A-LEVEL BIOLOGY, TOPIC EIGHT,8. GREY MATTER. Flashcards
1
Q
ORGANISM SURVIVAL.
A
ORGANISMS MUST RESPOND TO CHANGES IN THEIR EXTERNAL AND INTERNAL ENVIRONMENTS IN ORDER TO SURVIVE.
ORGANISMS NEED TO:
FIND FAVOURABLE EXTERNAL CONDITIONS, FOR EXAMPLE AVIODING LOCATIONS THAT ARE TOO HOT OR COLD.
FIND FOOD.
AVOID HARM, FOR EXAMPLE FROM PREDATORS OR HIGH BLOOD GLUCOSE.
2
Q
STIMULI.
A
SINGULAR STIMULUS.
3
Q
RECEPTOR CELLS, LOCATION.
A
RECEPTOR CELLS, ARE LOCATED IN SENSE ORGANS, SUCH AS THE NOSE AND EYES.
RECEPTOR CELLS CAN ALSO BE FOUND INSIDE THE BODY, SUCH AS PRESSURE RECEPTORS IN THE BLOOD VESSELS.
4
Q
CHANGES IN THE ENVIRONMENT, DETECTION AND RESPONSE.
A
CHANGES IN THE ENVIRONMENT, OR STIMULI, SINGULAR STIMULUS, ARE DETECTED BY SPECIALISED RECEPTOR CELLS.
GIVE THE LOCATION.
RECEPTOR CELLS, SEND SIGNALS VIA EITHER THE NERVOUS SYSTEM OR THE HORMONAL SYSTEM, TO THE BODYS CO-ORDINATION CENTRES IN THE BRAIN OR SPINAL CORD.
SIGNALS ARE THEN SENT ON TO THE PARTS OF THE BODY, WHICH RESPOND, KNOWN AS THE EFFECTORS.
5
Q
EFFECTORS.
A
EFFECTORS CAN EITHER BE MUSCLES OR GLANDS.
AN ARM MUSCLE WOULD RESPOND TO A HOT SURFACE BY CONTRACTING, TO MOVE THE HAND AWAY.
THE PANCREAS RESPONDS TO HIGH BLOOD SUGAR, BY SECRETING INSULIN.
6
Q
THE HUMAN NERVOUS SYSTEM, WHAT DOES IT CONSIST OF?
A
THE HUMAN NERVOUS SYSTEM CONSISTS OF:
CENTRAL NERVOUS SYSTEM, CNS, THE BRAIN AND SPINAL CORD.
PERIPHERAL NERVOUS SYSTEM, PNS, ALL OF THE NERVES IN THE BODY.
7
Q
THE NERVOUS SYSTEM, ROLE AND FUNCTION.
A
THE NERVOUS SYSTEM ALLOWS DETECTION OF STIMULI IN OUR SURROUNDINGS AND THE COORDINATION OF THE BODY’S RESPONSES TO THE STIMULI.
8
Q
THE NERVOUS SYSTEM, NERVES AND NEURONS.
A
INFORMATION, IS SENT THROUGH THE NERVOUS SYSTEM, IN THE FORM OF ELECTRICAL IMPULSES THAT PASS ALONG NERVE CELLS, KNOWN AS NEURONS.
A BUNDLE OF NEURONES IS KNOWN AS A NERVE.
THERE ARE DIFFERENT TYPES OF NEURONES INCLUDING SENSORY NEURONES, RELAY NEURONES, AND MOTOR NEURONES.
9
Q
NERVES, CONNECTION.
A
THE NERVES CONNECT THE RECEPTORS IN THE SENSE ORGANS WITH THE CENTRAL NERVOUS SYSTEM, CNS, AND CONNECT THE CNS, WITH EFFECTORS.
THE CNS, ACTS AS A CENTRAL COORDINATING CENTRE, FOR THE IMPULSES THAT COME IN FROM, AND ARE SENT OUT TO, ANY PART OF THE BODY.
10
Q
NERVE IMPULSES, WHAT DO THEY PASS THROUGH?
A
NERVE IMPULSES PASS THROUGH THE NERVOUS SYSTEM ALONG THE FOLLOWING PATHWAY:
STIMULUS -> RECEPTOR -> SENSORY NEURONE -> THE CENTRAL NERVOUS SYSTEM, CNS -> MOTOR NEURONE -> EFFECTOR.
11
Q
HORMONES.
A
HORMONES ARE CHEMICAL SUBSTANCES, PRODUCED BY ENDOCRINE GLANDS, AND CARRIED BY THE BLOOD.
HORMONES, ARE SOMETIMES KNOWN AS CHEMICAL MESSENGERS.
12
Q
HORMONES, ROLE.
A
HORMONES TRANSMIT INFORMATION, FROM ONE PART OF AN ORGANISM TO ANOTHER, AND BRING ABOUT CHANGE BY ALTERING THE ACTIVITY OF ONE OR MORE SPECIFIC TARGET ORGANS.
HORMONES, CAN LEAVE THE BLOOD, AND BIND TO SPECIFIC RECEPTORS ON THE CELL SURFACE MEMEBRANES OF TARGET ORGANS.
13
Q
HORMONES, ACTION.
