Module 1 Lecture 1: Membrane Structure and Function 1

Fluid mosaics

Phospholipids amphipathic hydrophilic head + hydrophobic tail

Membrane = phospholipid bilayer

Fluid mosaic model proteins embedded in fluid membrane

Membrane proteins embedded in bilayer

o

Hydrophobic protein regions = inside membrane

Hydrophilic protein regions = outside membrane

Membrane fluidity

Lateral movement two lipids on same side swap position

Flip-flop two lipids on opposite sides swap position

Double bond kinks unsaturated tails prevent closely packed arrangement

increased fluidity
o

Membrane remains fluid to lower temperature if it is rich in unsaturated tails

Saturated tails closely packed arrangement decreased fluidity

Cholesterol
o

Temperature buffer prevents fluidity changes due to temperature changes

Different effects on membrane fluidity at different temperatures

Body temperature decreased phospholipid movement decreased

fluidity

Low temperatures hinders close packing decreased temp

required for solidification

How do we know it is a fluid mosaic?

Experiment
o Labelled proteins of mouse and human cells fusion of cells mixed
proteins

Six major functions of membrane proteins

Transport
Enzymatic activity

Signal transduction

Cell-to-cell recognition

Intercellular joining

Attachment to cytoskeleton and extracellular matrix

Selective permeability

Membrane structure lipid bilayer selective permeability

Permeable to water, oxygen, carbon dioxide

Impermeable to charged ions, glucose, macromolecules (proteins, RNA) essential

Module 1 Lecture 2: Membrane Structure and Function 2

Passive transport

Diffusion/osmosis
Does not require ATP

Concentration equilibrium elimination of gradients

Down concentration gradient (high conc low conc)

Osmosis

Diffusion of water to region with higher solute concentration equal concentrations

Tonicity ability of a solution to cause a cell to gain or lose water

Isotonic solution equal concentrations no net movement of water

Hypertonic solution solute concentration greater outside cell cell loses water

Hypotonic solution solute concentration greater inside cell cell gains water

Transport proteins

Allow movement of hydrophilic substances across membrane (not lipid soluble)

Channel proteins = tunnels

Carrier proteins bind to molecule conformational change shuttle across

membrane

Transport proteins are specific

Facilitated diffusion

Passive transport aided by transport proteins faster diffusion

Channel proteins
o

Aquaporins channel proteins that regulate flow of water

Ion/gated channels open/close in response to stimulus

Active transport

Uses ATP
Against concentration gradient

Electrogenic pumps transport proteins that generate voltage across membrane

o

Na+/K+ ATPase (sodium potassium pump) animals

Proton pump plants/fungi/bacteria

Cotransport

Active transport of one solute indirectly drives transport of another solute

Bulk transport

Exocytosis
o Neurotransmitter release

Endocytosis
o

Phagocytosis cell engulfs particles

Pinocytosis cell drinks fluids containing molecules

Receptor-mediated inward budding of vesicles Clathrin-coated vesicles

Module 1 Lecture 3: Cell Communication

Local vs. long distance signalling

Autocrine signalling cell releases a chemical that affects itself (local)

Paracrine signalling cell secretes something that affects nearby cells (local)

Synaptic signalling neuron releases neurotransmitter into synapse which effects

nearby target cell (local)

Hormonal signalling hormone secreted into blood stream, can reach cells anywhere
in body (long distance)

3 stages of cell signalling

Reception Transduction Response

Reception
o

Signalling molecule binds to receptor on cell surface or inside cell

Hydrophilic signalling molecules

Water soluble

Move freely through blood

Surface receptors

Hydrophobic signalling molecules

Lipid soluble

Require transport proteins

Agonist drug that mimics effect of natural receptor

Ligand chemical that binds to receptor, first messenger

Transduction
o

Signal transduction pathway cellular response

Activated receptor molecule A molecule B molecule C

response

Receptor types

Plasma membrane receptors surface

o Ion channel receptors

G protein-coupled receptors

Biggest family, 7 transmembrane domains

Tyrosine kinase linked receptors

Fastest (<1s), signalling molecule binds to receptor and opens an ion

channel allowing ion to move rapidly down concentration gradient,
neurotransmission

Metabolism, cell growth, cell reproduction insulin

Intracellular receptors steroid receptors

G protein-coupled receptors

G proteins proteins that bind GTP

Heterotrimeric 3 different peptide chains

7 transmembrane domains

Sequence of events

1. Signalling molecule binds to receptor

2. Receptor conformational change
3. G protein binds to receptor and is activated
4. Activated G protein detaches and binds to enzyme
5. Activated enzyme catalyses conversion of ATP to cAMP
6. cAMP (second messenger) activates another enzyme
7. Activated enzyme causes cellular response

Responses

Response depends on target cell

Adrenaline

Airway cells relaxation of smooth muscle opening of airways

asthma treatment

Heart cells increase in heart rate

cAMP second messenger produced by activated adenylyl cyclase

Orphan GPCR with unknown signalling molecule

Amplification of signalling

Enzymes active long enough to process number molecules of substrate before they
become inactive again
Few enzymes many enzyme products

Tyrosine kinase linked receptors

Insulin binds to surface receptor phosphorylation cascade

Kinase enzyme that activates a protein through phosphate transfer (phosphorylation)

Phosphorylation cascade series of different molecules in pathway are

phosphorylated chain reaction

Phosphorylation protein conformational change

Steroid receptors

Intracellular
Nucleus genes regulation protein production control

Module 2 Lecture 1: Neural Transmission Cells and Ions

Cone snails

Cone snails produce toxins that attack nervous system of prey (immobilise)
Neuropathic pain treatment drug based on cone snail toxins

Organisation of mollusc nervous systems

All animals except sponges have a nervous system

Mollusc nervous system organisation depends on lifestyle (squid more complex
lifestyle than chiton therefore squid has more complex nervous system)

Giant axon of squid physiology model, action potentials (Hodgkin and Huxley)

Organisation of vertebrate nervous systems

Vertebrates all have CNS + PNS with regional specialisation

Information processing

3 stages of information processing

o sensory input (eye, ear etc)
o

integration (CNS)

motor output (PNS)

Reflex arc

Neural pathway that controls action reflex

Sensory neuron interneuron (spinal cord) motor neuron

Neuron structure

Dendrites receive signals

Cell body nucleus

Axon hillock initiation of signals

Axon signal transduction

Synapse communication between two neurons

Types of neurons

Sensory neurons, interneurons, motor neurons

o Sensory neurons dendrites joined to half of axon, then cell body, then rest of
axon

