- Created by: Abbie
- Created on: 16-09-19 17:02
Response to stimuli
- Responding to environmental stimuli (external environment) helps animals to avoid harmful environments. Also, response to internal environment helps to ensure conditions are always optimal for their metabolism.
- Plants also respond to environmental changes- they sense the direction of light, growing towards it to maximise photosynthesis, and gravity, so their shoots and roots can grow in the right direction
- A stimulus is any change in the internal/external environment, leading to a response. This response is due to receptors that detect the stimuli, prompting effectors to produce a response.
- Receptors can be cells or proteins on cell surface membranes- lots of different types that detect different stimuli, as sensory receptors are specific to one type of stimuli, e.g. heat
- Effectors are the cells that bring about a response to a stimuli to produce an effect. These include muscle cells and cells found in galnds, e.g. the pancreas
- Receptots communicate with effectors via the hormonal and/or nervous system
The Nervous System
The nervous system is made up of a network of cells called nerounes: sensory transmit impulses from receptors to the CNS, relay transmit impulses between sensory and motor nerounes, and motor transmit impulses from the CNS to effectors.
When a stimulus is detected in receptor cells, an electrical impulse is sent along the sensory neurone and upon reaching the axon terminal, neurotransmitters are released, triggering an electrical impulse when reaching the post-synaptic receptors. The CNS (coordinator) processes the info, sending impulses along the motor neurones to effectors. The Nervous system is subdivided into 2 systems:
- The CNS, which is made up of the brain and spinal cord.
- The PNS, which is made up of the neurones that connect the CNS to the rest of the body. Split into the SNS and ANS, which then breaks into the antagonistic sympathetic and parasympathetic nervous systems
Nervous system communication is localised, as when an electrical impulse reaches the end of a neurone, neurotransmitters are secreted directly into target cells. It's short-lived, as neurotransmitters are quickly removed after doing their job, and rapid, as electrical impulses are very fast, allowing animals to have quick response to stimuli
Reflexes are rapid, automatic responses to stimuli, as in this case, the body responds to a stimulus without making the conscious descision to do so. This is because reflex arcs bypass the brain, leaving it free to carry out more complex tasks and ensure it isn't overloaded. This means info travels very quickly from receptors to effectors in order to protect the body.
A simple reflex arc, e.g. hand-withdrawal due to heat, works as follows:
- thermoreceptors in skin detect heat stimulus
- sensory neurone carries impulse to relay, which connects to motor. This sends impulses to the effector, which moves the hand
If there's a relay neurone involves in the simple reflex arc, it's possible to override the response by involving the brain
A tropism is the response of a plant to a directional stimulus; they respond by regulating their growth. A positive tropism is growing towards the stimulus, and a negative one is growing away. Plant growth factors, e.g. light and gravity, impact the way in which a plant grows, as plants respond to such stimuli with growth factors; hormone-like chemicals made in cells throughout the plant that speed up/slow down plant growth. E.g IAA is an auxin that controls plant cell elongation- the cells become loose and stretchy, so the cells grow longer.
Phototropism in flowering plants:
- Cells in the shoot's tip produce IAA and it's transported down the shoot, evenly initially, but the light causes the IAA to build in a greater concentration on the shaded side of the shoot. This promotes greater elongation here, meaning the shoot bends towards the light
- Also controls the bending of roots in response to light, but as lots of IAA inhibits growth in roots, there is greater elongation on the lighter side than shaded, so the roots bend away from the light
Gravitropism in flowering plants:
- Cells in the tip of the root produce IAA, which is initially distributed evenly, but a greater concentration builds on the lower side, as gravity influences it. IAA inhibits the elongation of this side, causing the root to bend down towards gravity
- In shoots, greater IAA in the lower side causes it to elongate more, and grow up away from gravity
IAA's role in elongation:
- It increases cell wall plasticity, but only in young cell walls, as older cells develop greater rigidity over time, so the older parts won't be able to respond. The 'acid growth hypothesis' suggests IAA'e effect is to do with the active transport of hydrogen ions from the cytoplasm into cell wall spaces, causing it to become more elastic and elongate
- IAA moves around the plant to control tropisms via diffusion and active transport (short distances) and the phloem for longer distances
Reponses in simple mobile organisms
Simple moblie organisms have 2 types of responses that keep them in a favourable environment:
- Tactic responses (taxes)- the organisms move to (positive)/away (negative) from a directional stimulus. E.g. phototaxis in woodlice; they move away from light to help them stay in damp conditions
- Kinetic responses (kinesis)- the organisms' movement is affected by non-directional stimuli. It's to do with moving more/less, but not in a specific direction. The organism changes the speed at which it moves and the rate at which it changes direction. If it arrives in an unfavourable environment, rate of turning increases, helping it to return to a favourable one. But, if it moves a considerale distance into the UE, the rate of turning decreases, and it moves in long straight lines before turning sharply. This helps it to arrive in a new region with favourable conditions.