A
HORMONES ARE SLOWER IN ACTION THAN NERVE IMPULSES AND ARE THEREFORE USED TO CONTROL FUNCTIONS THAT DO NOT NEED INSTANT RESPONSES.
14
Q
ENDOCRINE GLANDS.
A
ENDOCRINE GLANDS, THAT PRODUCE HORMONES IN ANIMALS, ARE COLLECTIVELY KNOWN AS THE ENDOCRINE SYSTEM.
ENDOCRINE GLANDS, SECRETE HORMONES DIRECTLY INTO THE BLOOD.
ENDOCRINE GLANDS CAN BE STIMULATED TO SECRETE HORMONES, BY THE ACTION OF ANOTHER HORMONE, OR BY THE ARRIVAL OF A NERVE IMPULSE.
15
Q
THE PATHWAY, OF HORMONE ACTION.
A
THE PATHWAY OF HORMONE ACTION IS AS FOLLOWS,
STIMULUSE -> RECEPTORE -> HORMONE -> EFFECTOR.
16
Q
PITUITARY GLAND.
A
THE ‘MASTER GLAND”, SITUATED AT THE BASE OF THE BRAIN.
17
Q
THYROID GLAND.
A
PRODUCES THYROXINE.
18
Q
PANCREASE.
A
PRODUCES INSULIN.
THE PANCREASE PRODUCES HORMONES, TO REGULATE BLOOD GLUCOSE LEVELS, AS WELL AS DIGESTIVE ENZYMES, SUCH AS PANCREATIC AMYLASE, AND LIPASE.
19
Q
ADRENAL GLANDS.
A
PRODUCE ADRENALINE.
20
Q
TESTES.
A
PRODUCE TESTOSTERONE, THE MALE SEX HORMONE.
21
Q
OVARIES.
A
PRODUCE OESTROGEN, THE FEMALE SEX HORMONE.
22
Q
THE NERVOUS SYSTEM V.S, THE ENDOCRINE SYSTEM.
A
MADE UP OF:
THE NERVOUS SYSTEM, IS MADE UP OF NERVES, NEURONES, THE BRAIN, AND THE SPINAL CORD.
THE ENDOCRINE SYSTEM, GLANDS.
TYPE OF MESSAGE:
THE NERVOUS SYSTEM, ELECTRICAL IMPULSE.
THE ENDOCRINE SYSTEM, CHEMICAL HORMONE.
THE SPEED OF TRANSMISSION:
THE NERVOUS SYSTENM, VERY FAST.
THE ENDOCINE SYSTEM, SLOWER.
THE LENGTH OF EFFECT:
THE NERVOUS SYSTEM, SHORT, UNTIL NERVE IMPULSES STOP.
THE ENDOCRINE SYSTEM, LONGER, UNTIL HORMONE IS BROKEN DOWN.
23
Q
NEURONES.
A
NEURONES ARE SPECIALISED CELLS OF THE NERVOUS SYSTEM, WHICH CARRY ELECTRICAL IMPULSES AROUND THE BODY.
A BUNDLE OF NEURONES IS KNOWN AS A NERVE.
24
Q
NEURONES, FEATURES.
A
THERE ARE DIFFERENT TYPES OF NEURONES, BUT THE FOLLOWING FEATURES, ARE FOUND IN ALL TYPES:
A LONG FIBRE, KNOWN AS AN AXON.
A CELL BODY, THAT CONTAINS THE NUCLEUS AND OTHER CELLULAR STRUCTURES.
THE END OF THE AXON, KNOWN AS THE AXON TERMINAL, HAS MANY NERVE ENDINGS.
THE NERVE ENDINGS AT THE AXON TERMINALS, ALLOW NEURONES TO CONNECT TO AND RECIEVE IMPULSES FROM OTHER NEURONES, FORMING A NETWORK FOR EASY COMMUNICATION.
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MYELINATED.
SOME NEURONES ARE MYELINATED, MEANING THAT THEIR AXON IS INSULATED BY A FATTY LAYER, KNOWN AS THE MYELIN SHEATH.
THE MYELIN SHEATH IS MADE UP OF SPECIALISED CELLS, KNOWN AS SCHWANN CELLS, WHICH WRAP THEMSELVES AROUND THE AXON.
THERE ARE UNINSULATED GAPS, BETWEEN THE SCHWANN CELLS, KNOWN AS THE NODES OF RANVIER.
ELECTRICAL IMPULSES, IN MYELINATED CELLS DO NOT TRAVEL DOWN THE WHOLE AXON, BUT JUMP FROM ONE NODE TO THE NEXT, SPEEDING UP IMPULSE TRANSMISSION.
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NON-MYELINATED NEURONES.
IN NON-MYELINATED NEURONES THE AXON, IS NOT STIMULATED BY SCHWANN CELLS.
THE IMPULSE TRAVELS DOWN MORE SLOWLY, AS IT MOVES THROUGH THE ENTIRE LENGTH OF THE AXON.
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DENDRITES.
DENDRITES, ARE LOCATED AT THE NEURONE ENDING.
THEY FORM CONNECTION, WITH MANY OTHER NEURONES.
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HOW MANY MAIN TYPES OF NEURONES ARE THERE?
