Unit 6 Flashcards
Stimulus
A change in an organism’s internal or external environment.
Why is it important for organisms to respond to stimuli?
Increased chance of survival.
Tropism
-Growth of a plant in response to a directional stimulus.
-Positive tropism- towards a stimulus.
-Negative tropism- away from a stimulus.
Role of growth factors in flowering plants
-Specific growth factors move from growing regions to tips of roots or shoots.
-They regulate growth in response to directional stimuli.
How indoleacetic acid (IAA) affects cells in roots and shoots?
-In shoots, high conc of IAA stimulates cell elongation.
-In roots, high concentrations of IAA inhibit cell elongation.
Gravitropism in flowering plants
-Cells in tips of roots produce IAA.
-IAA diffuses down root.
-IAA moves to lower side of root so concentration increases.
-In the roots, IAA inhibits cell elongation.
-Upper cell elongates and roots bend towards gravity.
Phototropism in flowering plants
-Cells in tips of shoot produce IAA.
-IAA diffuses down shoot.
-IAA moves to shaded side of shoot so concentration increases.
-In the shoots, IAA stimulates cell elongation.
-Cells grow and bend towards the light.
Taxes
-Tactic response.
-Directional response.
-Movement towards or away from a directional stimulus.
Kinesis
-Kinetic response.
-Non-directional response.
-Speed of movement or rate of direction change changes in response to a non-directional stimulus.
-Depending on intensity of stimulus.
Basic structure of Pacinian corpuscle
-Lamaellae (layers of connective tissue).
-Sensory neurone ending.
-Sensory neurone axon.
-Gel.
-Myelin sheath.
-Stretch mediated sodium ion channel.
How is a generator potential established in a Pacinian corpuscle?
-Mechanical stimulus- pressure deforms lamellar and stretch mediated sodium channels open.
-Na+ diffuse into sensory neurone.
-Greater pressure causes more Na+ channels to open and more Na+ to enter.
-This causes depolarisation which leads to a generator potential.
-If generator potential reaches threshold, it triggers an action potential.
What does the Pacinian corpuscle illustrate?
-Receptors respond only to specific stimuli.
-Stimulation of a receptor leads to the establishment of a generator potential.
-When threshold is reached, action potential sent (all or nothing principle).
Rods sensitivity to light intensity
-Several rods connected to a single neurone.
-Spatial summation to reach threshold (as enough neurotransmitter released) to generate an action potential.
Cones sensitivity to light
-Each cone connected to one single neurone.
-No spatial summation.
Rod cells visual acuity
-Low visual acuity.
-Several rods connected to a single neurone.
-Several rods send a single set of impulses to brain (can’t distinguish between separate sources of light).
Cone cells visual acuity
-High visual acuity.
-Each cone connected to a single neurone.
-Cones send separate impulses to brain (can distinguish between 2 separate sources).
Rod cells sensitivity to colour
-1 type of pigment
-Monochromatic vision.
Cone cells sensitivity to colour
-3 types of cones- red-, green- and blue-sensitive.
-Different optical pigments- absorb different wavelengths.
-Stimulating different combinations of cones gives range of colour perception.
Cardiac muscle is myogenic?
-It can contract and relax without receiving electrical impulses from nerves.
Nodes on the heart
-Sinoatrial Node (SAN)
-Atrioventricular node (AVN)
-Purkyne tissue
-Bundle of His
Myogenic stimulation of the heart
-Sinoatrial node (SAN) acts as a pacemaker- releases regular waves of electrical activity across atria.
-Causes atria to contract simultaneously.
-Non-conducting tissue between atria/ ventricles prevents impulse passing directly to ventricles.
-Preventing immediate contraction of ventricles.
-Waves of electrical activity reach atrioventricular node (AVN) which delays impulse.
-Allowing atria to fully contract and empty before ventricles contract.
-AVN sends wave of electrical activity down bundle of His, conducting wave between ventricles to apex where it branches into Purkyne tissue.
