Topic 6 Homeostatsis

Taxes

Simple response in which an organism will move its entire body towards a favourable stimulus or away from an unfavourable stimulus → directional stimulus

Towards stimulus = positive taxis

Away from stimulus = negative taxis

Kinesis

An organism changes the speed of movement and rate due to non-directional stimulus

Positive area - less movement to stay where they are

Negative area - more movement to leave area to get positive

Plant tropism

Plant response via growth to stimulus

Positive = growth towards stimulus

Negative = growth away from stimulus

Responds to light, gravity and water

Indoleacetic acid (IAA)

Type of auxin, produced in the tips of shoots in flowering plants

Can diffuse to other cells

Phototropism positIve

IAA diffuses to the shaded side of the shoot resulting in high conc. of IAA on shaded side

IAA causes the cells on the shaded side to elongate and shoot bends towards the light

Phototropism negative

IAA diffuses to the shaded side of the root, so high conc. of IAA there

IAA causes cell elongation to be inhibited so root bends away from light

Gravitropism positive

IAA moves to the lower side of the root so high conc. of IAA there

Causes the upper side to elongate as IAA inhibits growth on the lower side so root bends down towards gravity and anchors in

Gravitropism negative

IAA diffuses to the underside of the shoots so there is high conc. of IAA there

Causes the cells to elongate so shoot bends upwards away from gravity

IAA stimulating growth

1. binding to a receptor in the target cell zone of cell elongation in shoots/roots membranes and activating a proton pump
2. These pump protons (H+) from the cytoplasm to their cell walls
3. The resulting decrease in pH activates an enzyme that breaks the bonds between cellulose microfibrils
4. This loosens the cell wall and so allows the cell to elongate under internal turgor pressure - Ψ more negative in cytoplasm than outside so water enters via osmosis so cell grows

Central Nervous System

CNS

brain and spinal cord

Peripheral Nervous System

PNS

Neurones that connect CNS to body

Splits into 2: somatic and autonomic nervous systems

Somatic nervous system

Controls conscious activities

Autonomic Nervous System

Controls unconscious activities

Splits into 2: sympathetic and parasympathetic

Sympathetic nervous system

Ready for action

Flight or fight

Parasympathetic nervous system

Calms

Rest and digest

Reflex arc

Body response to stimulus without making a conscious decision

Stimulus → receptors → sensory neurone → relay neurone → motor neurone → effectors → response

Sensory neurone

Transmits electrical impulses from receptors to CNS

Relay neurone

Transmits electrical impulses between sensory and motor neurones

Motor neurone

Transmits electrical impulses from CNS to effectors

Resting potential

Neurone not conducting a nerve impulse

Difference between electrical charge inside and outside of neurone

At -70mV → outside is positively charged compared to inside as there are more positive ions outside than inside

Establishing a resting potential

Maintained by sodium-potassium pumps → active transport using ATP

Pump moves:

* 2K+ into axon
* 3Na+ out of axon

This creates an electrochemical gradient

The membrane is more permeable to K+ so more are moved out via K+ channels via facilitated diffusion

* results in -70mV
* membrane becomes polarised

Action potential

Neurone voltage increases beyond a set point from the resting potential → this generates a nerve impulse

Increase in voltage (depolarisation) is due to membrane becoming more permeable to Na+

Action potential method

1. stimulus - excites the neurone cell membrane → Na+ channels open. The membrane becomes more permeable to Na+ so Na+ diffuses into neurone down Na+ electrochemical gradient. Makes the inside of neurone less negative
2. Depolarisation - if voltage reaches threshold of -55mV, more Na+ channels open causing more Na+ to diffuse rapidly into neurone
3. Repolarisation - at voltage +40mV, Na+ channels close and K+ channels open. Membrane is more permeable to K+ so K+ diffuse out of neurone down K+ concentration gradient. Membrane is back at resting
4. Hyperpolarisation - K+ channels are slow to close so slight ‘overshoot’, where too many K+ diffuse out of neurone. Voltage becomes more negative than the resting potential
5. Resting potential - ion channels reset. Na+/K+ pump returns membrane back to resting potential and maintains it until another stimulus