THERE ARE THREE,3, MAIN TYPES OF NEURONES.
THE SENSORY NEURONES,
THE RELAY NEURONES, AND THE MOTOR NEURONES.
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SENSORY NEURONES.
SENSORY NEURONES, CARRY IMPULSES FROM RECEPTORS, TO THE BRAIN AND THE SPINAL CORD, IN THE CENTRAL NERVOUS SYSTEM, THE CNS.
A CELL BODY, THAT BRANCHES OFF IN THE MIDDLE OF THE AXON.
THE DENTRITES, ARE ATTACHED TO A RECEPTOR CELL.
THE SECTION OF THE NEURONE, THAT LINKS THE AXON TERMINAL WITH THE CELL BODY, IS KNOWN AS A DENDRON.
THE SECTION OF THE NEURONE THAT CONNECTS THE BODY, WITH THE CENTRAL NERVOUS SYSTEM, IS THE AXON.
30
RELAY NEURONES.
RELAY NEURONES, ARE FOUND ENTIRELY WITHIN THE CENTRAL NERVOUS SYSTEM, THE CNS, AND CONNECT SENSORY, AND MOTOR NEURONES.
SHORT NERONES, WITH AXONS, AND HIGHLY BRANCHED DENDRITES.
31
MOTOR NEURONES.
MOTOR NEURONES, CARRY IMPULSES FROM THE CENTRAL NERVOUS SYSTEM, THE CNS, TO EFFECTOR MUSCLES OR GLANDS.
A LARGE CELL BODY AT ONE END, THAT LIES WITHIN THE SPINAL CORD OR BRAIN.
MANY HIGHLY-BRANCHED DENDRITES, EXTEDNING FROM THE CELL BODY, PROVIDING MANY CONNECTIONS, WITH THE AXON TERMINALS OF OTHER NEURONES.
32
RECEPTOR CELLS.
RECEPTOR CELLS DETECT CHANGES IN THE ENVIRONMENT, OR STIMULI.
33
NERVE IMPULSES.
NERVE IMPULSES, TRAVEL FROM THE RECEPTOR CELLS, ALONG SENSORY NEURONS, TO THE CENTRAL NERVOUS SYSTEM, OR THE CNS.
THE CENTRAL NERVOUS SYSTEM, THE CNS, ACTS AS A COORDINATING CENTRE, FOR THE IMPULSES THAT ARRIVE FROM THE RECEPTORS, DETERMINING WHICH PART OF THE BODY NEEDS TO RESPOND AND SENDING OUT A NEW SET OF IMPULSES ALONG MOTOR NEURONS.
MOTOR NEURONS SEND IMPULSES TO THE EFFECTORS, TO BRING ABOUT A RESPONSE.
EFFECTORS, MAY BE MUSCLES OR GLANDS.
34
CHANGING PUPIL DIAMETER.
CHANGING PUPIL DIAMTER, ENABLES THE EYE TO CONTROL THE AMOUNT OF LIGHT HITTING THE RETINA.
35
PUPIL RESPONSE.
THE DIMATER OF THE PUPIL IN THE EYE IS DETERMINED BY TWO,2, SETS OF MUSCLES.
THE CIRCULAR MUSCLES CONTRACT TO CONSTRICT THE PUPIL.
THE RADIAL MUSCLES CONTRACT TO DILATE THE PUPIL.
THE TWO,2, SET OF MUSCLES WORK ANTAGONISTICALLY, MEANING THAT WHEN ONE SET OF MUSCLES CONTRACTS, THE OTHER REALXES, AND VICE VERSA.
BRIGHT LIGHT,
LIGHT RECEPTORS IN EYES,
SENSORY NEURONE,
CNS,
MOTOR NEURONE,
CIRCULAR MUSCLES IN THE IRIS.
CONTRACTION OF THE CIRCULAR MUSCLES IN THE IRIS, OF THE EYE, CAUSES THE PUPIL TO CONSTRICT.
THIS LIMITS THE AMOUNT OF LIGHT ENTERING THE EYE AND PREVENTS DAMAGE TO THE RETINA.
LOW LIGHT,
LIGHT RECEPTORS IN EYES,
SENSORY NEURONE,
CNS,
MOTOR NEURONE,
RADIAL MUSCLES IN IRIS.
CONTRACTION OF THE RADIAL MUSCLES, IN THE IRIS, OF THE EYE, CAUSES THE PUPIL TO DILATE.
THIS MAXIMISES THE AMOUNT OF LIGHT ENTERING THE EYE, IMPROVING VISION.
36
THE RECEPTORS IN THE EYE.
PHOTORECEPTORS, DETECT CHANGE IN THE ENVIRONMENT.
BRIGHT.
DARK.
37
NEURONES, ELECTRICAL IMPULSES.
NEUROENS, TRANSMIT ELECTRICAL IMPULSES WHICH TRAVEL ALONG THE NEURONE CELL SURFACE MEMEBRANE, FROM ONE END OF A NEURONE TO THE OTHER.
38
IMPULSE.
AN IMPULSE, IS NOT AN ELECTRICAL CURRENT THAT FLOWS ALONG NEURONES AS IF THEY WERE WIRES.
