Muscles, Locomotion& Sensation

(Ch. 50)

Overview of information processing by nervous systems

Sensor

Effector

Motor output

Integration

Sensory input

Peripheral nervoussystem (PNS)

Central nervoussystem (CNS)

Animal Locomotion

What are the advantages of locomotion?

motilesessile

Lots of ways to get around…

Lots of ways to get around…

mollusk mammalbird reptile

Lots of ways to get around…

bird arthropodmammal bird

Muscle

voluntary, striated

involuntary, striated

auto-rhythmic

involuntary, non-striatedevolved first

multi-nucleated

digestive systemarteries, veins

heartmoves bone

• 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 MUSCLESmooth 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 MUSCLESmall 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 MUSCLEFusion of many cells so multi-nucleated. Attached by tendon to bone. Long thin cells called muscle fibers.

tendon

skeletal muscle

muscle fiber (cell)

myofilamentsmyofibrils

plasma membrane

nuclei

Organization of Skeletal muscle

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?

3

4

12

1

1

1

Cleaving ATP ADP allows myosin head to bind to actin filament

thin filament(actin)

thick filament(myosin)

ATP

myosin head

formcrossbridg

e

binding site

So that’s where those

10,000,000 ATPs go!Well, not all of it!

ADP

release

crossbridge shorten

sarcomere

1

Closer look at muscle cell

multi-nucleated

Mitochondrion

Sarcoplasmicreticulum

Transverse tubules(T-tubules)

Muscle cell organelles

• Sarcoplasm – muscle cell cytoplasm– contains many mitochondria

• Sarcoplasmic reticulum (SR)– 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

Ca2+ ATPase of SR

ATP

There’sthe restof theATPs!

But whatdoes theCa2+ 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 signal travels down T-tubule

– stimulates sarcoplasmic reticulum (SR) of muscle cell to release stored Ca2+

– flooding muscle fibers with Ca2+

Nerve trigger of 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

Ca2+ triggers muscle action

How Ca2+ controls muscle• Sliding filament model

– exposed actin binds to myosin

– fibers slide past each other• ratchet system

– shorten muscle cell• muscle contraction

– muscle doesn’t relax until Ca2+ is pumped back into SR • requires ATP

ATP

ATP

Put it all together…1

ATP

2

3

4

5

7

6

ATP

How it all works…• Action potential causes Ca2+ release from SR

– Ca2+ binds to troponin• Troponin moves tropomyosin uncovering myosin binding

site on actin• 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

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

Sensor

Effector

Motor output

Integration

Sensory input

Peripheral nervoussystem (PNS)

Central nervoussystem (CNS)

A bat using sonar to locate its prey

Sensory reception: two mechanisms

(a) Crayfish stretch receptors have dendrites embedded in abdominal muscles. When the

abdomen bends, muscles and dendrites

stretch, producing a receptor potential in the stretch receptor. The receptor potential triggers

action potentials in the axon of the stretch

receptor. A stronger stretch produces a larger receptor potential and higher frequency of

action potentials.

(b) Vertebrate hair cells have specialized cilia or microvilli (“hairs”) that bend when sur-

rounding fluid moves. Each hair cell releases an excitatory neurotransmitter at a synapse

with a sensory neuron, which conducts action potentials to the CNS. Bending in one direction depolarizes the hair cell, causing it to release

more neurotransmitter and increasing frequency

of action potentials in the sensory neuron. Bending in the other direction has the opposite

effects. Thus, hair cells respond to the direction of motion as well as to its strength and speed.

Muscle

Dendrites

Stretchreceptor

Axon

Mem

bran

epo

tent

ial (

mV

)

–50

–70

0

–70

0 1 2 3 4 5 6 7Time (sec)

Action potentials

Receptor potential

Weakmuscle stretch

–50

–70

0

–70

0 1 2 3 4 5 6 7Time (sec)

Strongmuscle stretch

–50

–70

0

–70

0 1 2 3 4 5 6 7Time (sec)

Action potentials

No fluidmovement

–50

–70

0

–700 1 2 3 4 5 6 7

Time (sec)

Receptor potential

Fluid moving inone direction

–50

–70

0

–70

0 1 2 3 4 5 6 7Time (sec)

Fluid moving in other direction

Mem

bran

epo

tent

ial (

mV

)

Mem

bran

epo

tent

ial (

mV

)

Mem

bran

epo

tent

ial (

mV

)