Refractory period

Neurone membrane can’t be excited straight away after an action potential due to ion channels recovering and can’t be made to open up again

So action potential can’t be regenerated

Act as a time delay between 1 action potential and next so:

* action potentials do not overlap but pass along as discrete (separate) impulses
* there is a limit to the frequency at which the nerve impulses can be transmitted
* action potentials are unidirectional

Propagation/wave of depolarisation

When action potential happens, some Na+ that enter neurone diffuse sideways

Causes Na+ channels in the next part of the neurone to open and Na+ diffuses in

Causes a wave of depolarisation to travel along the neurone

Waves move along from parts of membrane in the refractory period as these parts can’t have an action potential

All-or-nothing principle

If threshold isn’t reached, the action potential and the impulse are not produced - nothing

Any stimulus that reaches threshold will peak at the same voltage - all → bigger the stimulus increases the frequency of action potentials

Myelinated motor neurone

Factors affecting speed of conduction - myelination

Neurones have myelin sheath or Schwann cell which is an electrical insulator

Gaps between Schwann cells are nodes of Ranvier. Na+ channels are concentrated at nodes

In myelinated neurone, depolarisation only happens at the nodes of Ranvier

Saltatory conduction - neurone’s cytoplasm conducts enough electrical charge to depolarise the next node, so impulse jumps node to node

In a non-myelinated neurone, the impulse travels as a wave along whole of axon membrane so depolarisation occurs along the whole length of the membrane and is slower than saltatory conduction

Factors affecting speed of conduction - axon diameter

Wider diameter of axon, speed of conduction increases due to less resistance of flow of ions and less leakage so action potential travels faster

Factors affecting speed of conduction - temperature

A higher temperature increases the speed of conductance as ions diffuse faster as enzymes involved in respiration work faster → more ATP for active transport

Synapse

Junction between a neurone cell and another neurone or neurone and effector

Gap is synaptic cleft

Action potential is transmitted as neurotransmitters that diffuse across the synapse

Function of synapse

1. an action potential arrives at the synaptic knob. This causes depolarisation of synaptic knob leading to the opening of Ca2+ voltage-gated channels and Ca2+ diffuses into synaptic knob
2. This causes synaptic vesicles to move and fuse to presynaptic membrane. This releases acetylcholine into synaptic cleft
3. acetylcholine diffuses down concentration gradient, across the synaptic cleft to the postsynaptic membrane. This binds to specific cholinergic receptors on postsynaptic membrane
4. This causes Na+ channels to open on the postsynaptic membrane. The influx of Na+ causes depolarisation. If threshold is reached, this generates a new action potential in postsynaptic membrane
5. acetylcholine is hydrolysed by acetylcholinesterase into ethanoic acid and choline. These diffuse into synaptic cleft into presynaptic neurone. Na+ channels close and postsynaptic membrane can re-establish the resting potential
6. ATP released by mitochondria is used to recombine choline and ethanoic acid, stored in synaptic vesicles for future

Neuromuscular junction

Postsynaptic cleft is the muscle fibre membrane and depolarisation leads to contraction of muscle fibre

Neuromuscular junction features

Only excitatory synapse

Linkes neurone to muscle

Action potential ends here

Only motor neurones

Acetylcholine binds to receptors on muscle membrane

Cholinergic synapse features

Can be excitatory or inhibitory

Links neurones to neurones or neurone to effector

Another action potential may be generated along postsynaptic

Most neurones

Acetylcholine binds to receptors on postsynaptic membrane

Excitatory neurotransmitter

Post synaptic neurone is depolarised, triggering an action potential

Inhibitory neurotransmitter

Hyperpolarisation of postsynaptic neurone so no action potential is triggered

Inhibitory synapse

The presynaptic neurone releases an inhibitory neurotransmitter which binds to Cl- channels