INSTEAD, AN IMPULSE IS A MOMENTARY REVERSAL IN THE ELECTRICAL POTENTIAL DIFFERENCE ACROSS THE NEURONE CELL SURFACE MEMBRANE.
THE ELECTRICAL POTENTIAL DIFFERENCE ACROSS A MEMBRANE, CAN ALSO BE DESCRIBED AS THE VOLTAGE ACOSS A MEMBRNAE, THE DIFFERENCE IN CHARGE ACROSS A MEMBRANE, OR THE MEMBRANE POTENTIAL.
39
RESTING POTENTIAL.
IN A RESTING AXON, ONE THAT IS NOT TRANSMITTING IMPULSES, THE INSIDE OF THE AXON ALWAYS HAS A NEGATIVE ELECTRICAL POTENTIAL, COMPARED TO THE OUTSIDE OF THE AXON.
THE DIFFERENCE IN CHARGE, BETWEEN THE INSIDE AND OUTSIDE OF THE NEURONES, IS DUE TO DIFFERENT NUMBERS OF IONS ON EACH SIDE OF THE NEURONE CELL SURFACE MEMBANE.
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THE FACTORS, THAT CONTRIBUTE TO ESTABLISHING AND MAINTAINING RESTING POTENTIAL.
TWO,2, FACTORS CONTRIBUTE TO ESTABLISHING AND MAINTANING RESTING POTENTIAL.
THE ACTIVE TRANSPORT OF SODIUM IONS, AND POTASSIUM IONS.
A DIFFERENCE IN MEMBRANE PERMEABILITY TO SODIUM AND POTASSIUM IONS.
41
THE ACTIVE TRANSPORT OF SODIUM IONS, AND POTASSIUM IONS.
CARRIER PROTIENS, CALLED SODIUM-POTASSIUM PUMPS, ARE PRESENT IN THE CELL SURFACE MEMBRANES OF NEURONES.
THESE PUMPS USE ATP, TO ACTIVEL TRANSPORT SODIUM, Na+, IONS OUT OF THE AXON, AND POTASSIUM, K+, IONS INTO THE AXON.
THE TWO,2, TYPES OF IONS ARE PUMPED AT AN UNEQUAL RATE, FOR EVERY THREE,3, SODIUM IONS THAT ARE PUMPED OUT OF THE AXON, ONLY TWO,2, POTASSIUM IONS ARE PUMPED IN.
THIS CREATES A CONCENTRATION GRADIENT, ACROSS THE MEMBRANE FOR BOTH SODIUM IONS, AND POTASSIUM IONS.
42
DIFFERENCE IN MEMRANE PERMEABILITY, TO SODIUM IONS AND POTASSIUM IONS.
BECAUSE OF THE CONCENTRATION GRADIENT GENERATED BY THE SODIUM-POTASSIUM PUMPS, BOTH SODIUM AND POTASSIUM WILL DIFFUSE BACK ACROSS THE MEMBRANE.
THE NEURONE, CELL SURFACE MEMBRANE HAS SODIUM ION CHANNELS AND POTASSIUM ION CHANNELS, THAT ALLOW SODIUM AND POTASSIUM IONS TO MOVE ACROSS THE MEMBRANE BY FACILITATED DIFFUSION.
THE NEURONE MEMBRANE, IS LESS PERMEABLE TO SODIUM IONS THAN POTASSIUM IONS, SO POTASSIOUM IONS INSIDE THE NEURONE CAN DIFFUSE OUT AT A FASTER RATE THAN SODIUM IONS CAN DIFFUSE BACK IN.
THIS RESULTS IN MORE POSITIVE IONS ON THE OUTSIDE OF THE NEURONE, THAN ON TE INSIDE, GENERATING A NEGATIVE CHARGE INSIDE THE NEURONE IN RELATION TO THE OUTSIDE.
THE RESULS OF THIS, IS THAT THE NEURONE HAS A RESTING MEMBRANE POTENTIAL OF AROUND, -70 millivolts, mV.
43
ACTION POTENTIAL.
ONCE, RESTING POTENTIAL IS REACHED THE NEURONE MEMBRANE IS SAID TO BE POLARISED.
TO INITATE A NERVE IMPULSE, IN A NEURONE THE MEMEBRANE NEEDS TO BE DEPOLARISED.
DEPOLARISATION, IS THE REVERSAL OF THE ELECTRICAL POTENTIAL DIFFERENCE ACROSS THE MEMBRANE.
THE DEPOLARISATION OF THE MEMBRANE OCCURS WHEN AN ACTION POTENTIAL IS GENERATED.
ACTION POTENTIALS, LEAD TO THE REVERSAL OF RESTING POTENTIAL FROM AROUN -70mV, TO AROUND +30 mV.
ACTION POTENTIALS INVOLVE THE RAPID MOVEMENT OF SODIUM IONS AND POTASSIUM IONS ACROSS THE MEMBRANE OF THE AXON.
AN ACTION POTENTIAL, IS THE POTENTIAL ELECTRICAL DIFFERENCE PRODUCED ACROSS THE AXON MEMBRANE, WHEN A NEURONE IS STIMULATED.