Interneurons vary a lot (simple/common), lots of dendrites

Motor neurons many dendrites attached to cell body, with long axon

Radial nerve

Nerve that stimulates arm (baseball)

Glia

Support cells structural integrity/normal function

10-50x more glia than neurons in mammalian brain

2 types of glia astrocytes + oligodendrocytes/Schwann cells

o

Astrocytes

CNS

Structural support

Regulation of extracellular concentrations of ions and

neurotransmitters

Blood brain barrier formation

Blood brain barrier

Selectively determines which substances can move from blood to brain extracellular
fluid
o Lipid soluble compounds, H2O, O2, CO2, glucose, alcohol, nicotine,
anaesthetics YES
o

Proteins, lipids, toxins, antibiotics NO

Oligodendrocytes and Schwann cells

Form myelin sheaths around axons

o Myelin sheaths = insulators faster action potential transmission

Resting membrane potential

Negative (-70 mV)

o Ion gradients (imbalances between intracellular and extracellular fluids)

Intracellular net negative charge, extracellular net positive

charge

Outside concentrations 5 mM K+, 150 mM Na+

Gradients due to Na+/K+ ATPase

Pumps Na+ out and K+ in (3 Na+ for every 2 K+)

Goes against gradients uses ATP active transport

Resting membrane more permeable to K+ than Na+

Inside concentrations 140 mM K+, 15 mM Na+

K+ moves outward faster than Na+ moves inward

Nothing to do with voltage gated ion channels

Module 2 Lecture 2: Neural Excitability

Membrane potential

Membrane potential voltage of inside of membrane relative to outside

Depolarisation inside of membrane becomes more positive
o

Opening of voltage-gated Na+ channels Na+ in

Hyperpolarisation inside of membrane becomes more negative

o

Opening of voltage-gated K+ channels K+ out

Graded potentials

Slight increase or decrease in potential

Magnitude dependent on stimulus strength

Local and die out

Action potentials

Nerve impulses that carry information from one point of the body to another
Threshold stimulus threshold potential reached (-55 mV) action potential

Size of action potential unrelated to stimulus strength

o

If stimulus is strong enough to raises membrane potential to -55 mV then an

AP will be produced

All or nothing response threshold stimulus causes maximum response

Sequence of events

1. Resting state voltage gated ion channels closed, membrane potential -70 mV
2. Stimulus few Na+ channels open and Na+ rushes in
3. Depolarisation if threshold (-55 mV) is reached lots of Na+ channels open
and lots of Na+ rushes in
4. Repolarisation K+ channels open and K+ rushes out, Na+ channels
inactivated
5. Undershoot small hyperpolarisation + Na+/K+ ATPase restores resting
potential
Refractory period

Absolute refractory period

o Na+ channels inactivated AP cannot be generated

Relative refractory period (undershoot)

o

Hyperpolarised membrane (< -75) stronger than usual stimulus AP can

be generated

Mechanism of action of local anaesthetics

Prevent action potentials by blocking voltage-gated ion channels

Conduction speed

Influenced by axon diameter, temperature and degree of myelination

o Axon diameter

Increased diameter decreased resistance increased speed

Squid giant axon 100m/s

Temperature

Increased temperatureincreased speed

Degree of myelination

Factor that influences conduction speed the most (> axon diameter)

Increased myelination increased insulation increased speed

Saltatory conduction (myelinated axon)

AP jumps between nodes of Ranvier

Faster than smooth conduction (unmyelinated axons)

Synapses

Junctions through which impulses pass from one neuron (presynaptic) to another
(postsynaptic)

Module 2 Lecture 3: Synaptic transmission

Electrical synapses

Direct electrical currents between cells

Few synapses are electrical

Chemical synapses

Involve neurotransmitter release by presynaptic neuron

Majority of synapses are chemical

Neurotransmitter release

Exocytosis
o Action potential Ca2+ ion influx fusion of vesicles with membrane
neurotransmitter release

Types of chemical synaptic transmission

Direct transmission
Indirect transmission

Direct synaptic transmission

Neurotransmitter opens postsynaptic membrane ligand-gated ion channels graded

postsynaptic potential
o Excitatory postsynaptic potential depolarisation

Inhibitory postsynaptic potential hyperpolarisation

Increase membrane permeability to Na+ ions (inward)

Increase membrane permeability to K+ ions (outward)

Summation of postsynaptic potentials

o

Temporal summation (single presynaptic neuron)

Multiple consecutive EPSPs from same presynaptic neuron single

postsynaptic neuron

Spatial summation (multiple presynaptic neurons)

Multiple EPSPs from different presynaptic neurons single

postsynaptic neuron

Postsynaptic potential vs. action potential

Post synaptic potential

o Excitatory or inhibitory
o

Graded

At cell body or dendrites

Action potential
o

Depolarisation

All or nothing

EPSP summation can cause action potential

Generated at axon hillock and travels along axon

Indirect synaptic transmission

Neurotransmitter binds to postsynaptic membrane GPCR signal transduction

pathway (2nd messenger)

Amine neurotransmitters

Acetylcholine
Dopamine

Norepinephrine

Serotonin

Removal of neurotransmitters from synaptic cleft

Recycled by selective uptake by transporters (norepinephrine)

Taken up by astrocytes (glutamate)

Broken down by enzymes (acetylcholinerase breaks down acetylcholine)

Diffusion (dopamine)

Module 2 Lecture 4: Neuronal Organisation

Central nervous system

Brain + spinal cord

Peripheral nervous system

Cranial nerves + spinal nerves

Somatic nervous system

Voluntary control of movements

Autonomic nervous system

Sympathetic + parasympathetic
Involuntary functions homeostasis

Sympathetic division

Fight or flight
o Bronchi dilation
o

Increased heart rate

Glycogen breakdown

Adrenaline secretion

Digestion inhibition

Nerves that arise from thoracic and lumbar regions of spinal cord

Parasympathetic division

Rest and digest

o Calming
o

Opposite responses to sympathetic

Nerves that arise from sacral and cervical regions of spinal cord (two ends)

Spinal cord

White matter outside

Grey matter inside

Cerebrospinal fluid

Clear fluid
Subarachnoid space, ventricles and central canal

Cushions the brain and spinal cord

Supply of nutrients and hormones

Waste removal

Hydrocephalus
o

Blocked flow enlarged head

Brainstem

Medulla oblongata + pons + midbrain

Homeostasis
o

Information transfer
o

All info relayed between cerebrum/cerebellum and rest of body passes through
brainstem