Receptors are specific, as they only detect one particular stimulus, meaning there are many different types. Some are cells, e.g. photoreceptors are receptor cells, whilst others are proteins on cell surface membranes e.g. glucose receptors are proteins found in the cell membrane of some of the pancreas' cells. Some receptor cells communicate via the nervous system:
- when a NS receptor is in resting state, there's a difference in charge between the in and outside of the cell, which is generated by ion pumps and channels. This creates a voltage across the membrane, which is known as potential difference
- when a cell is resting, potential difference is called resting potential. Detected stimuli make cell membranes excited and more permeable, alloeing more ions to move in and out of the cell. This alters the potential difference; the change in PD due to a stimulus is called generator potential. The bigger the stimulus, more excitement, causing more movement of ions and a bigger change in PD- bigger generator potential
- If the generator potential is big enough to reach the threshold level, it'll trigger an action potential. These are all one size, so the strength of a stimulus is measured by the frequency of action potentials. If the stimulus is too weak, the threshold won't be reached, so there's no action potential
- These are pressure receptors deep in the skin that are specific to mechanical pressure (pressure and vibrations), so are called 'mechanoreceptors'. Most abundant in the fingers and soles of feet. Their job, as with all receptors, is to convert the (mechanical) energy of a stimulus into a nervous impluse called a generator potential.
- PCs contain the end of a sensory neurone (sensory nerve ending) with a stretch mediated sodium channel in its plasma membrane. Its permeability to sodium changes when deformed-in resting state it's too narrow to let sodium pass, so the neurone of the PC has a resting potential.
- When the PC is stimulated, it is deformed and the lamellae surrounding the sensory nerve ending becomes stretched and presses on it. This widens the neurone, widening the channels in the membrane, allowing sodium ions to diffuse out into the neurone
- This changes the potential of the membrane and produces a generator potential. If it reaches the threshold, an action potential is triggered
- The retina lines the inside of the eye, and contains photoreceptor cells, which detect light. Nerve impulses from the photoreceptors are carried from the retina to the brain via the optic nerve (a bundle of neurones). The optic nerve leaves the eye at the blind spot; it's not senstive to light, as there aren't any photoreceptors.
- When light hits the photoreceptors, it's absorbed by light-sensitive optical pigments. The light bleaches these, causing a chemical change and altering the membrane permeability to sodium ions. A generator potential is created, and if threshold is reached, a nerve impulse is sent down the bipolar neurone; these connect photoreceptors to the optic nerve
- 2 types of photoreceptors in the human eye- rods and cones. Rods are mainly in the peripheral parts of the retina, and cones packed together in the fovea
- Rods and cones contain different optical pigments, making them sensitive to different wavelengths of light- rods contain rhodopsin and give info in black and white (monochromatic vision). Cones contain iodopsin and give info in colour (trichromatic vision)- there are three types of cones, red, blue and green sensitive (all contain iodopsin). When they're stimulated in different proportions, you see different colours
Generator potentials in photoreceptors
- Light induces the rhosopisn/iodopsin pigment in the rod/cone cells to break down (bleaching). This depolaries the membrane of the rod/cone, producing a generator potential.
- This potential is passed onto the bipolar neurones and then to the sensory neurones as a nerve impulse (many rods are connected to a single bipolar cell, but cones are connected individually)
- The axons of the sensory neurones weave together to form the optic nerve and allow for the transmisiion of the nerve impulse to the brain
- If the threshold is met, an action potential is induced
Rods and cones
- Rods are very sensitive to light (work well in dim light) as many rods join to one bipolar neurone, allowing manyt weak generator potentials to combine to reach the threshold and trigger an action potential
- Cones are less sensitive (work best in bright light) as one cone joins to one neurone, so it takes more light to reach the threshold and trigger an action potential
Visual acuity (the ability to tell apart points that're close together):
- Rods give low visual acuity as many rods join the same neurone, which means light from 2 points close together can't be told apart
- Cones have high visual acuity as cones are close together and one cone joins one neurone. When light from 2 points hits 2 cones, two action potentials (one from each cone) go to the brain, so you can distinguish two points that're close together as two separate points
Control of heart rate
The cardiac muscle is myogenic, so contracts and relaxes on its own accord, withoyut outside stimulation:
- Process begins in the sinoatrial node (SAN); group of cells in the right atrium. SAN has a basic rhythm of stimulation that determines the beat of the heart (pacemaker) by sending out regular waves of electrical activity to the atrial walls (action potential). This causes the left and right atria to contract at the same time
- A layer of non-conductive tissue stops this wave crossing to the ventricles, instead it's transferred from the SAN to the atrioventricular node (AVN)
- After a short delay, to ensure the atria are empty, the AVN conveys a wave of electrical excitation between the ventricles along the bundle of His; a group of muscle fibres that conducts the waves between the ventricles to the bottom of the heart. Here, the bundle splits into the purkyne tissue, which is the finner muscle fibres in the left and right ventricle walls
- The purkyne tissue then carries the waves into the musclar walls of the ventricles, making then contract (ventricular systole) simultaneously from the bottom up
The brain/ANS (heart)
- A healthy human resting rate is around 70bpm, but this needs to be able to be altered to respond to internal stimuli and meet varying demands for oxygen. Changes to the heart rate are controlled by an area of the brain called the medulla oblongata. It has 2 centres concerning heart rate: a centre increasing heart rate, linked to the SAN by the sympathetic nervous system, and one decreasing heart rate that's linked by the parasympathetic nervous system.