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GENERATING, AN ACTION POTENTIAL.
SOME OF THE ION CHANNELS IN THE MEMBRANE OF A NEURONE, ARE VOLTAGE GATED, MEANING THAT THEY OPEN AND CLOSE IN RESPONSE TO CHANGES IN THE ELECTRICAL POTENTIAL ACROSS THE MEMBRANE.
VOLTAGE GATED ION CHANNELS ARE CLOSED WHEN THE MEMBRANE IS AT REST, BUT THEY ARE INVOLVED IN THE GENERATION AND TRANSMISSION OF ACTION POTENTIALS.
45
WHEN A NEURONE IS STIMULATED.
WHEN A NEURONE IS STIMULATED, THE FOLLOWING STEPS OCCUR:
A SMALL NUMBER OF SODIUM ION CHANNELS IN THE AXOX MEMBRANE OPEN.
SODIUM IONS, BEGIN TO MOVE INTO THE AXON, DOWN THE CONCENTRATION GRADIENT.
DURING RESTING POTENTIAL, THERE IS A GREATER CONCENTRATION OF SODIUM ION OUTSIDE THE AXON, THAN INSIDE DUE TO THE ACTION OF THE SODIUM-POTASSIUM PUMPS.
THIS REDUCES THE POTENTIAL DIFFERENCE ACROSS THE AXON MEMBRANE, AS THE INSIDE OF THE AXON BECOMES LESS NEGATIVE.
IF THE POTENTIAL DIFFERENCE, REACHES AROUND -55mV, KNOWN AS THE THRESHOLD POTENTIAL, MORE SODIUM IONS CHANNELS OPEN, LEADING A FURTHER INFLUX OF SODIUM IONS.
THIS SECOND SET OF SODIUM ION CHANNELS, ARE VOLTAGE GATED CHANNELS.
NOTE THAT AN ACTION POTENTIAL IS ONLY INITIATED IF THE THRESHOLD POTENTIAL IS REACHED.
ONCE THE CHARGE HAS BEEN REVERSE FROM -70mV, TO AROUND +30mV THE MEMEBRANE IS SAID TO BE DEPOLARISED, AND AN ACTION POTENTIAL, HAS BEEN GENERATED.
46
REPOLARISATION.
ABOUT ONE,1, MILLISECOND AFTER AN ACTION POTENTIAL IS GENERATED, ALL THE VOLTAGE GATED SODIUM CHANNES IN THIS SECTION OF THE MEMBRANE CLOSE.
VOLTAGE GATED POTASSIUM CHANNELS, IN THIS SECTION OF AXON MEMBRANE NOW OPEN, ALLOWING THE DIFFUSION OF POTASSIUM IONS, OUT OF THE AXON DOWN THE CONCENTRATION GRADIENT.
THIS MOVEMENT OF POTASSIUM IONS, CAUSES THE INSIDE OF THE AXON, TO BECOME NEGATIVELY CHARGED AGAIN, A PROCESS KNOWN AS REPOLARISATION.
THERE IS A SHORT PERIOD DURING WHICH THE MEMBRANE POTENTIAL IS MORE NEGATIVE THAN RESTING POTENTIAL, THIS IS KNOWN AS HYPERPOLARISATION.
THE PRIOD DURING WHICH THE MEMBRANE IS HYPERPOLARISED, IS KNWON AS THE REFRACTORY PERIOD.
THE MEMBRAZNE IS UNRESPONSIVE TO STIMULATION DURING THE REFRACTORY PERIOD, SO A NEW ACTION POTENTIAL CANNOT BE GENERATED.
THIS MAKES THE ACTION POTENTIALS DISCRETE EVENTS AND MEANS THE IMPULSE CAN ONLY TRAVEL IN ONE DIRECTION.
THIS IS ESSENTIAL, FOR THE SUCCESSFUL AND EFFICENT TRANSMISSION OF NERVE IMPULSES ALONG NEURONES.
THE VOLTAGE GATES POTASSIUM CHANELS CLOSE, AND THE SODIUM-POTASSIUM PUMPS WORK TO RESTORE RESTING POTENTIAL.
ONLY ONCE RESTING POTENTIAL IS RESTORES, CAN THE MEMBRANE BE STIMULATED AGAIN.
47
TRANSMISSION, OF AN ACTION POTENTIAL.
ONCE AN ACTION HAS BEEN GENERATED, IT CAN BE PROPOGATED, OR TRASNMITTED, ALONG THE LENGTH OF THE AXON.
THE DEPOLARISATION, OF THE MEMBRANE AT THE SITE OF THE FIRST ACTION POTENTIAL, CAUSES SODIUM IONS TO DIFFUSE ALONG THE CYTOPLASM, INTO THE NEXT SECTION OF THE AXON, DEPOLARISING THE MEMBRANE IN THIS NEW SECTION, AND CAUSING VOLTAGE GATED SOFIUM CHANELS TO OPEN.
THIS TRIGGERS ANOTHER ACTION POTENTIAL, IN THE SECTION OF THE AXON MEMBRANE.
THIS PROCESS THEN REPEATS ALONG THE LENGTH OF THE AXON.
THE ACTIO POTENTIAL IS SAID TO MOVE ALONG THE AXON, IN A WAVE OF DEPOLARISATION.