Complex movements
o

Heart rate, breathing rate, blood pressure

Running, climbing

Reticular formation
o

Arousal and sleep

Filters out unimportant sensory information

Cerebellum

Motor function complex movements

Coordination

Motor learning

Diencephalon

Thalamus + hypothalamus + epithalamus

Thalamus
o

Input via sensory neurons

Output via motor neurons

Hypothalamus
o

Homeostasis hormones

Biological clock

Temperature regulation

Hunger, thirst

Epithalamus
o

Connects limbic system to rest of brain

Pineal gland melatonin (sleep hormone)

Cerebrum

Right and left hemispheres

o Basal nuclei movement
o

Corpus callosum permits communication between hemispheres

Cerebral cortex (neocortex)

80% of brain mass

4 lobes frontal, parietal, temporal, occipital

Language and speech

Stroke destroys ability to speak

Brocas aphasia can understand speech but cant speak

Wernickes aphasia can speak but cant understand speech

Emotions

Limbic system

Amygdala fear

Hippocampus memory

Memory

Hippocampus
o Short term memory
o

STMLTM

Cerebral cortex
o

Long term memory

Long-term potentiation

Lasting increase in synaptic transmission strength

Caused by high frequency transmission

Involves glutamate

Fundamental process for storing memories and thus learning

Module 3 Lecture 1: Skeletal muscle

Skeletal muscular system 40-50% body mass, hypertrophied muscle = extraordinary bulk

Skeletal muscular system made up of organs, tissues, cells, molecules/chemicals

Organs muscle tendon units, heart, viscera (guts)

Tissues skeletal muscle tissue (voluntarily controlled), cardiac muscle tissue (striatic
muscle that occurs within the heart, does not tire), smooth muscle tissue (viscera)

Cells myocytes (muscle cells)

Molecules/chemicals actin, myosin, Ca2+

Function of muscular system

Convert chemical energy into mechanical work that enables:

Movement (bones, blood, food)

Support (bony and soft tissue)

Protection (skeletal and smooth muscle guard orifices)

Body temperature regulation (shivering generates heat)

Nutrient storage (glycogen used in muscle function, can use muscle tissue for
energy in times of starvation)

Characteristics of muscle tissue excitability and conductivity, contractility, extensibility,

elasticity

Excitability and conductivity - muscle tissue conductive, produce action potentials in

response to stimuli
Contractility muscle tissue able to shorten and thicken

Extensibility muscle tissue can be stretched without damage, skeletal muscles work
in pairs (one contracts, other relaxes)

Elasticity tendons (not muscles) good at temporarily storing energy as strain energy
that can be used for locomotion

Articulations (joints)

Ball and socket joints shoulder/hip, allow for free rotation

Hinge joints movement restricted to single plane

Pivot joints rotate forearm at elbow and move head side to side

Movement of synovial joints

Flexion decrease in joint angle, sagittal plane (bicep curl)

Extension increase in joint angle, sagittal plane (leg extension)

Adduction move limb towards midline, coronal plane

Abduction move limb away from midline, coronal plane

Anatomical planes

Coronal left to right, divides posterior and anterior

Sagittal back to front, divides left and right

Transverse midsection, divides upper and lower

Skeletal muscle structure

Muscle origin point where muscle attaches to bone

Muscle belly middle muscle section

Muscle insertion origin opposite, away from body (distal)

Connective tissue layers

Endomysium muscle fibre outer layer, microscopic

Perimysium encircles group of fibres, forming fasciculus

Fasciculus bundle of fibres

Epimysium encircles all fasciculi to form muscle, macroscopic

Skeletal muscle fibre components

Actin/myosin myofilaments myofibrils muscle fibre

Myofilaments

Thin myofilaments (actin)

o Actin, tropomyosin, troponin
o

Actin helix backbone

Tropomyosin spirals around helix and covers myosin binding sites

Troponin binds to tropomyosin to helix

Thick myofilaments (myosin)

o

Myosin = rod with two heads (double ended golf club)

Each head has actin binding site + myosin ATPase binding site

Myosin proteins bind together with heads projecting outwards

Sarcomere structure

Spatial organisation of contractile proteins cross banding

A band dark zone, myosin/actin overlap
o

M line binding of myosin

H zone myosin, no actin

I band light zone, thin filaments only

o

Z line adjacent thin filaments join

Myofibril structure

Sarcomeres distance between two Z lines

Sarcolemma muscle fibre membrane

Sarcoplasm muscle fibre cytoplasm

Sarcoplasmic reticulum network of membranous channels

Terminal cisternae chambers that sarcoplasmic reticulum tubes empty into, store
Ca2+ ions

Transverse T tubules internal extensions of sarcolemma that penetrate deep into

muscle fibre and allow action potential to be delivered from surface to centre

Muscle triad t tubule with terminal cisternae on both sides

Motor units

Motor unit motor neuron plus all muscle fibres it innervates

o More motor units with fewer fibre innervations per unit = greater
force/position control
o

Extrinsic eye muscles 6 fibres per MU (fine, highly coordinated movements)

Quadriceps 2000 fibres per MU (strength movements)

Neuromuscular junction

Space between motor neuron terminal and muscle fibre sarcolemma

Subneural clefts in sarcolemma increase surface area (increased SA = more receptors
= more acetylcholine neurotransmitters = more AP)

Sequence of events

1. AP travels to motor neuron terminal causing Ca2+ ion influx

2. Ca2+ ions cause synaptic vesicles to release acetylcholine into synaptic gap
3. AP radiates from receptors over sarcolemma and into muscle fibre via T tubules

Excitation-contraction coupling sliding filament theory of contraction

Sequence of events

1. Stimulation across neuromuscular junction initiates AP on muscle fibre sarcolemma,

AP spreads along sarcolemma and is transmitted into muscle fibre via T tubules
2. AP causes terminal cisternae to release Ca2+ ions
3. Ca2+ ions bind to and change structure of troponin on thin myofilaments, causes
tropomyosin to move aside and expose myosin binding sites
4. Myosin binds to thin myofilaments (cross bridge), cocked myosin head undergoes
conformational change that pulls thin myofilaments over thick myofilaments (power
stroke)

5. After power stoke ATP binds to head and causes detachment of cross bridge, ATPase
within head cleaves ATP to ADP + energy and uses energy to recock head, recocked
head can bind to another exposed binding site and produce another power stroke
6. Repeated power strokes pull in thin filaments and cause muscle contraction

Energy released by hydrolysis of ATP required to convert myosin head from low to
high energy configuration (uncocked cocked)

Actin and myosin filaments arranged within sarcomeres oriented in one direction,
sliding draws sarcomere ends towards centre which shortens muscle fibre to generate
movement

Cytosolic Ca2+ removed by active transport into sarcoplasmic reticulum after AP

ends, tropomyosin blockage of myosin-binding sites restored, contraction ends,
muscle fibre relaxes