-Causing ventricles to contract simultaneously from the base up.
Where are chemoreceptors and pressure receptors located?
In the aorta and carotid arteries
Rise in blood pressure, rise in pH
-Baroreceptors detect rise in bp and chemoreceptors detect blood fall in blood CO2 conc or rise in blood pH.
-Send impulses to medulla oblonganta/ cardiac control centre.
-Sends more frequent impulses to SAN along parasympathetic neurones.
-So less frequent impulses sent from SAN to AVN.
-Cardiac muscle contracts less frequently.
-Heart rate decreases.
Fall in blood pressure, fall in blood pH
-Baroreceptors detect fall in bp and chemoreceptors detect blood rise in blood CO2 conc or fall in blood pH.
-Send impulses to medulla oblonganta/ cardiac control centre.
-Sends more frequent impulses to SAN along sympathetic neurones.
-So more frequent impulses sent from SAN to AVN.
-Cardiac muscle contracts more frequently.
-Heart rate increases.
Structure of a myelinated motor neurone
-Dendrites
-Cell body (soma)
-Axon
-Myelin sheath
-Node of ranvier
Resting potential
Inside of the axon has a negative charge relative to the outside.
How is resting potential established?
-Na+/K+ pump actively transports 3Na out of the axon and 2K into the axon.
-Creates an electrochemical gradient.
-Higher K+ conc inside and higher Na+ conc outside.
-Differential membrane permeability.
-More permeable to K+- moved out by FD.
-Less permeable to Na+ (closed channels).
Stimulus
-Na+ channels open, membrane permeability to Na+ increases.
-Na+ diffuse into the axon down electrochemical gradient (causes depolarisation).
Depolarisation
-If threshold potential is reached, an action potential is triggered.
-As more voltage-gated Na+ channels open (positive feedback effect).
-More Na+ diffuse in rapidly.
Repolarisation
-Voltage-gated Na+ channels close.
-Voltage-gated K+ channels open, K+ diffuse out of axon.
Hyperpolarisation
-K+ channels slow to close so there’s a slight overshoot.
-Too many K+ diffuse out.
-Na+/K+ pump restore resting potential.
Action potential graph
Draw and label.
All-or-nothing principle
-For an action potential to be produced, depolarisation must exceed threshold potential.
-Action potentials produced are always same magnitude/size/peak at same potential.
-Bigger stimuli increase frequency of action potentials.
Action potential- non-myelinated axon
-Action potential passes as a wave of depolarisation.
-Influx of Na+ in one region increases permeability of adjoining region to Na+ by causing voltage-gated Na+ channels to open so adjoining region depolarises.
Action potential- myelinated axon
-Myelination provides electrical insulation.
-Depolarisation of axon at nodes of Ranvier only.
-Resulting in saltatory conduction (local currents circuits).
-So there is no need for depolarisation along the whole length of axon.
Damage to the myelin- slow/ jerky movements
-Less saltatory conduction- depolarisation occurs along whole length of axon.
-Nerve impulses take longer to reach neuromuscular junction, delay in muscle contraction.
-Ions may pass to other neurones.
-Causing wrong muscle fibres to contract.
Refractory period
-Time taken to resture axon to resting potential when no further action potential can be generated.
-As Na+ channels are closed/ inactive/ will not open.
Importance of the refractory period
-Ensures discrete impulses are produced- AP don’t overlap.
-Limits frequency of impulse transmission at a certain intensity- prevents over reaction to stimulus.
-But only up to a certain intensity.
-Also ensures action potentials travel in one direction- can’t be propagated in a refractory region.
-(In the second half of refractory period, an AP can be produced but requires greater stimulation to reach threshold).
Factors that affect speed of conductance
-Myelination
-Axon diameter
-Temperature
Myelination
-Depolarisation at Nodes of Ranvier only- saltatory conduction.
-Impulse doesn’t travel/ depolarise whole length of axon.