- The medualla oblongata controlls the rate SAN fires electrical impulses in accordance to the nerve impulses recieved by 2 types of receptors. These are pressure and chemical receptors, and they detect and respond to stimuli of either chemical or pressure changes in the blood:
- Pressure receptors- there are such receptors called baroreceptors in the aorta and carotid artieries (neck) that're stimulated by high and low blood pressure
- Chemoreceptors- these are found in the aorta, carotid arteries and medulla. They monitor oxygen level in the blood, as well as CO2/pH levels (indicators of oxygen level)
- Electrical impulses from receptors are sent to the medulla along sensory neurones. The medulla processes the info and sends impulses to the SAN along either sympathetic or parasympatheic neurones
Receptors and heart rate
If high blood presure/high blood oxygen(/low co2 or high pH) is the stimulus, then this will be detected by baroreceptors/chemoreceptors respectively. Impulses are then sent to the medulla, which will send impulses along the parasympathetic neurones. These will secrete the neurotransmitter acetylcholine, which binds to receptors on the SAN. The cardiac muscles will act as the effector that slows the heart rate down to return blood pressure/chemical levels to normal.
If low blood pressure/bloof oxygen levels are detected the same process will happen, except it will be the sympathetic nervous neurones that will be implicated, and these will secrete noradrenaline in order to allow the cardiac musces to speed up the heart rate to return blood pressure/chemical levels to normal
Mammalian motor neurone structure
- Cell body- which includes a nucleus and lots of RER (asso with the production of proteins and neurotransmitters)
- Dendrons- extend from the cell body and branch into dendrites. They carry nerve impulses towards the cell body
- Axon- carries nerve impulses away from the cell body. It's covered in myelin sheath and separated by nodes of ranvier
- Schwann cells- surround the axon to protect it and provide electrical insulation. They wrap around the axon many times as layers of their membranes build up around the axon. They carry out phagocytosis and help with nerve regeneration
- Myelin sheath- covers axon and is made up of membranes of schwann cells (myelinated neurones)
- Nodes of ranvier- constrictions between adjacent schwann cells (where there's no myelin sheath)
Establishing a resting potential
- In resting state, the outside of the axon membrane is positively charged compared to the inside as there are more positive ions outside. This means that the membrane is polarised, with a potential difference across it. At this point, the voltage is about -70 mV
- Resting potential is created by the movement of ions across the membrane by the Sodium- Potassium pump. Na is actively transported out of the axon and K into the axon. For every 3 Na that move out, only 2 K move in. Both of these ions are positive, with this movement ensuring more positive ions are outside the axon membrane
- Resting potential is maintained by the K and Na ion voltage-gated channels (channel proteins) in the phospholipid bilayer. Na begins to naturally diffuse back in and K out, due to the establishment of an electrochemical gradient by the Na-K pump. But, most of the K channels are open and most of the Na ones are closed. Because the phospholipid bilayer is not permeable to these ions, they can only diffuse across it if their channels are open
- Therefore, K ions diffuse out far quicker that Na diffuses back in, making the outside of the axon more and more positive, increasing the potential difference. This repells the (positive) Kions, complelling them to move back into the axon and stay there. This helps to establish an equilibrium and prevent the net movement of ions
Creating an action potential
If a big enough stimulus is detected, the energy of it causes a temporary reversal of charges either side of this part pf the axon, causing it to become depolarised and change to a positive charge of around +40 mV:
- The stimuli's energy causes more Na channels to open, allowing the ions to diffuse into the axon down the electrochemical gradient. This makes the inside of the membrane less negative, with the ions' positive charge triggering a reversal of potential difference.