IN THE BODY, THIS ALLOWS ACTION POTENTIALS TO BEGIN AT ONE END OF AN AXON, AND THEN PASS ALONG THE ENTIRE LENGTH OF THE AXON MEMBRANE.
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ACTION POTENTIALS, GENERATED OR NOT GENERATED.
ACTION POTENTIALS, ARE EITHER GENERATED OR NOT GENERATED, DEPENDING ON WHETHER THE THRESHOLD POTENTIAL IS REACJED.
THERE IS NO SUCH THING AS A SMALL OR LARGE ACTION POTENTIAL.
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THE ALL-OR-NOTHING PRINCIPLE.
IF A STIMULUS, IS WEAK, ONLY A FEW SODIUM ION CHANNELS WILL OPEN, AND THE MEMBRANE WILL NOT BE SUFFICIENTLY DEPOLARISED, TO REACH THE THRESHOLD POTENTIAL, AN ACTION POTENTIAL WILL NOT BE GENERATED.
IF A STIMULUS IS STRONG ENOIGH, TO RAISE THE MEMBRANE POTENTIAL, ABOVE THE THRESHOLD POTENTIAL, THEN AN ACTION POTENTIAL WILL BE GENERATED.
THIS IS THE ALL-OR-NOTHING PRINCIPLE,
AN IMPULSE IS ONLY TRANSMITTED IF THE INITIAL STIMULUS IS SUFFICIENT TO INCREASE THE MEMBRANE POTENTIAL ABOVE A THRESHOLD POTENTIAL.
50
THE ALL-OR-NOTHING PRINCIPLE, STIMULUS SIZE.
STIMULUS SIZE, CAN BE DETECTED BY THE BRAIN, BECAUSE AS THE INTENSITY OF A STIMULUS INCREASES, THE FREQUENCY OF THE ACTION POTENTIALS, TRANSMITTED ALONG THE NEURONE INCREASES.
THIS MEANS THAT A SMALL STIMULIS, MAY ONLY LEAD TO ONE ACTION POTENTIAL, WHILE A LARGE STIMULUS, MAY LEAD TO SEVERAL ACTION POTENTIALS IN A ROW.
51
UNMYELINATED NEURONES.
IN UNMYELINATED NEURONES, THE SPEED OF CONDUCTION IS RELATIVELY SLOW BECAUSE DEPOLARISATION MUST OCCUR ALONG THE WHOLE MEMBRANE OF THE AXON.
52
MYELINATION, DESCRIPTION.
BY INSULATING THE AXON MEMBRANE MYELIN, INCREASES THE SPEED AT WHICH ACTIION POTENTIALS CAN TRAVEL ALONG THE NEURONE.
IN SECTIONS OF THE AXON THAT ARE SURROUNDED BY A MYELIN SHEATH MEMBRANE, DEPOLARISITATION CANNOT OCCUR.
AS THE MYELIN SHEATH, STOPS THE DIFFUSION OF SODIUM AND POTASSIUM IONS.
ACTION POTENTIALS CAN ONLY OCCUR AT THE NODE OF RANVIER.
SODIUM IONS CAN DIFFUSE ALONG THE AXON WITHIN THE SCHWANN CELLS AND THE MEMBRANE AT THE NODES OF RANVIER DEPOLARISISES WHEN THE SODIUM IONS ARRIVE.
THE DIFFUSION OF SODIUM IONS IN THIS WAY IS KNOWN AS LOCAL CURRENT, OR LOCAL CIRCUITS.
THE ACTION POTENTIAL THEREFORE APPEARS TO JUMP, FROM ON ENODE TO THE NEXT, THIS IS KNOWN AS SALTATORY CONDUCTION.
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THE NODES OF RANVIER.
NODES OF RANVIER ARE THE GAPS, BETWEEN THE SCHWANN CELLS THAT MAKE UP THE MYELIN SHEATH.
54
PREVENTING IMPULSE TRANSMISSION.
USEFUL TO PREVENT NERVE TRANSMISSION, IN PAINKILLERS AND ANAESTHETICS.
SUCH DRUGS BIND TO SODIUM ION CHANNELS, PREVENTING THEM FROM OPENING ANF THEFORE PREVENTING AN INFLUX OF SODIUM IONS, WHEN AN AXON IS STIMULATED.
PREVENTING SODIUM ION INFLUX, PREVENTS MEMBRANE DEPOLARISTION AND AN ACTION POTENTIAL CANNOT BE GENERATED.
55
SYNAPSE, LOCATION.
STRUCTURES, KNOWN AS SYNAPSES ARE FOUND AT THE JUNCTIONS BETWEEN CELLS IN THE NERVOUS SYSTEM.
IN THE SENSE ORGANS, THERE ARE SYNAPSES, BETWEEN SENSORY RECEPTOR CELLS AND SENSORY NEURONS.
IN MUSCLES THERE ARE SYNAPSES BETWEEN MOTOR NEURONES AND MUSCLE FIBRES.
56
SYNAPSE STRUCTURE.
THE STRUCTURE OF SYNAPSE, INCLUDES THE FOLLOWING FEATURES:
A GAP BETWEEN THE NEURONES, KNOWN AS THE SYNAPTIC CLEFT.
