Muscles, Locomotion
& Sensation
(Ch. 50)
Overview of information processing by nervous
systems
Sensory input
Integration
Sensor
Motor output
Effector
Peripheral nervous
system (PNS)
Central nervous
system (CNS)
Animal Locomotion
What are the advantages of locomotion?
sessile
motile
Lots of ways to get around…
Lots of ways to get around…
mollusk mammal
bird reptile
Lots of ways to get around…
bird arthropod
mammal bird
Muscle
involuntary,
striated
auto-rhythmic
voluntary,
striated
heart
moves bone
multi-nucleated
evolved first
involuntary,
non-striated
digestive system
arteries, veins
•
All cells have a fine network of actin and myosin fibers that contribute to cellular
movement. But only muscle cells have them in such great abundance and far more
organized for contraction.
•
SMOOTH MUSCLE
Smooth muscle was the first to evolve.
Lining of blood vessels, wall of the gut, iris of the eye.
Some contract only when stimulated by nerve impulse. Others generate electrical
impulses spontaneously and then are regulated by nervous system.
•
CARDIAC MUSCLE
Small interconnected cell with only one nucleus. Interconnected through gap
junctions. Single functioning unit that contract in unison via this intercellular
communication. Mostly generate electrical impulses spontaneously. Regulated
rather than initial stimulation by nervous system.
•
SKELETAL MUSCLE
Fusion of many cells so multi-nucleated. Attached by tendon to bone. Long thin
cells called muscle fibers.
Organization of Skeletal muscle
skeletal muscle
plasma
membrane
nuclei
tendon
muscle fiber (cell)
myofibrils
myofilaments
Human endoskeleton
206 bones
Muscles movement
• Muscles do work by contracting
– skeletal muscles come in
antagonistic pairs
• flexor vs. extensor
– contracting = shortening
• move skeletal parts
– tendons
• connect bone to muscle
– ligaments
• connect bone to bone
Structure of striated skeletal muscle
• Muscle Fiber
– muscle cell
• divided into sections =
sarcomeres
• Sarcomere
– functional unit of muscle
contraction
– alternating bands of
thin (actin) & thick (myosin)
protein filaments
Muscle filaments & Sarcomere
• Interacting proteins
– thin filaments
• braided strands
– actin
– tropomyosin
– troponin
– thick filaments
• myosin
Thin filaments: actin
• Complex of proteins
– braid of actin molecules & tropomyosin fibers
• tropomyosin fibers secured with troponin molecules
Thick filaments: myosin
• Single protein
– myosin molecule
• long protein with globular head
bundle of myosin proteins:
globular heads aligned
Thick & thin filaments
• Myosin tails aligned together & heads pointed away
from center of sarcomere
Interaction of thick & thin filaments
• Cross bridges
– connections formed between myosin heads (thick
filaments) & actin (thin filaments)
– cause the muscle to shorten (contract)
sarcomere
sarcomere
Where is ATP needed?
binding site
thin filament
(actin)
myosin head
ADP
12
thick filament
(myosin)
ATP
So that’s
where those
10,000,000 ATPs go!
Well, not all of it!
form
cross
bridge
11
1
3
release
cross
bridge
Cleaving ATP  ADP allows myosin head 1
to bind to actin filament
shorten
sarcomere
4
Closer look at muscle cell
Sarcoplasmic
reticulum
Transverse tubules
(T-tubules)
multi-nucleated
Mitochondrion
Muscle cell organelles
Ca2+ ATPase of SR
• Sarcoplasm
– muscle cell cytoplasm
– contains many mitochondria
• Sarcoplasmic reticulum (SR)
There’s
the rest
of the
ATPs!
– organelle similar to ER
• network of tubes
– stores Ca2+
• Ca2+ released from SR through channels
• Ca2+ restored to SR by Ca2+ pumps
– pump Ca2+ from cytosol
– pumps use ATP
ATP
But what
does the
Ca2+ do?