Channels open causing facilitated diffusion of Cl- into postsynaptic neurone

May cause the opening of nearby K+ channels causing K+ to diffuse out

Cause an effect of more negative ions and less positive ions in cytoplasm of postsynaptic neurone causing hyperpolarisation

If an excitatory neurotransmitter was released at the same time, wouldn’t result in sufficient generator potential to reach threshold → no action potential is generated in postsynaptic neurone

Summation

The rapid build up of neurotransmitter in the synapse to help generate an action potential

This is needed as some action potentials do not result in sufficient concs of neurotransmitters being released to generate a new action potential

Spatial summation

Many different neurones collectively trigger a new action potential by combining the neurotransmitters they released to exceed threshold

Temporal summation

The neurone releases neurotransmitter repeatedly over a short period of time to add up to enough to exceed threshold

Effects of stimulating drugs

Enhanced response

Can mimic the shape of the neurotransmitter, triggering action potentials

Stimulate the release of more neurotransmitters

Inhibits enzymes which breakdown neurotransmitters causing prolonged stimulation

Effect of inhibitor drugs

Reduced response

Block response to stop neurotransmitters triggering action potentials

Bind to receptors and change their shape

Acetylcholine neurotransmitter

Parasympathetic nervous system

Noradrenaline neurotransmitters

Sympathetic nervous system

Pacinian Corpuscles

responds to changes in pressure

occur deep in skin, mainly feet and hands

consists of a single sensory neurone wrapped with layers of tissue separated by gel

Sensory neurone has special channel proteins in plasma membrane

* allows ion transportation
* Membranes surrounding sensory neurone have stretched-mediated Na+ channels
* Only open and allow Na+ to enter sensory neurone when stretched and deformed

Pacinian Corpuscles structure

At resting of pacinian corpuscles

Na+/K+ pumps move Na+ away from dendrite. Therefore high diffusion gradient for Na+

Na+ channels are too narrow for Na+ to diffuse into sensory neurone so resting potential maintained

Pressure applied on pacinian corpuscles

When pressure is applied, membrane stretches and deforms

Causes Na+ channels to open so Na+ diffuses into dendrite → this causes the generator potential

The greater the pressure, the more Na+ channels open so larger generator potential

If threshold is reached, an action potential occurs

Rod cells

Can’t distinguish between different wavelengths of light

Processes images in black and white

Can detect light at very low light intensities → many rod cells to 1 sensory neurone → retinal convergence

Contains light sensitive pigment, rhodopsin

* breaks down into opsin (protein) and retinal (vitamin A)

High visual sensitivity as spatial summation occurs

Low visual acuity as light from two close point aren’t able to be distinguished between

Rod cells generating action potential

1. rhodopsin is broken down by light - bleaching
2. Must be enough energy from low-intensity light to cause breakdown
3. Enough pigment needs to be broken down for threshold to be met in the bipolar cell - become hyperpolarised and causes an action potential

Threshold can be reached in low light as many rod cells are connected to a single bipolar cell - spatial summation

Rhodopsin is reformed in the dark → dark adaption occurs from light to dark

Visual acuity

Measure of the ability of the eye to distinguish shapes and the details of objects at a given distance

Cone cells

Three types: red, green, blue

Contain pigment iodopsin

Each detects a different range of wavelengths

Stimulated by very high light intensities and sensitive to different wavelengths of light

A single cone cell contains 1 type of iodopsin

Colour vision

Low visual sensitivity → temporal summation

Can determine exact source of stimulus due to temporal summation → high visual acuity

Iodopsin is only broken down by high light intensities so generator potential can only be generated with enough light

Fovea

Receives most light

Cone cells near

Rod cells far away at low light intensities

Blind spot

No rod or cone cells

Not sensitive to light

Optic nerve

Heart

Cardiac muscle

Myogenic:

* contracts without stimulus
* rate of contraction is controlled by wave of electrical activity

Sinoatrial node:

* located in right atrium
* known as pacemaker → sets rhythm of heart beat by sending out regular electrical activity to atrial walls

Atrioventricular node:

* near border of left and right ventricle still within atria

Bundle of His:

* conductive tissue that runs through septum and up the walls of the ventricles

Purkyne tisse

* conductive tissues that go through ventricle walls

Regular beating of heart

1. SAN sends out a wave of electrical activity (depolarisation) across atria, causing both atria to contract at the same time
2. Band of non-conductive collagen tissue prevents the waves from being passed directly to ventricles from atria
3. waves go to AVN
4. AVN is responsible for passing the waves onto the Bundle of His → there is a slight delay before AVN reacts to make sure atria have empties before ventricles contract
5. Bundle of His conducts the waves down the septum to purkyne tissue
6. Purkyne tissue carries the waves into muscular walls of right and left ventricles causing them to contract simultaneously from bottom up

Control of heart rate

1. SAN generates electrical impulses that cause cardiac muscle to contract
2. the rate at which the SAN fires is unconsciously controlled by medulla oblongata
3. stimuli are detected by internal receptors


1. pressure receptors, baroreceptors, in aorta or carotid arteries, stimulated by blood pressure
2. chemical receptors, chemoreceptors, in aorta, carotid arteries or medulla, stimulated by O2 and CO2 levels and pH
4. electrical impulses from receptors are sent to medulla along sensory neurones
5. medulla processes the information and sends impulses along sympathetic neurones (increases heart rate) or parasympathetic neurones (decreasing heart rate), part of autonomic nervous system

High blood pressure

Baroreceptor

Impulses are sent to medulla, then send impulses along parasympathetic neurones. They secrete acetylcholine which binds to receptors on SAN

Cardiac muscle

Heart rate slows to reduce blood pressure back to normal

Low blood pressure

Baroreceptor

Impulses are sent to medulla, then send impulses along sympathetic neurones. They secrete noradrenaline which binds to receptors on SAN

Cardiac muscle

Heart rate speeds up to increase blood pressure back to normal

High O2, low CO2, high pH

Chemoreceptors

Impulses are sent to medulla, then send impulses along parasympathetic neurones. They secrete acetylcholine which binds to receptors on SAN

Cardiac muscle

Heart rate decreases so O2, CO2 and pH return back to normal

Low O2, high CO2, low pH

Chemoreceptors

Impulses are sent to medulla, then sends impulses along sympathetic neurones. They secrete noradrenaline, which binds to receptors on SAN

Cardiac muscle

Heart rate increases to return O2, CO2 and pH back to normal

Muscle structure

sarcolemma

sarcoplasm

invaginations

sarcoplasmic reticulum

lots of mitochondria and nuclei for ATP for contraction

contains myofibrils

Sarcolemma

cell membrane of muscle fibre cells

Invaginations

parts of sarcolemma folding inwards

they stick to sarcoplasm forming transverse (T) tubules

* help spread electrical impulses in sarcoplasm to reach all of muscle fibres

Sarcoplasmic reticulum

Network of internal membrane through sarcoplasm

Stores and releases Ca2+ needed for contraction

Myofibrils

Made up of thick myosin and thin actin filaments

Myosin: 2 heads and form cross bridges

Actin: troponin and tropomyosin

Under electron microscope:

* dark bands = A-bands = thick myosin and some overlapping actin
* light bands = I-bands = thin actin only

Made of many short sarcomeres

Muscle contraction with bands

A-bands = stay the same length

I-bands = get shorter

H-zones = get shorter

Sarcomeres get shorter

Sliding filament theory

Myosin and actin filament slide over one another to make the sarcomere contract

Simultaneous contraction of lots of sarcomere means myofibrils and muscle fibres contract

Sarcomere return to original length as muscle relaxes

Cross-bridge cycle

1. ATP binds to myosin head, causes the myosin head to be released from actin
2. ATP is hydrolysed while myosin head is unattached. ADP + Pi is formed and remain bound to myosin head
3. Energy released by hydrolysis of ATP is absorbed by myosin head changes shape. ADP + Pi are released from myosin head
4. Power stroke occurs, myosin head changes shape. This draws actin filament over myosin filament. Then binds to actin filament

