes fusion of synaptic vesicles with axon membrane
• Exocytosis of neurotransmitter occurs
Information Transfer
• Neurotransmitter diffuses and binds to receptors (often chemically gated ion channels) on the postsynaptic neuron
• Ion channels are opened, causing an excitatory or inhibitory event (graded potential)
Figure 11.17
Action potentialarrives at axon terminal.
Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Ca2+ entry causesneurotransmitter-containing synapticvesicles to release theircontents by exocytosis.
Chemical synapsestransmit signals fromone neuron to anotherusing neurotransmitters.
Ca2+
Synapticvesicles
Axonterminal
Mitochondrion
Postsynapticneuron
Presynapticneuron
Presynapticneuron
Synapticcleft
Ca2+
Ca2+
Ca2+
Neurotransmitterdiffuses across the synapticcleft and binds to specificreceptors on thepostsynaptic membrane.
Binding of neurotransmitteropens ion channels, resulting ingraded potentials.
Neurotransmitter effects areterminated by reuptake throughtransport proteins, enzymaticdegradation, or diffusion awayfrom the synapse.
Ion movement
Graded potentialReuptake
Enzymaticdegradation
Diffusion awayfrom synapse
Postsynapticneuron
1
2
3
4
5
6
Postsynaptic Potentials
• Graded potentials• Strength determined by:
– Amount of neurotransmitter released– Time the neurotransmitter is in the area
• Types of postsynaptic potentials 1. EPSP—excitatory postsynaptic potentials 2. IPSP—inhibitory postsynaptic potentials
Table 11.2 (1 of 4)
Table 11.2 (2 of 4)
Table 11.2 (3 of 4)
Table 11.2 (4 of 4)
Excitatory Synapses and EPSPs
• Neurotransmitter binds to and opens chemically gated channels that allow simultaneous flow of Na+ and K+ in opposite directions
• Na+ influx is greater that K+ efflux, causing a net depolarization
• EPSP helps trigger AP at axon hillock if EPSP is of threshold strength and opens the voltage-gated channels
Figure 11.18a
An EPSP is a localdepolarization of the postsynaptic membranethat brings the neuroncloser to AP threshold. Neurotransmitter binding opens chemically gated ion channels, allowing the simultaneous pas-sage of Na+ and K+.
Time (ms)
(a) Excitatory postsynaptic potential (EPSP)
Threshold
Stimulus
Mem
bra
ne p
ote
nti
al (m
V)
Inhibitory Synapses and IPSPs
• Neurotransmitter binds to and opens channels for K+ or Cl–
• Causes a hyperpolarization (the inner surface of membrane becomes more negative)
• Reduces the postsynaptic neuron’s ability to produce an action potential
Figure 11.18b
An IPSP is a localhyperpolarization of the postsynaptic membraneand drives the neuron away from AP threshold. Neurotransmitter binding opens K+ or Cl– channels.
Time (ms)
(b) Inhibitory postsynaptic potential (IPSP)
Threshold
Stimulus
Mem
bra
ne p
ote
nti
al (m
V)
Integration: Summation
• A single EPSP cannot induce an action potential
• EPSPs can summate to reach threshold• IPSPs can also summate with EPSPs, canceling
each other out
Integration: Summation
• Temporal summation– One or more presynaptic neurons transmit
impulses in rapid-fire order
• Spatial summation– Postsynaptic neuron is stimulated by a large
number of terminals at the same time
Figure 11.23
1
2
3
4
5
Receptor
Sensory neuron
Integration center
Motor neuron
Effector
Stimulus
ResponseSpinal cord (CNS)
Interneuron