Muscle relaxation

Caused by active transport of Ca2+ ions from cytosol back into transverse cisternae,
reverting thin myofilaments to regular shape (covering myosin binding sites) and
causing them to slide back into original position

Death (Rigor mortis)

Ca2+ ions leaks into cytosol and causes contraction, remaining ATP used to sustain
contraction,
After ATP spent myosin heads cannot unbind, leading to stiffening of the body

As contractile proteins degrade rigor mortis subsides

Electromyography (EMG)

Records electrical activity of muscles

o Surface electrodes (superficial muscles)
o

Fine-wire electrodes (deep or small muscles)

Rhabdomyolysis

Breakdown of massive amounts of muscle tissue, caused by crush injuries

Broken down tissue cleaned out by kidneys, results in renal failure

Muscle twitch and wave summation

Latent period time between stimulation and start of contraction

Muscle contraction strength dependent on size and number of muscle units recruited

All or none law when a motor unit is stimulated, all of its muscle fibres will contract
(more muscle fibres = more force = stronger contraction)

Muscle twitch rapid, unsustained contraction due to single AP

Summation additional shortening due to rapid succession of two or more AP

Tetanus overlapping twitches summing to one steady contraction, maximum tension

The ability to generate tension depends on muscle fibre length

highly extended muscle no overlap between myosin and actin therefore no

cross bridges and no tension produced

optimal resting length results in maximum tension

The ability to generate tension depends on passive tissue behaviour

o

Increased stretch = increased passive force (tension)

Module 3 Lecture 2: Skeletons

Types of skeletons

Hydroskeletons fluid filled chambers

Exoskeleton external skeleton

Endoskeleton internal skeleton (humans)

Hydroskeletons

Fluid held under pressure in closed body compartment (nematode)

Muscles control shape of compartment (worms have longitudal and circular muscles
that enable elongation and contraction)

Exoskeletons

Calcium carbonate shell or chitin cuticle

Arthropods enlarge or shed and replace exoskeleton

Chitin protein matrix

Endoskeletons

Skeletal elements conserved across species (humans, cats, whales, bats)

Axial and appendicular skeletons

Axial central axis (head, neck, chest)

Appendicular limbs (arms, legs)

80 (axial) + 126 (appendicular) = 206

Ossification/ontogenesis

Skeletons change throughout lifetime

Ossification centre point where ossification commences

Epiphesial growth plates responsible for lengthening of bones

o

Damage to growth plates can cause premature closure (bone stops lengthening
or curves) and growth disorders

Skeleton organisation

Organs bones, cartilages, ligaments, bone marrow

Tissues connective tissues

Cells osteocytes, osteoblasts, osteoclasts

Molecules/chemicals Ca2+

Vertebrate skeleton role/s

Mechanical roles support, protection, function

Metabolic roles calcium storage and blood cell formation (haematopoiesis)

Haematopoiesis major role of adult axial skeleton and child appendicular

skeleton (occurs in liver/spleen of embryo)

Types of bones

Long bones length > width, shaft with ends, leverage/movement (femur)
Short bones square, movement (kneecap)

Flat bones skull, protection/haematopoiesis (adults)

Irregular bones specific shapes (hip)

Long bone composition and structure

Compact bone hard, long bone shaft (hollow)

Trabecular bone spongy, long bone ends (honeycomb)
o

No secondary osteons (replacement bone)

Can be remodelled

Compact and trabecular same material but different arrangement

Bone matrix

Hydroxyapatite + collagen (reinforced concrete brittle concrete + steel bars)

Hydroxyapatite
o

65% bone tissue, 99% of bodys calcium

Bone brittleness

Hydroxyapatite deficiency causes deformities such as rickets

Collagen
o

33% bone tissue

Bone flexibility and toughness

Collagen deficiency causes brittleness and lack of flexibility

Maintained by osteoblasts, osteocytes and osteoclasts

o

Osteocytes maintain bone matrix

Communicate via canaliculi

Osteoblasts create bone matrix

Osteoclasts breakdown bone matrix

Skeleton turning over constantly but slowly

Why are bones hollow?

More resistant to bending

Cortical microstructure

Primary bone
o First bone that is formed (embryo)

Secondary bone
o

Secondary osteons/Haversion systems replacement bone

Cortical remodelling

Osteoclasts chew tunnel (resorption)

Osteoblasts refill with osteoid that mineralises

Osteoporosis

Net loss of bone (rate of formation < rate of destruction)

Architectural change that increases risk of bone fracture

Synovial joints

Free movement
Between most long bones

Structural differences
o

Joint capsules (lining)

Synovial cavities (fluid)

Module 3 Lectures 3+4: Locomotion

Locomotion in water

Types of aquatic locomotion

o Undulation (shark)
o

Flapping (manta ray)

Rowing (beetle)

Jet propulsion draw in and rapidly expel water (jellyfish, squid)

Buoyancy
o

Passive approach = gas bladders

Gas bladders allow fish to control buoyancy and depth

Active approach = dynamic lift

Pectoral fins create lift which allows fish to swim up and down

Constantly swimming

Friction
o

Bigger organism bigger Reynolds number more friction

Locomotion in air

Types of aerial locomotion

o Flapping flight

Continuous wing beat sequence

Upstroke + downstroke

Bounding flight

Muscles used at optimum power output, economical

Small birds only

Soaring

Most economical

Hovering

Highly energetic

Very small birds only (hummingbirds)

Continuous downward flow of air that supports body weight

Structural adaptations that contribute to low body mass

o

Light bones

No teeth/urinary bladder

Locomotion on land

Types of terrestrial locomotion

o Crawling

Two-anchor (inchworm)

Pedal wave (snail)

Peristalsis (earthworm)

Serpentine/side winding/concertina (sidewinder snake)

Amoeboid (pseudopodia formation and extension)

Walking

Cursorial posture straight limb

Non-cursorial posture bent limb

Body form, posture and size strongly influence energetic costs more
muscle activity needed to walk with bent limb

We use a nearly straight-legged posture when load-bearing during

walking because it reduces the muscle moments about the knee joint,
making walking energetically economical

Running

Plantigrade foot flat (humans)

Digitigrade on toes (dog, cat)

Unguligrade on fingertips (horse)

Less digits = reduced skeletal elements = lighter skeleton = high speed

more economical

Jumping

Bipedal hopping elastic strain energy temporarily stored in stretched

tendons makes it highly economical (kangaroo)

Locomotion in primates

Types of primate locomotion

o Brachiation swing from tree to tree using only arms (gibbon)
o

Quadrapedalism knuckle walking (gorilla)

Bipedalism (humans)