Muscle contraction method

1. action potential arrives at the presynaptic neurone and this causes depolarisation of the membrane
2. Ca2+ channels open and Ca2+ diffuse in
3. This causes vesicles to move and fuse with presynaptic membrane. Vesicles release acetylcholine
4. Acetylcholine diffuses across the synaptic cleft and binds to receptors on sarcolemma of muscle
5. Causes Na+ channels to open and diffuse in. This causes depolarisation
6. Action potential is carried quickly into t-tubules and causes Ca2+ to be released from sarcoplasmic reticulum
7. Ca2+ binds to tropomyosin and causes to change shape
8. This exposes myosin binding site on actin
9. Myosin heads bind to actin filament forming actinomyosin cross bridges
10. Myosin heads bends pulling the actin filaments
11. ATP binds to myosin head breaking actinomyosin cross bridges
12. Hydrolysis of ATP releases energy used to recock the myosin head so it can bind to another binding site further away

Muscle relaxation

1. repolarisation of sarcolemma and sarcoplasmic reticulum
2. Causes Ca2+ channels to close and Ca2+ pumps remove Ca2+ into sarcoplasmic reticulum by active transport using ATP
3. Ca2+ dissociates from ATP hydrolase on myosin heads and this prevents ATP from binding so cross bridge stops
4. Ca2+ dissociates from tropomyosin causing it to change shape, covering up the myosin binding site on actin, dislodging the myosin head so cross bridges are broken
5. Actin filaments slide back and sarcomere lengthens

Phosphocreatine (PCr)

Serves as a high-energy phosphate reservoir for rapid regeneration of ATP

Creatine is phosphorylated during rest by ATP produced by respiration

Replaces ADP’s lost phosphate to reform ATP

Process is much faster than making new ATP

Slow twitch muscles

Aerobic respiration, limited by rate of O2 supply

Long periods of contraction

Slow contraction speeds

No lactate produced, not susceptible to fatigue

Lots of mitochondria and myoglobin → red colour

Heart, leg and back

Fast twitch muscles

Anaerobic respiration → not limited by blood supply

Only short bursts of energy

Fast contraction speed

Lots of glycogen but few mitochondria and myoglobin → white

Lactate produced

pH is low and muscle fatigue

Rigor mortis

Soon after death, aerobic respiration is inhibited

ATP not available for repolarisation of sarcoplasmic reticulum and Ca2+ pumps to remove Ca2+ from myofibrils

Ca2+ remains bound to tropomyosin so binding sites are not broken down

Slowly Ca2+ diffuses out of muscle cell into surrounding tissue, decreasing conc of Ca2+ in myofibrils

Ca2+ will eventually dissociate from tropomyosin ending rigor mortis

Homeostasis

In mammals involves physiological control system that maintain the internal environmental within restricted limits

Negative feedback

Restores system to their original level

Control of body temperature - too hot

Increase in temperature

Detected by thermoreceptors

Sweating and vasodilation

Decrease in temperature

Negative feedback for heat loss and positive feedback for heat gain

Control of body temperature - too cold

Decrease in temperature

Detected by thermoreceptors

Shivering and vasoconstriction

Increase in temp

Negative feedback for heat gain and positive feedback for heat loss

Control of blood glucose

Pancreas detects changes in the blood glucose levels

* contain endocrine cells in the Islet of Langerhans which release the hormones insulin and glucagon to bring levels back to normal

Islets of Langerhans contain 2 different types of secretory cells:

* alpha cells which secrete glucagon
* beta cells which secrete insulin

Adrenaline is released by adrenal glands when your body anticipates danger

* this results in more glucose being released from stores of glycogen in the liver