Muscle at rest
• Interacting proteins
– at rest, troponin molecules hold tropomyosin fibers so
that they cover the myosin-binding sites on actin
• troponin has Ca2+ binding sites
The Trigger: motor neurons
• Motor neuron triggers muscle contraction
– release acetylcholine (Ach) neurotransmitter
Nerve trigger of muscle action
• Nerve signal travels
down T-tubule
– stimulates
sarcoplasmic
reticulum (SR) of
muscle cell to
release stored Ca2+
– flooding muscle fibers
with Ca2+
Ca2+ triggers muscle action
• At rest, tropomyosin blocks
myosin-binding sites on
actin
– secured by troponin
• Ca2+ binds to troponin
– shape change
causes movement
of troponin
– releasing tropomyosin
– exposes myosin-binding
sites on actin
How Ca2+ controls muscle
• Sliding filament model
– exposed actin binds to
myosin
– fibers slide past each
other
• ratchet system
ATP
– shorten muscle cell
• muscle contraction
– muscle doesn’t relax
until Ca2+ is pumped
back into SR
ATP
• requires ATP
Put it all together…
1
2
3
ATP
7
4
6
ATP
5
How it all works…
• Action potential causes Ca2+ release from SR
– Ca2+ binds to troponin
• Troponin moves tropomyosin uncovering myosin binding
site on actin
ATP
• Myosin binds actin
– uses ATP to "ratchet" each time
– releases, "unratchets" & binds to next actin
• Myosin pulls actin chain along
• Sarcomere shortens
– Z discs move closer together
• Whole fiber shortens  contraction!
• Ca2+ pumps restore Ca2+ to SR  relaxation!
– pumps use ATP
ATP
Fast twitch & slow twitch muscles
• Slow twitch muscle fibers
– contract slowly, but keep going for a long time
• more mitochondria for aerobic respiration
• less SR  Ca2+ remains in cytosol longer
– long distance runner
– “dark” meat = more blood vessels
• Fast twitch muscle fibers
– contract quickly, but get tired rapidly
• store more glycogen for anaerobic respiration
– sprinter
– “white” meat
Muscle limits
• Muscle fatigue
– lack of sugar
• lack of ATP to restore Ca2+ gradient
– low O2
• lactic acid drops pH which
interferes with protein function
– synaptic fatigue
• loss of acetylcholine
• Muscle cramps
– build up of lactic acid
– ATP depletion
– ion imbalance
• massage or stretching
increases circulation
Diseases of Muscle tissue
• ALS
– amyotrophic lateral sclerosis
– Lou Gehrig’s disease
– motor neurons degenerate
• Myasthenia gravis
– auto-immune
– antibodies to
acetylcholine
receptors
Stephen Hawking
Botox
• Bacteria Clostridium botulinum toxin
– blocks release of acetylcholine
– botulism can be fatal
muscle
Rigor mortis
 So why are dead people “stiffs”?
no life, no breathing
 no breathing, no O2
 no O2, no aerobic respiration
 no aerobic respiration, no ATP
 no ATP, no Ca2+ pumps
 Ca2+ stays in muscle cytoplasm
 muscle fibers continually
contract

 tetany or rigor mortis

eventually tissues breakdown
& relax
 measure of time of death
Overview of information processing by nervous
systems
Sensory input
Integration
Sensor
Motor output
Effector
Peripheral nervous
system (PNS)
Central nervous
system (CNS)
A bat using sonar to locate its prey
Sensory reception: two mechanisms
Weak
muscle stretch
Muscle
Strong
muscle stretch
Membrane
potential (mV)
Dendrites
Stretch
receptor
Axon
–50 Receptor potential
–50
–70
–70
Action potentials
0
0
–70
–70
(a) Crayfish stretch receptors have dendrites
embedded in abdominal muscles. When the
abdomen bends, muscles and dendrites
“Hairs” of
hair cell
0 1 2 3 4 5 6 7
Time (sec)
stretch, producing a receptor potential in the
stretch receptor. The receptor potential triggers
action potentials in the axon of the stretch
No fluid
movement
Fluid moving in
one direction
More
neurotransmitter
Neurotransmitter at
synapse
0 1 2 3 4 5 6 7
Time (sec)
receptor. A stronger stretch produces a larger
receptor potential and higher frequency of
action potentials.