THE NEURONE, BEFORE THE SYNAPSE IS KNWON AS THE PRESYNAPTIC NEURONE, AND HAS A ROUNDED END KNOWN AS THE SYNAPTIC KNOB.
THE NEURONE AFTER THE SYNAPSE, IS KNOWN AS THE POSTYSYNAPTIC NEURONE.
NERVE IMPULSES, ARE PASSED ACROSS THE SYNAPTIC CLEFT, BY THE DIFFUSION OF CHEMICALS KNOWN AS NEUROSTANSMITTERS, SUCH AS ACETYLCHOLINE.
NEROTRANSMITTERS, ARE CONTAINED WITHIN VESICLES, IN THE SYNAPTIC KNOB.
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SYNAPTIC TRANSMISSION.
ELECTRICAL IMPULSES CANNOT 'JUMP" ACROSS THE SYNAPTIC CLEFT.
WHEN AN ACTION POTENTIAL ARRIVES AT THE ENED OF THE AXON OF PRESYNAPTIC NEURONE, THE MEMBRANE BECOME DEPOLARISED.
THIS CAUSES THE VOLTAGE GATED CALCIUM ION CHANNELS TO OPEN.
CALCIUM IONS DIFFUSE INTO THE SYNAPTIC KNOB, VIA CALCIUM ION CHANNELS IN THE MEMBRANE.
THE CALCIUM ION CAUSE VESICLE IN THE SYNAPTIC KNOB, TO MOVE TOWARDS THE PRESYNAPTIC MEMBRANE, WHERE THEY FUSE WITH IT, AND RELEASE CHEMICAL MESSENGERS, CALLED NEUROTRANSMITTERS, INTO THE SYNAPTIC CLEFT, VIA EXOCYTOSIS.
THE NEUROTRANSMITTERS, DIFFUSE ACROSS THE SYNAPTIC CLEFT, AND BIND WITH RECEPTOR MOLECULES ON THE POSTSYNAPTIC MEMBRANE.
THIS CAUSES ASSOCITAED SODIUN ION CHANNELS ON THE POSTSYNAPTIC MEMEBTRANE TO OPEN, ALLWOING SODIUM IONS TO DIFFUSE INTO THE POSTSYNAPTIC CELL.
IF ENOUGH TRANSMITTER MOLECULES BIND WITH THEESE RECPETORS, THEN AN ACTION POTENTIAL IS GENERATED, WHICH THEN TRAVELS DOWN THE AXON OF THE POSTSYNSAPTIC NEURONE.
HERE THE POSTSYNAPTIC MEMBRANE, IS DEPOLARISED.
THE NEUROTRANSMITTERS ARE THEN BROKEN DOWN TO PREVENT CONTINUED STIMULATION OF THE POSTSYNAPTIC NUEORNE.
THE ENZYME THAT BREAKS DOWN ACETYLCHOLINE IS ACETYLCHOLINESTERASE.
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SYNAPSE ROLE, UNIDIRECTIONALITY.
SYNAPSES ENABLE, UNIDIRECTIONALITY OF IMPULSE TRANSMISSION.
SYNAPSES ENSURE THE ONE-WAY TRANSMISSION OF IMPULSES.
IMPULES CAN ONLY PASS IN ONE DIRECTION AT SYNAPSES, BECAUSE NEUOTRANSMITTERS IS RELEASED ON ONE SIDE AND ITS RECEPTORS ARE ONE THE OTHER.
CHEMICAL TRANSMISSION CANNOT OCCUR IN THE OPPOSITE DIRECTION.
59
SYNAPSES, DIVERGECE.
SYNAPSES ENABLE, THE DIVERGENCE OF NERVE IMPULSES.
ONE NEURONE CAN CONNECT TO SEVERAL OTHER NEURONES AT A SYNAPSE, ALLOWONG NERVE SIGNALS TO BE SENT IN SEVERAL DIRECTIONS FROM A SIGNEL PRESYNAPTIC NEURONE.
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SYNPASES, AMPLIFICATION.
SYNAPSES ENABLE, THE AMPLIFICATION OF NERVE SIGNALS BY SUMMATION.
WHEN AN IMPULSE ARRIVES AT A SYNAPSE, IT DOES NOT ALWAYS CAUSE AN IMPULSE TO BE GENERATED IN THE NEXT NEURONE.
A SINGLE IMPULSE THAT ARRIVES AT A SYNAPTIC KNOB MAY BE INSUFFICIENT TO GENERATE AN ACTION POTENTIAL, IN THE POST-SYNAPTIC NEURONE.
REASONS:
ONLY A SMALL AMOUNT OF ACETLYCHOLINE MAY RELASE INOT THE SYNAPTIC CLEFT.
A SMALL NUMBER OF SODIUM ION CHANNELS ARE OPENED, INTO THE POSTSYNAPTIC AXON MEMBRANE.
AN INSUFFICENT NUMBER OF SODIUM IONS PASS THROUGH THE MEMBRANE.
THE THRESHOLD POTENTIAL IS NOT REACHED.