Blood glucose levels increase

Blood glucose levels increase

Detected by beta cells in Islets of Langerhans

Liver cells become more permeable to glucose and enzymes are activated to convert glucose to glycogen

Glucose is removed from the blood and stored as glycogen in cells

Normal blood glucose levels

Blood glucose levels decrease

Blood glucose levels decrease

Detected by alpha cells in the Islets of Langerhans

Alpha cells release glucagon and adrenal gland releases adrenaline

Second messenger model occurs to activate enzymes to hydrolyse glycogen

Glycogen is hydrolysed to glucose and more glucose is released back into the blood

Normal blood glucose levels

Glycogenesis

The process of excess glucose being converted to glycogen when blood glucose is higher than normal

Occurs mainly in the liver

Glycogenolysis

The hydrolysis of glycogen back into glucose in the liver

Occurs when blood glucose levels are lower than normal

Gluconeogenesis

The process of creating glucose from non-carbohydrate stores in the liver

Occurs if all glycogen has been hydrolysed into glucose and body still needs more glucose

Action of insulin

1. Insulin binds to specific receptors on the cell membrane of liver and muscle cells. This changes the tertiary structure of the channel proteins resulting in more glucose being absorbed by facilitated diffusion
2. It increases the permeability of muscle cell membrane to glucose so takes up more glucose. This involves increasing the number of channel proteins in the cell membrane
3. Insulin also activates enzymes in the liver and muscle cells that convert glucose into glycogen
4. The cells are able to store glycogen in their cytoplasm, as an energy store → glycogenesis
5. Insulin also increase the rate of respiration of glucose, especially in muscle cells

Action of glucagon

1. Glucagon binds to specific receptors on cell membranes of liver cells
2. Glucagon activates enzymes in liver cells that breakdown glycogen into glucose. The glucagon binding causes a protein to be activated into adenyl cyclase and to convert ATP in a molecule, cyclic AMP (cAMP). CAMP activates an enzyme, protein kinase, that can hydrolyse glycogen into glucose → glycogenolysis
3. Glucagon also activates enzymes that are involved in the formation of glucose from glycerol and amino acids → gluconeogenesis
4. Glucagon decreases the rate of respiration of glucose in cells

Action of insulin and glucagon

Second messenger model

1. Glucagon binds to glucagon receptors
2. Once bound, it causes a change in shape to the enzyme adenyl cyclase, which activates it
3. Activated adenyl cyclase enzymes convert ATP into cyclic AMP (cAMP). CAMP is the second messenger
4. CAMP activates an enzyme, protein kinase A. Protein kinase A activates a cascade (a chain of reactions) of glycogenolysis

Role of adrenaline in second messenger model

Increases blood glucose levels


1. Adrenaline attaches to receptors on surface of target cells. This causes G protein to be activated and to convert ATP into cAMP

Other hormones influencing plasma glucose conc.

Thyroxine → increases the basal metabolic rate, so and increase rate of energy release is required

Corticosteroids → promote reactions that result in the synthesis of glucose from non-carbohydrate sources → glucogenesis

Diabetes Type I

Body is unable to produce insulin

Starts in childhood and could be result of an autoimmune disease where the beta cells were attacked

Treatment involves injections of insulin

Diabetes Type II

Due to receptors on target cells losing their responsiveness to insulin

Develops in adults because of obesity and poor diet

Controlled by regulating in take of carbohydrates, increasing exercise and sometimes insulin injections

Hyperglycaemic coma

Too much glucose

Excessive ketone production

Insulin treatment

Hypoglycaemic coma

Low glucose

Brain cells starved

Treated by glucose or adrenaline

Kidneys

Osmoregulation occurs within nephrons

Nephrons are long tubules surrounded by capillaries

Approx 1 million nephrons in each kidney

Nephron structure

1. Renal capsule with glomerulus
2. Proximal convoluted tubule
3. Loop of Henle
4. Distal convoluted tubule
5. Collecting ducts

Function of nephron

Filter blood to remove waste and selectively reabsorb useful substances back into blood