- If the potential diference reaches the threshold of -55 mV, more Na channels open, increasing the influx of Na diffusion. A 'wave' of depolraisation then begins to move along the axon, as some of the Na ions that enter the neurone diffuse sideways, causing the Na channels of the next region of the axon to open, and the Na to diffuse into that part too. (The 'wave' only moves in one direction, as it moves away from the parts of the axon in the refractory period, as they can't fire an action potential)
- Once an action potential of around +40 mV has been created, the Na gates close and the K gates open. The electrochemical gradient previously preventing the outward movement of K ions has now been reversed, allowing them to diffuse out of the axon and reploraise it
Hyperpolarisation and the Refractory Period
- There is a temporary overshoot of the electrical gradient, as the K channels are too slow to close, meaning that the inside of the axon becomes more negative tha usual
- Once the gates of both channels are shut, the Na-K pump returns the membrane to its resting potential by move Na out and K in
- After an action potential, the membrane can't be excited again straight away, as the channels are recovering and can't be opened. This is called the refractory period, and it acts as a time delay between action potentials, ensuring that they're discrete (don't overlap), only travel in one directon and limits the frequency at which nerve impulses can be transmitted
The 'all or nothing' principle
Action potentials have an 'all or nothing' principle, meaning that once the threshold is reached, an action potential will always fire with the same change in voltage, no matter how big the stimulus is. Bigger stimuli will just cause the action potentials to fire more frequently. Also, if the threshold isn't reaches, and action potential will never fire
Action potential- unmyelinated axon
- Resting potential-relative negative charge inside membrane, polarised membrane
- Stimulus causes an action potential-sudden influx of sodiumions, causing the membrane to transmit a nerve impulse; a temporary reversal of electrical potential difference that depolarises the membrane
- Causes sodium voltage gated channels to open further along- wave of depolarisation, and behind they close and potassium channels open so potassium ions can leave the axon
- Whilst the wave of depolarisation moves along, the outward movement of potassium ions repolarises the membrane behind it
- The sodium potassium pump actively transports sodium ions out and potassium in, helping to return the axon to its resting potential, ready for a new stimulus
Action potential- myelinated axon
- Myelin sheath is an electrical insulator that prevents action potentials from forming. Nodes of ranvier break it up, and action potentials can occur here- they jump between these points during a process called saltatory conduction, making them travel faster than along an unmyelinated axon.
- Travels faster because deploarisation only has to occur in a few places, rather than along the whole axon as it does with an unmyelinated neurone.
Factors affecting speed of action potential
- Myelin sheath- saltatory conduction is faster
- Diameter of axon- larger diameters have faster potentials as there's less leakage of ions from a larger axon. This allows deploraisation to travel quicker as there's less resistance
- Temperature- higher temp creates faster speed as the ions diffuse faster. But at around 40 degrees, the enzymes controlling the sodium potassium pump begin to denature and the speed decreases
Structure of a synapse
This is teh point where 2 neighbouring neurones meet and communicate with each other:
- Synapses send info by sending neurotransmitters across the synpatic cleft
- The presynpatic neurone has a 'synaptic knob' at the axon terminal, which is a swelling that contains vesicles with neurotransmitters inside
- Neurotransmitters are made in the axon of the pre-synpatic neurone; the synaptic knob processes many mictocondria and RER in order to make the neurotransmitter
Features of synpases
- Unidirectionality- impulses can only travel in order direction, as the receptor sites are only in the post-synpatic membrane. Neurotransmitters are then removed from the cleft so the response doesn't keep happening
- Spatial summation- many neurones connecting to one neurone with their combined amount of neurotransmitter being enough to reach the threshold in the postsynaptic membrane
- Temporal summation- 2/more nerve impulses arrive in quick succession from the same presynaptic neurone; the increased neurotransmitter makes an action potential more likely
- Inhibition- inhibitory synpases make it less likely a new action potential will be created on the postsynpatic neurone by releasing a neurotransmitter that binds to the chloride ion (Cl-) channels on postsynpatic neurone, causing them to open and Cl- move in. This causes the opening of the K+ channels, cause it to move out into the synpase. Creates hyperpolarisation (-80mV instead of -65), meaning a lot more sodium ions that ususal will be needed to create an action potential. Excitatory neurotransmitters depolarise the neurone- action potential fires if threshold is reached
- Synpases that produce new action potentials when a neurotransmitter binds to them are called excitatory synpases
ACh- cholinergic synapse
A cgolinergic synpase is one where acetylcholine (ACh) is released- made of acetyl and choline. These synpases occur in the CNS and at neromuscular junctions in vertibrates:
- Action potential arrives at synpatic knob, stimulating voltage gates calcium channels to open, and Ca2+ to enter the knob via facilitated diffusion. The influx causes the synaptic vesicles to fuse with presynpatic membrane and release ACh into the cleft via exocytosis
- ACh diffsues across and binds to cholinergic receptors found on the sodium channels of the postsynaptic membrane. This causes them to open, allowing an influx of Na+ to diffuse down a concentration gradient into the membarne, depolarising it, An action potential will then be created if the threshold is reached
- ACh is removed from the synaptic cleft so the response doesn't keep happening. It's broken down by enzyme acetylcholinesterase, breaking it down into acetyl and choline. The products are reabsorbed by the presynpatic neurone, and ATP from the mitochondria recombines them into ACh,
- Without ACh in the receptor sites, the sodium channels close
Effects of drugs on synpases
- Some drugs stimulate the nervous system by creating more action potentials in postsynaptic neurones. For example, drugs the same shape as the neurotransmitter can mimic their action at receptors, stimulating the release of more neurotransmitter or inhibiting the enzyme that breaks it down. This aims to enhance the body's responses to impulses passed along the postsynaptic neurone
- Some drugs inhibit the nervous system by creating fewer action potentials in postsynaptic neurones. For example, drugs can inhibit the release of neurotransmitters- fewer receptors activared or can block receptors on the postsynaptic receptors so they can't be activated by neurotransmitters. Aims to reduce impulses passed along the postsynaptic neurone
The effects of drugs on synapses depends upon the type of neurotransmitter- a drug that inhibits an excitatory neurotransmitter will reduce an effect, but one that inhibits an inhibitory neurotransmitter will enhance a particular effect
- Muscles are effectors that respond to stimuli by bringing about movement. Skeletal muscle makes up the bulk of body muscle in vertebrates. It is attached to skeletal bone, and operates under volunatry control.