“Hairs” ofhair cell

Neuro-trans-

mitter at synapse

Axon

Lessneuro-trans-mitter

Moreneuro-trans-mitter

Sensory receptors in human skinHeat

Light touch PainCold

Hair

Nerve Connective tissue Hair movement Strong pressure

Dermis

Epidermis

The Structure of the Human Ear

Pinna

Auditory canal

Eustachian tube

Tympanicmembrane

Stapes

Incus

Malleus

Skullbones

Semicircularcanals

Auditory nerve,to brain

Cochlea

Tympanicmembrane

Ovalwindow

Eustachian tube

Roundwindow

Vestibular canal

Tympanic canal

Auditory nerve

BoneCochlear duct

Hair cells Tectorialmembrane

Basilarmembrane

To auditorynerve

Axons of sensory neurons

1 Overview of ear structure 2 The middle ear and inner ear

4 The organ of Corti 3 The cochleaOrgan of Corti

Outer earMiddle

ear Inner ear

Transduction in the cochlea

Cochlea

Stapes

Oval window

Apex

Axons ofsensoryneurons

Roundwindow Basilar

membrane

Tympaniccanal

Base

Vestibularcanal Perilymph

Cochlea(uncoiled)

Basilarmembrane

Apex(wide and flexible)

Base(narrow and stiff)

500 Hz(low pitch)1 kHz

2 kHz

4 kHz

8 kHz

16 kHz(high pitch)

Frequency producing maximum vibration

How the cochlea distinguishes pitch

Organs of equilibrium in the inner earThe semicircular canals, arranged in three spatial planes, detect angular movements

of the head.

Body movement

Nervefibers

Each canal has at its base a swelling called an ampulla,

containing a cluster of hair cells.

When the head changes its rateof rotation, inertia prevents

endolymph in the semicircular canals from moving with the head, so the endolymph presses against

the cupula, bending the hairs.

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.

Vestibule

Utricle

Saccule

Vestibular nerve

Flowof endolymph

Flowof endolymph

CupulaHairs

Haircell

Structure of the vertebrate eyeCiliary body

Iris

Suspensoryligament

Cornea

Pupil

Aqueoushumor

Lens

Vitreous humor

Optic disk(blind spot)

Central artery andvein of the retina

Opticnerve

Fovea (centerof visual field)

Retina

ChoroidSclera

Focusing in the mammalian eye

Lens (flatter)

Lens (rounder)

Ciliarymuscle

Suspensoryligaments

Choroid

Retina

Front view of lensand ciliary muscleCiliary muscles contract, pulling

border of choroid toward lens

Suspensory ligaments relax

Lens becomes thicker and rounder, focusing on near objects

(a) Near vision (accommodation)

(b) Distance vision

Ciliary muscles relax, and border of choroid moves away from lens

Suspensory ligaments pull against lens

Lens becomes flatter, focusing on distant objects

Cellular organization of the vertebrate retina

Opticnervefibers

Ganglioncell

Bipolarcell

Horizontalcell

Amacrinecell

Pigmentedepithelium

NeuronsCone Rod

Photoreceptors

Retina

RetinaOptic nerve

Tobrain

Rod structure and light absorptionRod

Outersegment

Cell body

Synapticterminal

Disks

Insideof disk

(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.

(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.

Retinal

OpsinRhodopsin

Cytosol

HC

CH2C

CH2C C

HCH3

CH3

HC

C

CH3 H CH3

CC

CC

CC

C

H

H

H

H

OH

H3C

HC

CH2C

CH2C C

HCH3

CH3

HC

C

CH3 H CH3

CC

CC

HH

CH3

H

CC

CH

O

CH3

trans isomer

cis isomer

EnzymesLight

Neural pathways for visionLeft

visualfield

Rightvisualfield

Lefteye

Righteye

Optic nerve

Optic chiasm

Lateralgeniculate

nucleus

Primaryvisual cortex

Smell in humansBrain

Nasal cavity

Odorant

Odorantreceptors

Plasmamembrane

Odorant

Cilia

Chemoreceptor

Epithelial cell

Bone

Olfactory bulb

Action potentials

Mucus

Chemoreceptors in an insect

0.1

mm

Sensory transduction by a sweetness receptorTaste pore Sugar molecule

Sensoryreceptor

cells

Sensoryneuron

Taste bud

Tongue

G protein Adenylyl cyclase

4 The decrease in the membrane’s permeability to K+ depolarizes the membrane.

5 Depolarization opens voltage-gated calcium ion (Ca2+) channels, and Ca2+ diffuses into the receptor cell.

6 The increased Ca2+ concentration causes synaptic vesicles to release neurotransmitter.

3 Activated protein kinase A closes K+ channels in the membrane.

2 Binding initiates a signal transduction pathway involving cyclic AMP and protein kinase A.

—Ca2+

ATP

cAMP

Proteinkinase A

Sugar

Sugarreceptor

SENSORYRECEPTOR

CELL Synapticvesicle

K+

Neurotransmitter

Sensory neuron

1 A sugar molecule binds to a receptor protein on

the sensory receptor cell.

Specialized electromagnetic receptors

(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, apparentlysense Earth’s magnetic field and use the information, along with

other cues, for orientation.

Eye

Infraredreceptor

The lateral line system in a fish

Nerve fiber

Supportingcell

Cupula

Sensoryhairs

Hair cell

Segmental muscles of body wall Lateral nerve

Scale EpidermisLateral line canal

Neuromast

Opening of lateralline canal

Lateralline

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.