Chimpanzees can only temporarily be bipedal because not adapted for

upright posture and will fatigue various muscle groups

Evolution of human locomotion

Benefits of bipedalism
o Visual scanning of environment
o

Specialisation of upper limbs (toolmaking, cooking, carrying)

Walking speed

Maximum speed directly proportional to leg length

Vmax = gh

Six determinants of human walking

1. Forward pelvic rotation increases stride length and decreases energy consumption
2. Lateral pelvic tilt reduces movement of centre of gravity when standing on one leg
3. Knee flexion reduces movement of COG when standing on one leg and reduces
shock
4. Foot mechanism reduces movement of COG when standing on one leg and reduces
shock
5. Muscular control of ankle/foot ensures that foot delivers mechanical benefits and
reduces shock, foot meets ground in controlled manner instead of slapping it

6. Lateral body displacement maintains balance during single limb stance, too little =
unstable, too much = movement too costly
Module 4 Lecture 1: Circulation 1

Mechanisms for environmental exchange

Unicellular organisms exchange substances directly with environment through

diffusion
o Diffusion is inefficient because only rapid over short distances

Animals that exchange substances by diffusion (jellyfish)

body plan that doesnt require circulatory system

All cells close to external environment

Multicellular organisms require specialised systems for both exchange and transport
o

Diffusion distances are too great for adequate exchange

Open and closed circulatory systems

Circulatory system 3 components circulatory fluid, tubing, pump

Interstitial fluid
o

Main component of extracellular fluid

In open system circulatory fluid = interstitial fluid (hemolymph)

In closed system circulatory fluid is not the same as interstitial fluid and is
confined to vessels (blood)

Advantages of open system

o

Lower pressures requires less energy

Advantages of closed system

o

Increased pressure efficient delivery

Differential regulation of blood flow to organs

Different areas of body require different amounts of blood at certain

time (runningheart)

Circulation in vertebrates

Amphibians/reptiles have three chambered heart

o Underwater blood flow diverted from lungs

Mammals/birds have four chambered heart

o

Divided into two sides (left atrium/ventricle, right atrium/ventricle)

Four chambered heart key adaptation of endotherms

10x energy consumption of ectotherms require 10x more oxygen

Closed circulatory systems

Two types of closed circulatory system single or double loop

o Single loopBlood passes through heart once in each complete circuit
o

Double loop

Two circuits pulmonary and systemic

RVLCLALVSCRA

Increased blood flow to organs

Heart repressurizes blood as it moves from PC to SC

Mammal (human) circulatory system

Sequence of events

1. Deoxygenated blood pumped out of RV

2. Deoxygenated blood pumped from RV to LC via pulmonary arteries
3. Deoxygenated blood flows through LC (O2 in, CO2 out)
4. Oxygenated blood flows to LA via pulmonary veins
5. Oxygenated blood flows into LV
6. Oxygenated blood pumped out of LV via aorta
7. Oxygenated blood supplied to upper SC (head and forelimbs) via aorta branch
8. Oxygenated blood supplied to lower SC (abdominal organ and hind limbs) via aorta
branch
9. Deoxygenated blood flows to RA from upper SC via superior vena cava
10. Deoxygenated blood flows to RA from lower SC via inferior vena cava

11. Deoxygenated blood flows from RA to RV

Mammalian heart

Atria chambers that receive blood entering heart

Ventricles chambers that pump blood out of heart
o

Thicker walls than atria because they work harder

Left side of heart (LA/LV) has thicker walls than right side
o

LV pumps blood to extremities

RV pumps blood to lungs

Cardiac muscle
o

Involuntary, striated, electrically coupled, does not tire

Cardiac cycle

Complete sequence of contraction (systole) and relaxation (diastole)

Cardiac output
o

Volume of blood pumped per minute

CO = HR (bpm) x SV (litres)

Heart rate rate of contraction

Stroke volume blood vol pumped per contraction

Sequence of events

1. AD, VD blood flows into A+V through AV valves

2. AS, VD contraction pushes remaining blood from A to V
3. VS, AD ventricles pump blood into large arteries

Heart conduction

Cardiac myocytes
o Auto rhythmic contract without signal from NS

Cardiac cells are electrically coupled gap junctions

o

Allow electrical activity to move between cells

Sinoatrial (SA) node

Atrioventricular (AV) node

o

Pacemaker sets rate and timing of contraction

Impulses delayed here before moving to apex

Sequence of events

1. SA node generations signals that cause contraction and send to AV node

2. SA node signals delayed at AV node
3. Signals pass from AV node to apex
4. Signals spread throughout ventricles via Purkinje fibres
Physiological control of hearth rhythm

Sympathetic division (fight or flight)

Parasympathetic division (rest and digest)

Hormones (adrenaline)

Temperature

Module 4 Lecture 2: Circulation 2

Blood vessel structure and function

Structural differences functional differences

Endothelium
o

Innermost layer

Smooth surface minimise blood flow resistance

Contains heparan sulfate prevents clotting

Smooth muscle
o

Middle layer

Regulation of smooth muscle contractions and relaxation controlled blood

flow

Thicker in arteries than veins

Connective tissue
o

Outer layer

Capillaries
o

Smallest vessels

Very thin walls facilitate substance exchange

Arteries
o

Thicker walls blood pumped at high pressure by the heart

Greater elastic recoil keeps blood pressure constant when heart relaxes
between contractions

Blood pressure

Hydrostatic force that blood exerts against the wall of a vessel

Diastolic pressure pressure in the arteries during ventricular diastole (relaxation)

Systolic pressure pressure in the arteries during ventricular systole (contraction)

o

Systolic pressure always higher than diastolic pressure

Blood pressure decreases as distance from heart increases

o

Highest in aorta/arteries

Ventricular BP = 120/80

Decreases dramatically as blood passes through arterioles and capillaries

Narrow diameter resistance to flow decreased pressure

Lowest in vena cavae

Blood pressure arteries

Artery elasticity constant blood flow

o Arteries stretch to accommodate increased pressure when heart
contracts/empties
o

Arteries shrink to accommodate decreased pressure when heart relaxes/fills

Blood pressure veins

Veins function at lower pressures

Valves allow blood flow in one direction only

Skeletal muscle pump helps to move blood against gravity

o

Person standing motionless for long periods of time

Pooling of blood in distended veins increased pressure swollen

ankles/feet

Increased exercise increased skeletal muscle activity venous

return

Person stops exercising

No skeletal muscle pump activity rapid decrease in heart rate

Cooling down exercise gradual HR drop reduced stress on heart

Blood pressure arterioles

Nervous and hormonal stimuli vasoconstriction/vasodilatation regional

regulation of blood flow
Vasoconstriction
o

Smooth muscle contraction narrowed arterioles increased BP

Vasodilatation
o

Smooth muscle relaxation widened arterioles decreased BP

Measurement of blood pressure

Inflatable cuff inflated until pressure closes artery

Cuff deflated gradually until sounds generated (turbulent flow) systolic pressure