Axon diameter
-Bigger diameter means less resistance to flow of ions in cytoplasm.
Temperature
-Increases rate of diffusion of Na+ and K+ as more KE.
-But proteins/ enzymes could denature at a certain temp.
Cholinergic Synapse
-A gap in between two neurones that uses the neurotransmitter acetylcholine (ACh).
-Draw it!!!
Describe transmission across a cholinergic synapse
-Depolarisation of pre-synaptic membrane causing opening of voltage-gated Ca2+ channel.
-Ca2+ diffuse into pre-synaptic knob.
-Causing vesicles containing ACh to move and fuse with pre-synaptic membrane.
-Releasing ACh into the synaptic cleft by exocytosis.
-ACh diffuses across synaptic cleft to bind to specific receptors on post-synaptic membrane.
-Causing Ligand-gated sodium channels to open.
-Na+ diffuse into post-synaptic knob causing depolarisation.
-If threshold is met, AP is initiated.
What happens to acetylcholine after synaptic transmission?
-It is hydrolysed by acetylcholinesterase.
-Into acetate and choline.
-Products are reabsorbed by the presynaptic neurone.
-To stop overstimulation- if not removed it would keep binding to receptors causing depolarisation.
Unidirectional nerve impulses
-Neurotransmitter only made in pre-synaptic neurone.
-Receptors only on post-synaptic membrane.
Summation by synapses
-Addition of a number of impulses converging on a single post-synaptic neurone.
-Causing rapid buildup of neurotransmitter (NT).
-So threshold more likely to be reached to generate an AP.
Spatial summation
-Many pre-synaptic neurones hare one synaptic cleft.
-Collectively release sufficient neurotransmitter to reach threshold to trigger an action potential.
Temporal summation
-One pre-synaptic neurone releases neurotransmitter many times over a short time.
-Sufficient neurotransmitter to reach threshold to trigger an action potential.
Inhibition by inhibitory synapses
-Inhibitory neurotransmitters hyperpolarise postsynaptic membranes as:
-Cl- channels open- Cl- diffuses in.
-K+ channels open- K+ diffuses out.
-This means the inside of axon has a more negative charge relation to outside (below resting potential).
-More Na+ required to enter for depolarisation.
-Reduces likelihood of threshold being met and AP being established.
Structure of a neuromuscular junction
-Receptors are on muscle fibre sarcolemma instead of postsynaptic membrane and there are more.
-Muscle fibre forms clefts to store enzyme to break down neurotransmitter.
Compare transmission across cholinergic and neuromuscular junctions.
-Neurone to neurone vs motor neurone to muscle.
-Excitatory or inhibitory vs always excitatory.
-AP initiated in postsynaptic neurone vs AP propagates along sarcolemma down T tubules.
Effect of drugs on a synapse
-Some drugs stimulate the nervous system, leading to more action potentials.
-Similar shape to neurotransmitter.
-Stimulate release of more neurotransmitter.
-Inhibit enzyme that breaks down neurotransmitter- Na+ contains to enter.
-Some drugs inhibit the nervous system, leading to fewer action potentials.
-Inhibit release of neurotransmitter.
-Block receptors by mimicking shape of neurotransmitter.
How muscles work?
-Work in antagonistic pairs and pull in opposite directions.
-One muscle contracts (agonist)- pulling on bone- producing force.
-One muscle relaxes (antagonist).
-Skeleton is incompressible so muscles transmit force to bone.
Gross structure of skeletal muscle
-Made of many bundles of muscle fibres (cells) packaged together.
-Attached to bones by tendons.
Microscopic structure of skeletal muscle
-Muscle fibres contain:
-Sarcolemma- cell membrane which folds inwards to form transverse T tubules.
-Sarcoplasm- cytoplasm.
-Multiple nuclei.
-Many myofibrils.
-Sarcoplasmic reticulum- endoplasmic reticulum.
-Many mitochondria.