Fluid moving in
other direction
Less
neurotransmitter
–50
–50 Receptor potential
–50
–70
–70
–70
0
–70
0
–70
Membrane
potential (mV)
Action potentials
Membrane
potential (mV)
Membrane
potential (mV)
Axon
0
–70
0 1 2 3 4 5 6 7
0 1 2 3 4 5 6 7
0 1 2 3 4 5 6 7
Time (sec)
Time (sec)
Time (sec)
(b) Vertebrate hair cells have specialized cilia
with a sensory neuron, which conducts action
of action potentials in the sensory neuron.
or microvilli (“hairs”) that bend when surpotentials to the CNS. Bending in one direction Bending in the other direction has the opposite
rounding fluid moves. Each hair cell releases
depolarizes the hair cell, causing it to release effects. Thus, hair cells respond to the direction of
an excitatory neurotransmitter at a synapse more neurotransmitter and increasing frequency
motion as well as to its strength and speed.
Sensory receptors in human skin
Cold
Light touch
Pain
Hair
Heat
Epidermis
Dermis
Nerve
Connective tissue Hair movement
Strong pressure
The Structure of the Human Ear
1 Overview of ear structure
2 The middle ear and inner ear
Incus
Outer ear
Middle
ear Inner ear
Stapes
Skull
bones
Semicircular
canals
Malleus
Auditory nerve,
to brain
Pinna
Tympanic
membrane
Hair cells
Cochlea
Eustachian
tube
Auditory
canal
Tectorial
membrane
Tympanic
membrane
Oval
window
Eustachian
tube
Round
window
Cochlear duct
Bone
Vestibular canal
Auditory nerve
Basilar
membrane
Axons of
sensory neurons
4 The organ of Corti
To auditory
nerve
Tympanic canal
3 The cochlea
Organ of Corti
Transduction in the cochlea
Cochlea
Stapes
Oval
window
Axons of
sensory
neurons
Vestibular
canal
Perilymph
Base
Round
window
Tympanic
canal
Basilar
membrane
Apex
How the cochlea distinguishes
pitch
Cochlea
(uncoiled)
Apex
(wide and flexible)
Basilar
membrane
1 kHz
500 Hz
(low pitch)
2 kHz
4 kHz
8 kHz
16 kHz
(high pitch)
Base
(narrow and stiff)
Frequency producing
maximum vibration
Organs of equilibrium in the inner ear
The semicircular canals, arranged in three
spatial planes, detect angular movements
of the head.
Each canal has at its base a
swelling called an ampulla,
containing a cluster of hair cells.
When the head changes its rate
of rotation, inertia prevents
endolymph in the semicircular
canals from moving with the head,
so the endolymph presses against
the cupula, bending the hairs.
Flow
of endolymph
Flow
of endolymph
Vestibular nerve
Cupula
Hairs
Hair
cell
Nerve
fibers
Vestibule
Utricle
Body movement
Saccule
The utricle and saccule tell the brain which
way is up and inform it of the body’s
position or linear acceleration.
The hairs of the hair cells
project into a gelatinous cap
called the cupula.
Bending of the hairs increases the
frequency of action potentials in
sensory neurons in direct
proportion to the amount of
rotational acceleration.
Structure of the vertebrate eye
Sclera
Choroid
Retina
Ciliary body
Fovea (center
of visual field)
Suspensory
ligament
Cornea
Iris
Optic
nerve
Pupil
Aqueous
humor
Lens
Vitreous humor
Central artery and
vein of the retina
Optic disk
(blind spot)
Focusing in the mammalian eye
Ciliary muscles contract, pulling
border of choroid toward lens
Choroid
Suspensory ligaments relax
Front view of lens
and ciliary muscle
Lens (rounder)
Retina
Ciliary
muscle
Lens becomes thicker and rounder,
focusing on near objects
Suspensory
ligaments
(a) Near vision (accommodation)
Ciliary muscles relax, and border of
choroid moves away from lens
Suspensory ligaments pull
against lens
Lens becomes flatter, focusing on
distant objects
(b) Distance vision
Lens (flatter)
Cellular organization of the vertebrate retina
Retina
Optic nerve
To
brain
Retina
Photoreceptors
Neurons
Cone Rod
Amacrine
cell
Optic
nerve
fibers
Ganglion
cell
Horizontal
cell
Bipolar
cell
Pigmented
epithelium
Rod structure and light absorption
Rod
Outer
segment
H
H
C
H2C
H2C
Disks
C
CH3
CH3
C
H
C
C
C
H3C
C
H
C
C
CH3 H
H
C
C
C
C
H
O
H
CH3 H
cis isomer
Inside
of disk
Cell body
Enzymes
Light
Synaptic
terminal
H
H
C
H2C
H2C
Cytosol
Rhodopsin
Retinal
Opsin
(a) Rods contain the visual pigment rhodopsin, which is embedded
in a stack of membranous disks in the rod’s outer segment.