Cuff further deflated until sounds stop (laminar flow) diastolic pressure

Capillaries

Diffusion facilitated by thin walls and low blood flow velocity

Pores small, water-soluble substances can cross capillary wall

Capillary blood supply

Major organs capillaries filled

Meal increased digestive tract blood supply

Exercise increased muscle blood supply (oxygen)

Two mechanisms for control of blood flow to capillaries

o

Arteriole wall smooth muscle contraction + sphincters

Relaxed smooth muscle/sphincters blood can enter capillaries

Net movement of fluid across capillary wall

Determined by the balance of blood/osmotic pressures

When BP > OP net loss of fluid from capillaries, but when BP < OP net gain
of fluid

Osmotic pressure caused by blood proteins

Fluid drawn back into capillaries at venous end because OP > BP at

venous end

Protein malnutrition decreased OP decreased net gain at venous

end

Capillaries total cross-sectional area > arterioles TCSA lower BP in capillaries

(30mmHg)

Lymphatic system

85% of fluid leaving capillaries re-enters due to OP, remaining fluid returned to blood
via lymphatic system
Defence

Module 4 Lecture 3: Circulation 3

Blood composition

Blood = 55% plasma, 45% erythrocytes, 1% buffy coat

Buffy coat platelets + white blood cells

Haematocrit packed cell volume

Bicarbonate electrolyte that buffers blood pH changes

Albumin plasma protein that maintains osmotic balance

Fibrinogen plasma protein involved in clotting

Immunoglobulins plasma protein involved in defence (antibodies)

Concentration of ions in plasma affects blood composition

Erythrocytes
o

Biconcave larger surface area increased diffusion

Lack mitochondria and nuclei more space to pack in haemoglobin

increased oxygen transport

Inflammatory responses

Mast cells
o Store histamine in granules for secretion histamine secretion
vasodilatation phagocytes traverse capillary wall to get to where they are
needed
o

Vasodilatation increased blood flow redness and heat overflowing

capillaries blood leakage into neighbouring tissues swelling

Regeneration of blood cells

Blood cells all develop from multipotent stem cells in bone marrow
o Multipotent able to form multiple cell types

Lymphoid stem cells lymphocytes (T cells, B cells)

Myeloid stem cells erythrocytes, platelets

Erythrocytes lifespan of 3-4 months

Erythrocyte production

Erythropoietin (EPO) protein that stimulates erythrocyte production

Decrease in oxygen increase in erythropoesis

Kidneys detect reduced oxygen-carrying capacity erythropoietin secretion

stimulation of erythropoiesis in bone marrow more erythrocytes more oxygen

Patients with kidney failure often have anaemia as well

o

Anaemia = lack of erythrocytes damaged kidneys cant detect deficiency

and thus do not release erythropoietin to fix problem, resulting in permanently
low erythrocyte count

Blood doping

Increasing number of erythrocytes in blood increased oxygen capacity

enhanced athletic performance
Detect blood doping by analysing proportion of mature and immature erythrocytes in
circulation
Extremely high erythrocyte production increased blood viscosity heart failure
(Zyzz)

Blood clotting

Endothelium antithrombotic surface

Clotting process

1. Vessel endothelium damaged, connective tissue exposed, platelets become sticky

2. Temporary platelet plug
3. Temporary platelet plug reinforced by fibrin clot, allowing regeneration of underlying
tissue

Fibrin formation process

1. Clotting factors mix, forming activation cascade

2. Prothrombin converted to thrombin
3. Thrombin catalyses conversion of fibrinogen to fibrin

Cardiovascular disease

Hypertension chronic elevation of blood pressure (>140/90 mmHg)

o Increase in blood pressure structural changes to small vessels reduced
downstream perfusion
o

Can cause myocardial infarction, stroke, and renal failure

Myocardial infarction = heart attack

Atherosclerosis hardening of arteries by accumulation of fatty deposits

o

Narrowing reduced perfusion

Stable and unstable plaques

Unstable plaque rupture thrombosis/embolism

Module 4 Lecture 4: Gas Exchange 1

3 components of respiratory system

respiratory surface
respiratory medium

means of ventilation (movement of medium over surface)

Partial pressure

Pressure exerted by a particular gas in a mixture of gases

PP of oxygen = 160 mmHg

Gases diffuse from high partial pressures to low partial pressures

Respiratory media

Air better than water

Water = viscous aquatic animal gas exchange is energy intensive

Respiratory surfaces

Increased surface area increased diffusion

Decreased surface thickness increased diffusion

Large surface area, thin surface maximum diffusion (capillaries)

Some aquatic animals (sea star, zebrafish) have large, thin surface area no
specialised organ required

Respiratory organs: gills

Concurrent exchange exchange of a substance between two fluids flowing in

opposite directions
Partial pressure gradient from water to blood exists along entire length of capillary

Net diffusion of O2 from water to blood

Respiratory organs: tracheal systems in insects

Extensively branched tubes deliver air directly to body cells independent of

circulatory system
Adaptation for high metabolic demand during flight

Respiratory organs: lungs

Trachea windpipe, branches into two bronchi

Bronchi two tubes that connect trachea to two lungs, branch into bronchioles

Bronchioles fine tubes

o

Mucous layer that traps foreign particles

Cilia that move mucus up to pharynx where it can be swallowed into

oesophagus

Alveoli

Air sacs clustered at tips of terminal bronchioles

Pulmonary capillary beds surround alveoli O2 in and CO2 out

Lung surfactants
o

Reduce surface tension prevent collapse of alveoli

Premature babies surfactant deficiency alveoli collapse and respiratory problems

Ventilation

Positive pressure breathing

o Force air into lungs across pressure gradient (amphibians)

Negative pressure breathing

o

Diaphragm contraction increased lung volume decreased pressure air

enters lungs when lung pressure < atmospheric pressure (mammals)

Pneumothorax pleural cavity penetrated air enters and builds up prevents

normal lung expansion

Lung volumes

Tidal volume volume of air inhaled and exhaled during normal breathing
Inspiratory reserve volume additional air that can be forcibly inhaled after TV
inspiration (deep breath)

Expiratory reserve volume additional air that can be forcibly exhaled after TV
expiration

Residual volume volume of air remaining in lungs after ERV volume exhalation

Total lung capacity maximum amount of air that can fill lungs (TV+IRV+ERV+RV)