- Skeletal muscle is attached to bones by tendons, with ligaments attaching bones to other bones.
- Pairs of skeletal muscles contract and relax to move bones to a joint. Skeletal bones are incompressible and rigid, so act as levers and give the muscles something to pull against
- Muscles that work together are called 'antagonistic pairs', with the contracting muscle being the agonist and the relaxing musce being the antagonist
Overall skeletal muscle structure
- Skeletal muscle is made up of striped muscle fibres and controls voluntary reactions. The muscle fibre has a cytoplasm called a sacroplasm, with separate cells being joined by shared nuclei and sacroplasms to ensure junctions between muscle cells don't deduct from the overall strength of the muscle. This makes muscle fibres multinucleate.
- The sarcoplasm has a high concentration of mitochondria (ATP) and endoplasmic reticulum, and is mostly found around the circumference of the fibre. It also contains smaller muscle fibres cakked myoibrils, which can collectively be very powerful.
- The sarcoplasmic reticulum stores and releases calcium ions needed for muscle contraction
- The cell membrane of muscle fibres is called the sarcolemma, and has traverse tubules that fold into the sacroplasm to ensure electrical impulses reach all of the muscle fibre
Microscopic structure of myofibrils
Myofibrils are made up of 2 types of protein filament:
- Action- thin filaments of two wtisted strands with tropomyosin running down the middle
- Myosin- thicker filaments, with long tails and myosin heads that project to the side
When looking at a myofibril under a microscope, it appears striped due to the pattern of alternating light and dark bands. I bands are lighter as they only contain actin filaments. A bands are the darkest as rget contain both filaments as they overlap. The H-zone in the middle of A bands is slightly lighter, as it only contains myosin filaments. Down the centre of this is an M line, that marks the middle of the sarcomere. The centre of the I bands is marked by a z line. A sarcomere is the space in between adjacent z lines.
When muscles contract, the space between the z lines gets smaller, changing the pattern of light and dark bands.
Types of muscle fibre
Slow twitch muscles:
contract sowly, weaker contractions, endurance, posture, calf muscles, aerobic respiration, large number of mitochondria present, high myoglobin concentration (stores oxygen), less sarcoplasmic reticulum
Fast twitch muscles:
Contract quickly, powerful contractions, short periods of time, intense exercise, biceps, thicker, shorter and more myosin, high glycogen concentration, anaerobic respiration, lots of phosphocrestine in cytoplasm, more sarcoplasmic reticulum (calcium ions), easily fatigued- lactate build up
Sliding Filament Theory
This explains muscle contraction by saying actin and myosin filaments slide over each other to make sacromeres contract, rather than the myofilaments themselves contracting. This stimulates the contraction of many sacromeres, causing muscle fibres to contract. As the sacromeres return to their original length, the muscle relaxes.
If this theory is correct, a greater overlap of myofilaments should be seen in contracted muscles. When a muscle contracts, a number of changes occur in sacromeres; I bands become narrower, z lines move closer together and the H zone becomes shorter (A bands stay the same width)
Proteins involved in the theory include:
- myosin- which is made of two types of protein; a fiborous protein arranged in a tail, and a globular protein that forms the head
- Actin is a globular protein with molecules that are arranged to form a helical strand
- Tropomyosin form long thin threads that are wound around actin filaments
Myosin has globular heads that're hinged, so they can move back and forth. Each one has a binding site for actin and another for ATP. Actin too has a binding site for myosin that allowed them to form cross-bridges by binding and flexing in unison. This allows them to them pull the actin filaments along the myosin, become detached and then use the ATP to re-attach themselves further along the actin filaments
Tropomyosin allows the myofilaments to move past each other- in resting muscles, this is what blocks the actin-myosin binding site, preventing the cross bridges from forming
Muscle stimulation- Action potentials reach many neuromuscular junctions simultaneously, sending the action potential across the synapse to the muscle
- The action potential depolarises the sarcolemma; this continues down the T-tubules to the sacroplasmic reticulum, causing the calcium channels to open and release stored calcium down a concentration gradient into the sacroplasm.
- The calcium binds to a protein called troponin, which is attached to tropomyosin, causing it to change shape and release the tropomyosin from the actin-myosin binding site. This allows the myosin heads to bind to it, forming cross bridges
- The myosin heads change angle to bind, releasing the molecule of ADP that was attached to it, and pulling the actin towards the centre of the sarcomere (power stroke). ATP then binds to the head, causing it to detach from the actin.
- The calcium ions activate ATP hydrolase, hydrolysing ATP to provide the energy for the head to detach and return to its original position. It reattaches itself further along and the process repeats as long as calcium ions are present.