Ultrastructure of a myofibril
-Two types of protein filaments arranged in parallel- myosin (thick) and actin (thin).
-Arranged in functional units called sarcomeres.
-Ends- Z line
-Middle- M line
-H zone- contains only myosin.
Banding pattern seen in myofibrils
-I-band- light bands containing only thin actin filaments.
-A-band- dark bands containing thick myosin filaments.
-H zone contains only myosin.
-Darkest region contains overlapping actin and myosin.
Evidence for sliding filament theory
-Myosin heads slide actin along myosin causing the sarcomeres to contract.
-Stimultaneous contraction of many sarcomeres causes myofibrils and muscle fibres to contract.
-When sarcomeres contract:
-H zones get shorter
-I band get shorter
-A band stays the same
-Z lines get closer
Muscle contraction mechanism
-Depolarisation spreads down sarcolemma via T tubules causing Ca2+ release from sarcoplasmic reticulum which diffuse to
myofibrils.
-Ca2+ bind to tropomyosin causing it to move which exposes binding sites on actin.
-Allowing myosin head, with ADP attached, to bind to binding sites on actin which forms an actinmyosin crossbridge.
-Myosin heads change angle, pulling actin actin along myosin (ADP released), using energy from ATP hydrolysis.
-New ATP binds to myosin head causing it to detach from binding site.
-Hydrolysis of ATP by ATP(hydrol)ase (activated by Ca2+) releases energy for myosin heads to return to original position.
-Myosin reattaches to a different binding site further along actin. Process is repreated as long as Ca2+ concentration is high.
During muscle relaxation
-Ca2+ actively transported back into the endoplasmic reticulum using energy from ATP.
-Tropomyosin moves back to block myosin binding site on actin again.
-So no more actinmyosin crossbridges can form.
Role of phosphocreatine
-Source of Pi.
-Rapidly phosphorylates ADP to regenerate ATP.
-ADP + phosphocreatine = ATP + creatine.
-Runs out after a few seconds, used in short bursts of vigorous exercise.
-Anaerobic and alactic.
Slow twitch skeletal muscle fibres
General properties
-Specialised for slow, sustained contractions- long distance running, posture.
-Produce more ATP slowly from aerobic respiration.
-Fatigues slowly.
Location
-High proportion in muscles used for posture- back, calves.
-Legs of long distance runners.
Structure
-High conc of myoglobin- stores oxygen for aerobic respiration.
-Many mitochondria- high rate of aerobic respiration.
-Many capillaries- supply high conc of oxygen/ glucose for aerobic respiration and to prevent build-up of lactic acid causing muscle fatigue.
Fast twitch skeletal muscle fibres
General properties
-Specialised for brief, intensive contractions- sprinting.
-Produces less ATP rapidly from anaerobic respiration.
-Fatigues quickly due to high lactate conc.
Location
-High proportion in muscles used for fast movement- biceps, eyelids.
-Legs of sprinters.
Structure
-Low levels of myoglobin.
-Lots of glycogen- hydrolysed to provide glucose for glycolysis, anaerobic respiration which is inefficient so large quantities of glucose required.
-High conc of enzymes involved in anaerobic respiration in cytoplasm.
-Store phosphocreatine.
Homeostasis in mammals
-Maintenance of a stable internal environment within restricted limits.
-By physiological control systems- normally involve negative feedback.
Importance of maintaining stable core temperature
-If temp is too high
-Hydrogen bonds in tertiary structure of enzymes break.
-Enzymes denature, active sites change shape and substrates can’t bind.
-So fewer enzyme-substrate complexes.
-If temp is too low
-Not enough kinetic energy so fewer enzyme-substrate complexes.
Importance of maintaining stable blood pH
-Above or below optimal pH, ionic/ hydrogen bonds in tertiary structure break.
-Enzymes denature, active sites change shape and substrates can’t bind.
-So fewer enzyme-substrate complexes.
Low blood glucose conc (hypoglycaemia)
-Not enough glucose (respiratory substrate) for respiration.