Vital capacity total amount of air that can be expired after fully inhaling
(TV+IRV+ERV)

Inspiratory capacity maximum amount of air that can be inspired (TV+IRV)

Functional residual capacity amount of air remaining after normal exhalation

(RV+ERV)

Measured using spirometer

Regulation of breathing

Medulla oblongata and pons = breathing control centres

Blood CO2 cerebrospinal fluid pH (detected by chemoreceptors in medulla/pons)

Exercise increased blood CO2 decreased CSF pH increased breathing

O2 detected in aorta/carotids in extreme conditions (trauma)

Module 4 Lecture 5: Gas Exchange 2

Coordination of gas exchange

Driving force = differences in partial pressure of gases, gas flows from high to low
Oxygen flows from alveolus to blood and then from blood to body tissue

Blood (pO2=40) alveolus (pO2=100) blood (pO2=100 body tissue (pO2=40)

blood (pO2=40)

Carbon dioxide flows from body tissue to blood and then from blood to alveolus

Blood (pCO2=40) body tissue (pCO2=46) blood (pCO2=46) alveolus

(pCO2=40) blood (CO2=40)

Respiratory pigments

Low solubility of oxygen limits ability of circulatory system to deliver it

Respiratory pigments (haemoglobin) increase amount of oxygen that can be carried
(5mL/L200mL/L)

Aid in transport and buffering of CO2

Haemoglobin

Haemoglobin molecule = 4 subunits = 4 heme groups = 4 iron atoms = 4 molecules of

oxygen
Iron = reversible oxygen binding site (oxygen can dissociate and move to body tissue)
Cooperativity binding of oxygen to one site increases affinity for oxygen of the
remaining sites

Haemoglobin dissociation

Affinity oxygen saturation of haemoglobin

Increased affinity shift of curve to left (increased pO2)

Decreased affinity shift of curve to right (increased temp, increased pCO2,

decreased pH)

Fetal haemoglobin greater oxygen affinity than maternal haemoglobin because it can
function at lower partial pressure (50% saturation when pO2 = 19 instead of when
pO2 = 26.8), therefore shift of curve to left

Carbon monoxide 200x greater affinity for haemoglobin than oxygen inhibition of
oxygen delivery

Carbon dioxide transport

Carbonic acid (H2CO3) bicarbonate (HCO3-) and H+ ions

Buffering of H+ ions by haemoglobin prevents shift to right of dissociation curve

Diving mammals

Two adaptations oxygen storage and oxygen conservation

o Storage

70% of oxygen stored in blood 2x human blood volume/kg body

mass

High myoglobin muscle concentration more oxygen stored in

muscles than humans

Conservation

Decreased muscular effort/heart rate/oxygen consumption/blood flow

to muscles

PNS rest and digest vasoconstriction decreased HR

SNS fight or flight decreased blood flow to muscles

Module 5 Lecture 1: Principles of Endocrine Systems 1

Hormonal signalling

Endocrine cells/glands secrete hormones into bloodstream that can reach all cells
Long distance

Types of chemical signalling

Endocrine signalling hormones bloodstream trigger responses in target cells

anywhere Synaptic signalling neurotransmitters diffuse across synapse trigger
response in cells of targeted tissue
Neuroendocrine signalling neurohormones blood stream trigger responses in
target cells anywhere

Paracrine signalling secreted regulators trigger response in neighbouring cells

Autocrine signalling secreted regulators trigger response in cell which secreted them

Regulation and homeostasis

Homeostasis used to maintain internal balance irrespective of external environmental

conditions

Endocrine function in animals

Hormones = long distance communication, messengers that tell target cells how to
behave
Endocrine cells in various organs and tissues secrete hormones into bloodstream

Specificity

Hormone will only bind to cells with specific receptor

o Hormones released straight into blood stream able to induce certain responses
from certain cells

Types of hormones

Polypeptide hormones
o Water soluble, bind to surface receptors
o

Insulin, vasopressin, ACTH, oxytocin

Steroid hormones
o

Lipid soluble, bind to intracellular receptors

Cortisol, aldosterone, testosterone

Amine hormones
o

Most water soluble (epinephrine)

Some lipid soluble (T3, T4)

Module 5 Lecture 2: Principles of Endocrine Systems 2

Hormone functions

One hormone multiple receptors multiple functions in different target cells

Epinephrine = adrenaline = stress hormone, different responses
o

Liver beta receptors glycogen breakdown and glucose release

Skeletal muscle beta receptors blood vessel dilation and increased blood
flow

Heart beta receptors increased cardiac output

Intestines alpha receptors blood vessel constriction and reduced blood

flow

Blood diverted to skeletal muscle

Neurohormones

Integration of nervous and endocrine systems

Nervous system signals initiate and regulate endocrine signals hypothalamus and
pituitary gland

Feedback

Feedback loop stimulus endocrine gland hormone target tissue response

Negative feedback response inhibits stimulus, homeostatic

Positive feedback reinforces stimulus, increases deviation from normal values thus
not homeostatic

Hormone cascade pathway

Negative feedback
Hormone + anterior pituitary + target endocrine gland = hormone cascade pathway

Thyroid hormones

Regulate homeostasis (metabolism/temperature) and development (tadpole to frog)

Cold hypothalamus TRH anterior pituitary TSH thyroid gland T3
and T4 body tissue increased metabolism

Production of T3 and T4 inhibits production of TRH and TSH negative feedback

T3 and T4 thyroid hormones contain iodine

o

Iodine deficiency hypothyroidism mental retardation

Neurohormone pathway

Stimulus hypothalamus/ posterior pituitary hormone blood stream target

cells response

Antagonistic hormones

Hormones with opposing effects that counterbalance each other to maintain internal
balance
o Insulin + glucose blood glucose homeostasis

Blood glucose homeostasis

Insulin + glucagon
Increased blood glucose (meal) insulin released into bloodstream by pancreas beta
cells increased glucose uptake by body cells and liver (stored as glycogen)
decreased blood glucose

Decreased blood glucose (skipped meal) glucagon released into blood stream by
pancreas alpha cells glycogen broken down by liver and glucose released into
blood increased blood glucose

Blood pressure homeostasis

RAAS = Renin Angiotensin-Aldosterone System

o Renin converts angiotensinogen to angiotensin I ACE converts angiotensin
I to angiotensin II angiotensin II constricts arterioles AND causes adrenal
gland to produce aldosterone which increases water absorption in distal
tubules increase in blood pressure and volume

Module 5 Lecture 3: Hypothalamus and Pituitary Hormones

Posterior pituitary hormones

Oxytocin and vasopressin

o Produced in hypothalamus and stored in posterior pituitary

Posterior pituitary stores but does not produce hormones

Vasopressin (ADH)