When muscle stimulation stops, calcium ions leave their binding sites and are moved by active transport back into the endoplasmic reticulum (using enery from the ATP hydrolysis). This allows the tropomyosin to block the actin mysoin binding sites again, preventing the cross bridges form being fomed. This causes the contraction to cease.
The antagonistic muscles pull the actin filaments out from between the myosin back to their relaxed position. This lengthens the sacromere back to its original state.
Energy supply for muscle contraction
- Aerobic respiration- most ATP is regenerated from ADP during respiration of pyruvate (then in OP) in mitochondria- but only works if there's sufficient oxygen present. Good for long, low-intensity periods of exercise
- Anaerobic respiration- useful in very active muscles- demand for ATP is greater than the rate blood can supply the oxygen. But, as lactate quickly builds up during lactate fermentation, it causes muscle fatigue. Good for short, intense bursts of exercise
- ATP- Phosphocreatine (PCr) System- another way of overcoming oxygen shortage. ATP is produced by phosphorylating ADP with a phosphate group from PCr. This is because PCr can't directly supply energy to muscles, so instead regenerates ATP. PCr is stored in muscles as a reserve supply of phosphates, with this system regenerating ATP very quickly; however PCr runs out in a few seconds. As well as producing ATP, it produces creatine (Cr). The system is both anaerobic and a lactic
Homeostasis is the maintenance of a stable internal environment. This 'internal environment' consists of blood and the tissue fluid that surrounds cells; the use of control systems allows this to remain roughly constant to protect from changes to the external environment, let cells function normally and protect them from damage. It's esp important to maintain core body temp and blood pH as they influence enzyme activity, which controls the rate of metabolic reactions:
- If body temp is too high, enzyme denatures, it can't act as a catalyst and metabolic reactions are less efficient. If it's too low, enzyme activity reduces, reducing rate of reactions. 37 degrees is the optimum temp in humans
- If blood pH is too low/high, enzymes are denatures. Optimum pH is around 7 in humans
Also need to maintain blood glucose conc as it's needed for energy and impacts blood water potential. If glucose conc is too high, water potential is reduced- water exits cells via osmosis- lysis. If it's too low, it impairs cell activity- not enough glucose for respiration- can't provide energy.
Organisms that can maintain a constant internal environment are more independent of changes to their external environment- may have a wider geogrpahical field.
- Receptors- thermoreceptors in the skin and hypothalamus
- Coordinator- the thermoregulatory centre in the hypothalamus- subdivided into heat gain and heat loss centres
- Effectors- sweat glands, hair errector muscles, aterioles supplying blood to skin capillaries etc
Sweat glands produce sweat onto the skin. The water has a high latent heat of vaporisation, allowing the water loss to cool the organism down without losing too much water
The control of a self-regulating system involves the following stages:
- the optimum point- the point at which the system operates best. It's monitored by a
- receptor- detects any deviation from the optimum point and informs the
- coordinator- which coordiates info from receptors and sends instructions via an electrical impulse to an appropriate
- effector- a muscle/gland which brings about the changes needed to return the system to the optimum point. This return to normality creates a
- feedback mechanism- by which a receptor responds to a stimulus created by the change to the optimum point. Most biological systems make use of negative feedback mechanisms, which bring about the reversal of any changes in conditions
- Positive feedback- amplifies the orginial change, causing effectors to further increase the level away from the normal level. This is useful to rapidly activate something. It also occurs when a homeostatic system breaks dow
- Negative feedback- occurs when there is a deviation from the optimum level and works to restore this by reverting any changes made. However, it may not work if the change is too big- effectors may not be able to counteract.
Homeostasis allows multiple negative feedback mechanisms for each thing being controlled, giving you more control ober changes in your internal environment, as you can actively increase or decrease a level so it returns to normal. This produces a faster response with greater control.
It's important that info provuded by recpetors is analysed by the coordinator before action is taken. This means the info must be analysed from all the detectors so that they brain can decide the best course of action. The control centre must then coordinate the actions of the effectors so they can operate in harmony.
Control of blood glucose
- produced in endocrine glands and secreted directly into the blood. They act as messengers between these glands and their target organs/tissues
- carried in blood plasma to target cells, which are complementary to specific cells. They then activate these cells, triggering a response
- effective in very low concentrations, producing widespread and lasting effects
Factors influencing blood glucose concentration
Blood glucose comes from three sources:
- directly from the diet- absorption of glucose
- from glyconeogenesis
- from glycogenolysis of glycogen storesd in liver and muscle cells
The pancreas and blood glucose
The pancreas is a gland located in the upper abdomen; it produced enzymes for digestion and hormones (insulin and glucagon) for regulating bloof glucose concentration. Insulin and glucagon are secreted on cells within the pancreas called islets of Langerhans. These cells include:
- Alpha cells, which are larger, and secrete glucagon. When alpha cells detect that blood gluocse conc has fallen too low, they secrete glucagon which binds to receptors on cell-surface membrane of liver cells, activating enzymes in the liver that convert glycogen to glucose (glucogenolysis) and those involved in gluconeogenesis. Glucagon also decreases the rate of respiration of glucose in cells. Glucagon production stops when glucose levels raise and return to normal (negative feedback)
- Beta cells, which are larger and secrete insulin. When beta cells detect glucose is too high, they secrete insulin, which binds to receptors on liver and muscle cells. This alters structure of glucose carrier proteins, increasing the permeability or cell membrane to glucose so they take in more glucose. This also increases the rate of respiration of glucose in cells (esp muscle cells). Insulin activates enzymes in the liver and muscles to convert glucose to glycogen (glycogenesis). As glucose levels lower and return to normal, insulin release stops (negative feedback)
This is a metabolic disorder caused by an inability to control blood glucose concentration due to a lack of insulin or loss of responsiveness to it.