Rhodopsin consists of the light-absorbing molecule retinal
bonded to opsin, a protein. Opsin has seven  helices that span
the disk membrane.
CH3
CH3
C
H
C
C
C
C
CH3 H
H
H
H
C
C
C
C
C
C
CH3
CH3
CH3
C
O
H
trans isomer
(b) Retinal exists as two isomers. Absorption of light
converts the cis isomer to the trans isomer, which
causes opsin to change its conformation (shape).
After a few minutes, retinal detaches from opsin.
In the dark, enzymes convert retinal back to its cis
form, which recombines with opsin to form rhodopsin.
Neural pathways for vision
Left
visual
field
Left
eye
Optic nerve
Optic chiasm
Lateral
geniculate
nucleus
Primary
visual cortex
Right
visual
field
Right
eye
Smell in humans
Brain
Action potentials
Odorant
Olfactory bulb
Nasal cavity
Bone
Epithelial cell
Odorant
receptors
Chemoreceptor
Plasma
membrane
Odorant
Cilia
Mucus
0.1 mm
Chemoreceptors in an insect
Sensory transduction by a sweetness receptor
Taste pore
Sugar molecule
Taste bud
Sensory
receptor
cells
Sensory
neuron
Tongue
1 A sugar molecule binds
to a receptor protein on
the sensory receptor cell.
Sugar
G protein
Sugar
receptor
Adenylyl cyclase
2 Binding initiates a signal transduction pathway
involving cyclic AMP and protein kinase A.
ATP
cAMP
Protein
kinase A
SENSORY
RECEPTOR
CELL
3 Activated protein kinase A closes K+ channels in
the membrane.
K+
4 The decrease in the membrane’s permeability to
K+ depolarizes the membrane.
Synaptic
vesicle
—Ca2+
5 Depolarization opens voltage-gated calcium ion (Ca2+)
channels, and Ca2+ diffuses into the receptor cell.
Neurotransmitter
6 The increased Ca2+ concentration causes
synaptic vesicles to release neurotransmitter.
Sensory neuron
Specialized electromagnetic receptors
Eye
Infrared
receptor
(a) This rattlesnake and other pit vipers have a pair of infrared receptors,
one between each eye and nostril. The organs are sensitive enough
to detect the infrared radiation emitted by a warm mouse a meter away.
The snake moves its head from side to side until the radiation is detected
equally by the two receptors, indicating that the mouse is straight ahead.
(b) Some migrating animals, such as these beluga whales, apparently
sense Earth’s magnetic field and use the information, along with
other cues, for orientation.
The lateral line system in a fish
Lateral
line
Lateral line canal
Scale
Epidermis Neuromast
Segmental muscles of body wall
Opening of lateral
line canal
Lateral nerve
Cupula
Sensory
hairs
Supporting
cell
Nerve fiber
Hair cell
So don’t be a stiff!
Ask Questions!!
Make sure you can do the following:
1. Label all parts of a striated motor unit and explain how
those structure contribute to the function of the
motor unit.
2. Explain the sliding filament model of muscle
contraction
3. Compare and contrast the major sensory apparatus
used by mammals and other animals
4. Explain the causes of sensory and motor system
disruptions and how disruptions of the sensory and
motor systems can lead to disruptions of homeostasis.