Regulates blood osmolarity

Produced in hypothalamus and stored in posterior pituitary

Main target cells = distal tubules and collecting duct in kidneys

Negative feedback

Sweating increased blood osmolarity hypothalamus osmoreceptors detect

change vasopressin release and thirst increased number of aquaporins in distal
tubule and collecting duct cellsincreased permeability to water of distal tubules and
collecting ducts increased renal reabsorption of water inhibition of further blood
osmolarity increase

Thirst drinking decreased blood osmolarity

Vasopressin binds to receptors more aquaporins increased water reabsorption

Diabetes insipidus

Caused by mutations that affect ADH production, ADH receptors, aquaporins

Increased urine volume severe dehydration, solute imbalances

Anterior pituitary hormones

Controlled by hypothalamic releasing and inhibitory hormones

Hypothalamic hormones travel from hypothalamus to anterior pituitary via portal
vessels
o

Hypothalamus portal vessels anterior pituitary

Tropic hormones

Hormones that regulate function of endocrine cells or glands

o TSH acts on thyroid to stimulate release of T3 and T4 thyroid hormones
o

ACTH acts on adrenal cortex to stimulate production and release of steroid

hormones

Nontropic hormones

Hormones that target nonendocrine tissues

o Prolactin mammary gland growth and mammal milk synthesis, delayed
amphibian metamorphosis

Nontropic and tropic hormone (Growth hormone)

Metabolic effects increased blood glucose

Major target = liver

Liver stimulation IGF release bone and cartilage growth stimulation

IGF = insulin-like growth factor

Module 5 Lecture 4: Stress and Adrenaline

Adrenal glands

Supra-renal organs
Adrenal cortex (endocrine) + adrenal medulla (neuroendocrine)

Adrenal cortex

True endocrine tissue

Release corticosteroids (long term stress response)
o

Two types of corticosteroids mineralocorticoids and glucocorticoids

Mineralocorticoids mineral metabolism (aldosterone)

Aldosterone secretion controlled by RAAS

Glucocorticoids glucose metabolism (cortisol)

Adrenal medulla

Neural tissue
Releases catecholamines (short term stress response)
o

Catecholamines trigger fight or flight response

Two catecholamines epinephrine, norepinephrine

Role of the hypothalamus in stress response

Activates adrenal medulla (and short term responses) via autonomic nerve impulses
Activates adrenal cortex (and long term responses) via hormonal signals

Role of the anterior pituitary in long term stress response

Hypothalamus CRH anterior pituitary ACTH bloodstream adrenal

cortex corticosteroids
o CRH = neuroendocrine signal released by hypothalamus that stimulates
anterior pituitary (and thus release of ACTH)

Head of School Lecture: Viruses

Major advances in gene therapy

Virus-based
Viral genes in human genome placenta

Cell culture virus growth and manipulation

Reverse transcriptase
o

Retrovirus uses to convert their RNA into DNA that can be incorporated into
our genome

Recombinant viral vectors

o

Retroviral life cycle and gene regulation gene therapy

Retroviral genomes modified to make recombinant vector genomes

Production of retroviral particles

o

Viruses 3 components GAG (structure), POL (polymerase), ENV

(envelope)

Cell + DNA insert artificial virus that produces gene

Gene therapy
o

Take stem cells that differentiate into WBC out of blood

Put retrovirus into blood to replace genes that were damaged

Return white blood cells to blood disease treatment

SCID

Took WBC out, inserted retrovirus, returned WBC treatment

4/20 children treated developed leukemia

Virus-based clinical trials

Advantages of adeno-associated virus (AAV)

Parvovirus 95% of people already infected

o Non-pathogenic
o

Low immunogenicity (lack of massive immune response)

Long term transgenic expression (1 injection couple of years)

Integrates in one place Chromosome 19

Can target muscle, liver, neurons

Making AAV in the lab

o

Requires adenovirus to replicate

Scale

Duchenne muscular dystrophy (DMD) and micro-dystrophin

X linked recessive
Caused by mutations in dystrophin gene
o

Normal muscle vs DMD muscle

o

Dystrophin gene binds to cell surface proteins but not actin nonfunctional
dystrophin

DMD muscle doesnt have structure to maintain skeletal muscle function

Mdx mouse model

Mutation DMD

Potential replacement micro-dystrophin

o

Two ends package in virus inject in animals increased lifespan

Dystrophin knockout decreased lifespan

RNAi clinical trials

Destroy mRNA that codes for proteins decreased protein production

DsRNA (similar to mRNA that codes for protein) can destroy mRNA

DsRNA delivery selective knockout of protein expression

RNAi in eye
o

Eye = readily accessible

Macular degeneration treatment

Final Lectorial: Practicals

Osmosis

C1V1=C2V2
Effects of tonicity on red blood cells
o

Hypertonic shrinking (crenation)

Isotonic no change

Hypotonic swelling/hemolysis

Osmolarity = (molarity)*(number of dissociable ions)

o

Example: osmolarity (250mM KCl solution) = 250*2 = 500

Action potentials

Strength of stimulus vs. compound action potential (CAP)

o Increased strength increased CAP magnitude until all nerve fibres have
fired AP (plateau)

Action potential vs. compound action potential

Sciatic nerve collection of nerve fibres compound action potential

Nerve bundle finite number of nerve fibres

Temperature vs. CAP and latency

o

Increased temperature increased membrane fluidity increased CAP

speed decreased latency

Lignocaine vs. CAP and latency

o

Increased lignocaine decreased CAP increased latency

Skeletal muscle

Strength of stimulus vs. force of contraction

o Increased strength increased force of contraction until all motor units
recruited (plateau)

Frequency of stimulus vs. force of contraction

o

Increased frequency summation of twitches increased force of

contraction tetanus

Length of muscle vs. force of contraction

o

Passive vs. active tension

Passive tension force generated by non contractile units (tendons etc)

Increased length increased stretch increased passive

tension

Active tension force generated by sliding of actin and myosin (usual)

Active tension bell curve

Optimal length maximum force of contraction

> optimal length disrupted sarcomeres reduced

force of contraction

Experimental design

Hypothesis
o Falsifiable and testable

Methods
o

All important conditions Ringers solution, controls

Results and discussion

o

Scientific writing recruitment of motor units

Short answer question

Interpret/draw graph
Axis labels (with units)
o

Example: The effect of stimulus interval (ms) of two 1V pulses on the second
peak CAP (mV) generated by the ulnar nerve of Rattus norvegicus. Data
represents the mean of three replicates.

Explain biological processes that cause results