- Type I- immune system attacks beta cells in the islets of langerhands so they can't produce insulin. This means that after eating, bloof glucose conc rises and stays high, causing hyperglycaemia. The kidenys can't reabsorb all of the glucose, so some of it is excreted in the urine. This is treated with insulin therapy; has to be injected, or would be broken down by enzymes in the mouth. Dose has to match glucose intake, as too much insulin results in hypoglycaemia. Eating regularly and controlling sugar intake can help to manage it.
- Type II- usually occurs later in life and often linked to obesity. Poss because of B cells not producing enough insulin and also because the insulin receptors on liver and muscle cells don't respond properly, due to high levels of insulin making them less responsive. May also be due to an inadequate supply of insulin. It's usually controlled by regulating carb intake and matcing this to the amount of exercise done. Also can lose weight. Eventually, insluin injections may need to be used.
The liver and blood glucose
Insulin and glucagon have their impacts within the liver. There are 3 possible effects that they can produce:
- glycogenesis- conversion of glucose to glycogen. Occurs when blood glucose in too high, so the liver converts it. Blood can store 75-100g of glycgen. This can maintain blood glucose for approximately 12 hours when the body is at rest
- glycogenolysis- breakdown on glycohen into glucose. The liver can convert stored glucogen if glucose concentration is too low
- gluconeogenesis- production of glucose from non-carbohydrate sources such as glycerol and amio acids. This occurs if the glycogen supply has been exhausted
The Kidneys- overview
- Control of blood water potential via homeostasis is 'osmoregulation'; this is carried out my a part of the kidneys called nephrons
- One of the main roles of the kidney is to filter out substances such as water and small molecules (e.g. urea, salt and sugar) when blood passes through capillaries in the cortex of the kidney. This is known as ultrafiltration; useful substances are then reabsorbed into the blood during selective reabsoption. Following this, the remaining unwanted substanes pass along into the bladdee and are excreted as urine
Structure of the Kidney
Structure of nephron
- Blood arrives from the renal artery, entering the afferent arteriole in the kidney's cortex, The arterioles branch into a bundle of capillaries that form a knot called the glomerulus. This is held within Bowman's capsule.
- The afferent arteriole that takes blood into the glomerulus has a larger diameter than the efferent arteriole, which takes it away. This puts the blood under high pressure as it leaves the glomerulus.
- This high pressure forced liquid and small molecules in the blood out of the capillaries and into Bowman's capsule. This includes water, amino acids, glucose, urea and inorganic ions. Blood cells and proteins are too large to be forced out, so remain in the capillaries. This means that the blood in the capillaries is left with a very low water potential, helping the capillaries to later reasorb enough water back into the blood.
- The barrier between the blood in the capillaries and the lumen of Bowman's capsule consists of the endothelium, basement membrane and podocytes. When they pass through, they enter the nephron tubules. These substances are known as 'glomerular filtrate'
- Selective reasbroption then occurs as the filtrate passes along the nephron, with the remaning filtrate flowing through the collecting duct and passing out of the kidney along the ureter
The nephron- PCT cells
- Selective reabsorption occurs as the glomerular filtrate flows along the proximal convoluted tubule, through loop of Henle and along the distal convoluted tubule. Most reabsorption occurs from the PCT where 85% of filtrate is reabsorbed.
- Useful substances leave the nephron tubules and enter the capillary network. All sugars (glucose and amino acids etc), most salts and some water are reabsorbed by the PCT
PCT cell adaptation:
- The epithelium on the wall of the PCT (tissue between the tubule and the capillaries) has microvilli to provide a large SA for the reabsoption of useful materials from the tubules into the blood in the capillaries.
- They have many mitochonria in the cell cytoplasm- ATP needed for active transport
- Have co-transport proteins in the membrane furtherest from the capillaries and sodium potassium pumps in the membrane closest to them
The nephron- selective reabsorption
- Sodium potassium pump moves Na from the PCT cells into the capillaries, lowering sodium concentration within the PCT cells. This allows Na to be transported into the cells at the other side of the membrane by facillitated diffusion, bringing glucose or amino acids with it via the co-transporter proteins.
- As the concentration of the useful molecules increases (e.g. glucose), they can then diffuse out of the other side of the PCT membrane, into the tissue fluid that is directly before the capillaries. Here, they diffuse into the blood and are then carried away.