-So less ATP produced.
-Active transport- can’t happen- cell death.
High blood glucose conc (hyperglycaemia)
-Water potential of blood decreases.
-Water lost from tissue to blood via osmosis.
-Kidneys can’t absorb all glucose- more water lost in urine causing dehydration.
Role of negative feedback in homeostasis
-Receptors detect change from optimum.
-Effectors respond to counteract change.
-Returning levels to optimum/normal.
Importance of conditions being controlled by negative feedback
-Departures in different directions from the original state can all be controlled/ reversed.
-Giving a greater degree of control over changes in internal envrionment.
Positive feedback
-Receptors detect change from normal.
-Effectors respond to amplify change.
-Producing a greater deviation from normal.
Factors that influence blood glucose concentration
-Consumption of carbohydrates- glucose absorbed into blood.
-Rate of respiration of glucose.
Glycogenesis
Converts glycose to glycogen
Glycogenolysis
Converts glycogen to glucose
Gluconeogenesis
Converts amino acids and glycerol into glucose.
Action of insulin
-Beta cells in islets of Langerhans in pancreas detect blood glucose concentration is too high- secretes insulin.
-Attaches to specific receptors on cell surface membranes of target cells.
-Causes more glucose channel proteins to join cell surface membrane.
-Increasing permeability to glucose.
-So more glucose can enter cell by facilitated diffusion.
-Activates enzymes involved in conversion of glucose to glycogen.
-Lowering glucose concentration in cells, creating a concentration gradient.
-Glucose enters cell by facilitated diffusion.
Action of glucagon
-Alpha cells of islets of Langerhans in pancreas detect low blood glucose concentration- secretes glucagon.
-Attaches to specific receptors on cell surface membranes of target cells.
-Activates enzymes involved in hydrolysis of glycogen to glucose.
-Activates enzymes involved in conversion of glycerol/ amino acids to glucose.
-Establishes a conc gradient- glucose enters blood by facilitated diffusion.
Role of adrenaline
-Adrenal glands secrete adrenaline.
-Attaches to specific receptors on cell surface membranes of target cells.
-Activates enzymes involved in hydrolysis of glycogen to glucose.
-Establishes a concentration gradient- glucose enters blood by facilitated diffusion.
Second messenger model
-Adrenaline/ glucagon attach to specific receptors on cell membrane
-Activates enzyme adenylate cyclase (changes shape).
-Which converts many ATP to many cyclic AMP (cAMP).
-cAMP acts as the second messenger- activates protein kinase enzymes.
-Protein kinases activate enzymes to break down glycogen to glucose.
Advantage of second messenger model
-Amplifies signal from hormone.
-As each hormone can stimulate production of many molecules of second messenger (cAMP).
-Which can in turn activate many enzymes for rapid increase in glucose.
Causes of type 1 diabetes
-Beta cells in islets of langerhans in pancreas produce insufficient insulin.
-Normally develops in childhood due to an autoimmune response destroying beta cells.
Causes of type 2 diabetes
-Receptor loses responsiveness/ sensitivity to insulin.
-So fewer glucose transport proteins- less uptake of glucose- less conversion of glucose to glycogen.
-Risk factor- obesity.
How can type 1 diabetes be controlled?
-Injections of insulin as pancreas doesn’t produce enough.
-Blood glucose conc monitored with biosensors, dose pf insulin matched to glucose intake.
-Eat regularly and control carbohydrate intake.
-Avoid sudden rise in glucose.
Why insulin can’t be taken as a tablet?
-Insulin is a protein.
-Would be hydrolysed by endopeptidases/ exopeptidases.
How can type 2 diabetes be controlled?
-Not normally treated with insulin injections but may use drugs which target insulin receptors to increase their sensitivity.
-To increase glucose uptake by cells/ tissues.
-Reduce sugar intake- low glycaemic index- less absorbed.
-Reduce fat intake- less glycerol converted to glucose.
-More exercise- uses glucose/ fats by increasing respiration.
-Lose weight- increased sensitivity of receptors to insulin.
Structure of the nephron
-Nephron- basic structural and functional unit of the kidney- millions in the kidney.
-Associated with each nephron are a network of blood vessels.
Bowman’s/ renal capsule
Formation of glomerular filtrate (ultrafiltration)
Proximal convoluted tubule
Reabsorption of water and glucose- selective reabsorption
Loop of Henle
Maintenance of a gradient of sodium ions in the medulla.
Distal convoluted tubule/ collecting duct
Reabsorption of water- permeability controlled by ADH.
Formation of glomerular filtrate
-High hydrostatic pressure in glomerulus as afferent arteriole (in) is wider than efferent arteriole (out).
-Small substances (water, glucose, ions, urea) forced out into glomerular filtrate.
-It is filtered by- pores/ fenestrations between capillary endothelial cells, capillary basement membrane, podocytes.
-Large proteins/ blood cells remain in blood.
Reabsorption of glucose by the proximal convoluted tubule
-Na+ actively transported out of epithelial cells to capillary.
-Na+ moves by facilitated diffusion into epithelial cells down a concentration gradient, bringing glucose against its concentration gradient.
-Glucose moves into capillary by facilitated diffusion down its concentration gradient.
Reabsorption of water by the proximal convoluted tubule
-Glucose etc. in capillaries lower water potential.
-Water moves by osmosis down a water potential gradient.
Features of the cells in the PCT which allow the rapid reabsorption of glucose
-Microvilli/ folded cell-surface membrane- provides a large surface area.
-Many channel/ carrier proteins- for facilitated diffusion/ co-transport.
-Many carrier proteins- for active transport.
-Many mitochondria- produce ATP for active transport.
-Many ribosomes- produce carrier/ channel proteins.
Diabetic person- glucose in urine
-Blood glucose concentration is too high so noy all glucose is reabsorbed at the PCT.
-As glucose carrier/ cotransporter proteins are saturated, working at maximum rate.
Importance of maintaining a gradient of sodium ions in medulla
-So water potential decreases down the medulla- compared to filtrate in collecting duct.
-So a water potential gradient is maintained between the collecting duct and medulla.
-To maximise reabsorption of water by osmosis from filtrate.
Role of loop of Henle in maintaining a gradient of sodium ions in the medulla
Ascending limb-
-Na+ actively transported out (so filtrate conc decreases).
-Water remains as ascending limb is impermeable to water.
-This increases concentration of Na+ in the medulla, lowering water potential.
Descending limb-
-Water moves out by osmosis then reabsorbed by capillaries (so filtrate conc increases).
-Na+ ‘recycled’- diffuses back in.
Why animals have long loops of Henle?
-More Na+ moved out- Na+ gradient is maintained for longer in medulla/ higher Na+ conc.
-So water potential gradient is maintained for longer.
-So more water can be reabsorbed from collecting duct by osmosis.
Reabsorption of water by DCT and collecting duct
-Water moves out of DCT and collecting duct by osmosis down a water potential gradient.
-Controlled by ADH which increases their permeability.
Osmoregulation
Control of water potential of the blood- by negative feedback.
Role of hypothalamus in osmoregulation
-Contains osmoreceptors which detect increase or decrease in blood water potential.
-Produces more ADH when water potential is low or less ADH when water potential is high.
Role of posterior pituitary gland in osmoregulation
Secretes more/less ADH into blood due to signals from the hypothalamus.
Role of antidiuretic hormone (ADH) in osmoregulation
-Attaches to receptors on collecting duct and DCT.
-Stimulating addition of channel proteins (aquaporins) into cell-surface membranes.
-So increases permeability permeability of cells of collecting duct and DCT to water.
-So increases water reabsorption from collecting/ DCT (back into blood) by osmosis.
-So decreases volume and increases concentration of urine produced.