- This reabsorption of glucose and other materials reduces the water potential within the cells and increases it in the tubule fluid (water doesn't bind to the solutes anymore). So, water travels through the PCT cells and into the capillary, entering the blood via osmosis. It is reabsorbed from the PCT, loop of Henle, DCT and the collecting duct.
- The filtrate that remains is urine, which passes along the ureter to the bladder. Urine is usually made of water and dissolved salrs, urea and other substances such as horomes and excess vitamins. It doesn't contain proteins, blood cells or glucose.
- Water potential of fluid- initially decreased by addition of salts and removal of water, then increased as salts are removed by active transport (loop of Henle), then decreased at collecting duct by removal of water- ensures urine has a low water potential.
Control of blood water
Water is lost during excretion, as mammals excrete waste products in solution. It's also lost in sweat. Because of this, it's important for osmoregulation to occur.
If blood water potential is too low (dehydration), more water is reabsorbed during osmosis into the blood via the nephron tubules. This produces urine that is more concentrated, ensuring less water is lost during excretion. Conversly, if blood water potential is too high. less water is reabsorbed, meaning the urine is more dilute and more water is lost during excretion.
Although water is reabsored along the majority of the nephron, it mainly takes place in the loop of Henle. DCT and the collecting duct. The volume of water that's reabsorbed by the DCT and collecting duct is controlled by hormones.
The Loop of Henle
Located in the medulla of the kidney, the loop of Henle is made up of ascending and descending 'limbs'. These control the movement of sodium ions so that the water can be reabsorbed by the blood. This concentrates the urine so it has a lower water potential than the blood. The loop acts as a countercurrent multiplier:
- Near the top of the ascending limb, Na+ is actively transported out using ATP from the mitochondria in cell wall. The AL is impermeable to water, so water stays inside the tubule, creating a low water potential in the medulla due to the high conc of ions (NaCl)
- DL is permeable to water, so the conc gradient causes water to move out of here into medulla by osmosis. The water enters the blood capillaries via osmosis and is carried away. This makes a more concentrated filtrate as the ions can't diffuse out (DL isn't permeable to them).
- The filtrate loses water in this way as it moves down the DL, lowering the water potential. It reaches the lowest potential at the tip of the hairpin
- At the thin AL, Na+ diffuse out filtrate passively and are actively transported out at the thick AL. As AL is impermeable to water, it stays in, further increasing its water potential.
- In the interstitial space (betwen the limbs) there is a conc gradient- highest water/lowest ions in the coretx; this reverses the further into the medulla you go. So, the longer the loop, and
The Loop of Henle (2)
deeper you go into the medulla, the lower the water potential in the medulla
- Water moves out of the DCT by osmosis and is reabsorbed into the blood
- The collecting duct is permeable to water, so when the filtrate moves down it, water moves out of the duct and into the blood vessels that occupy this space, via osmosis
- When water passes out of the filtrate, its water potential is lowered, but at the same time, the water potnetial in the intersitial space is also lowered (due to ion movement), meaning that water does continue to move out via osmosis down the whole of the collecting duct. The counter-current multiplier ensures there's always a water potential gradient drawing water out of the tubule.
- Water passing out of the collecting duct does so through water-specific channel proteins (aquaporins)
Counter-current multiplier- the filtrate in the collecting duct with a lower water potential meets interstitial fluid with an even lower water potential- this means that the small water potential gradient between the two is able to exist for the whole length of the collecting duct, ensuring there's a steady flow of water to enter the interstitual fluid and then the blood. If the two flows occured in the same direction, less water would be able to enter the blood.
Water reabsorption and hormones
- Blood water potential is monitored by osmoreceptors in the hypothalamus. When water potential decreases, water moves out of the osmoreceptor cells by osmosis, causing the cells to decrease in volume. This signals other cells in the hypothalamus to send a signal to the posterior pituitary gland. This gland releases a hormone called antidiuretic hormone (ADH) into the blood.
- ADH controls water reabsorption by making the walls of the DCT and collecting duct more or less permeable to water. Cells in the walls have membrane bound receptors for ADH; if it binds to them, a chain of enzyme controlled reactions within the cell occurs, causing aquaporins to be inserted in the cell surface membrane, making the walls more permeable to water.
- A higher permeability to water causes more water to be reabsorbed from the tubules into the medulla and then the blood via osmosis. This means that a small amount of concentrated urine will be produced, resulting in less water being lost from the body
Blood ADH levels
Blood ADH levels rise when you're dehydrated: water blood content drops, so water potential drops. This is detected by osmoreceptors and posterior pituitary gland is stimulated to release more ADH into the blood. This causes the DCT and CD to become more permeable so more water is reabsorbed into the blood by osmosis. Small amount of highly concentrated urine is produced
Blood ADH levels fall when you're hydrated: water content of blood rises, so water potential rises. Detected by osmoreceptors, so PPG releases less ADH into the blood. The cell surface membrane folds inwards to create new vesicles that remove the aquaporins from the membrane, causing the membranes to become less permeable so less water is reabsorbed into the blood by osmosis. A large amount of dilute urine is produced and more water is lost.