THE EFFECT:
THE EFFECT OF MULTIPLE IMPULSES CAN BE ADDED TOGETHER TO OVERCOME THIS IN A PROCESS KNOWN AS SUMMATION.
SUMMATION CAN BE ACHIEVED BY:
SEVETAL PRESYNAPTIC NEURONES CONVEGING TO MEET A SINLGE POSTSYNAPTIC NEURONE.
THIS IS KNOWN AS SYNAPTIC CONVERGENCE.
MANY ACTION POTENTIALS ARRIVING AT A POSTYSYNAPTIC KNOB, IN QUICK SUCCESSION.
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THE EYES.
THE EYES IS A SENSE ORGAN, CONTAINING RECEPTORS SENSITIVE TO LIGHT INTENSITY AND WAVELENGTH.
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WHAT ARE RECEPTORS?
RECEPTORS, ARE SPECIALISED CELLS THAT GENERATE AN ELECTRICAL IMPULSE IN A SENSORY NEURONE, WHEN STIMULATED BY A PARTICULAR STIMULUS.
FOR EXAMPLE, LIGHT RECEPTORS ARE STIMULATED WHEN LIGHT FALLS ON THEM.
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EYE, LIGHT STIMULUS.
LIGHT ENTERS THE EYE, THROUGH THE PUPIL AND IS FOCUSED ONTO A REGION OF THE RETINA, CALLED THE FOVEA.
THE AMOUNT OF LIGHT THAT ENTERS THE EYE, IS CONTROLLED BY THE MUSCLES OF THE IRIS.
LIGHT IS FOCUSED USING THE LENS, THE SHAPE OF WHICH IS CONTROLLED BY THE CILARY MUSCLES, ATTACHED TO THE LENS BY THE SUSPENSORY LIGAMENTS.
THE FOVEA CONTAISN MANY LIGHT RECEPTORS, OR PHOTORECEPTORS.
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THE RETINA, PHOTORECEPTORS.
THE RETINA, CONTAINS TWO,2, TYPES OF PHOTORECEPTORS.
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ROD CELLS.
PRIMARILY LOCATED AROUND THE OUTER RETINA.
SENSITIVE TO LIGH INTENSITY, SO CAN DETECT THE PRESENCE AND BRIGHTNESS OF LIGHT.
IMAGES GENERATED, USING INFORMATION FROM ONLY ROD CELLS IS BLACK AND WHITE.
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CONE CELLS.
MOSTLY FOUND GROUPED TOGETHER IN THE FOVEA.
SENSITIVE TO DIFFERENT WAVELENGTHS OF VISIBLE LIGHT, AND SO CAN DETECT COLOUR.
CONCE CELLS CAN BE, RED-SENSITIVE, GREEN-SENSITIVE, OR BLUE-SENSITIVE.
THE NUMBER OF RED, GREE AND BLUE SESNITIVE CONCE CELLS STIMULATED, WILL DETERMINE THE COLOUR SEEN.
IMAGES GENERATED USING INFORMATION FROM CONE CELLS WILL BE IN COLOUR.
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EYES, ACTION POTENTIALS.
ACTION POTENTIALS GENERATED IN THE PHOTORECEPTORS, ARE TRANSMITTED TO THE BRAIN VIA THE OPTIC NERVE.
THE OPTIC NERVE, LEAVES THE BACK OF THE EYE FROM A REGION KNOWN AS THE BLIND SPOT.
THE BLIND SPOT CONTAINS NO PHOTORECEPTORS.
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PHOTORECEPTORS, GENERATE NERVE IMPULSES.
PHOTORECEPTORS IN THE EYE GENERATE ACTION POTENTIALS WHEN STIMULATED BY BRIGHT ENOUGH LIGHT, RODS, OR BY LIGHT OF A PARTICULAR WAVELENGTH, CONES.
LIGHT-SENSITIVE PIGMENTS INSIDE PHOTORECEPTORS ARE BELACHED WHEN LIGHT FALLS ON THEM.
ROD CELLS CONTAIN A LIGHT-SENSITIVE PIGMENT CALLED RHODOPSIN.
WHEN LIGHT HITS RHODOSPIN, ITS BREAKS APART INTO CONSTITUENT PARTS, RETINAL AND OPSIN.
THE BREAKING APART OF RHODOPSIN, IS KNOWN AS BLEACHING.
THE BLEACHING OF LIGH-SENSITIVE PIGMENTS CAUSES A CHEMICAL CHANGE IN THE PHOTORECEPTORS, THAT RESULTSA IN THE GENERATION OF A NERVE IMPULSE.
NERVE IMPULSES TRAVEL ALONG A BIPOLAR NEURONE, TO THE OPTIC NERVE, WHICH CARRIES INFORMATION TO THE BRAIN.
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ROD CELLS ACTION, DESCRIPTION.
THE WAY IN WHICH ROD CELLS PASS INFORMATION TO THE OPTIC NERVE, IS A BI BACK-TO-FRONT.
RATHER THAN INITIATING AN ATION POTENTIAL, WHEN THEY ARE DEPOLARISED.
ROD CELLS INITIATE ACTION POTENTIALS, IN NEIGHBOURING BIPOLAR NEURONES WHEN THEY ARE HYPERPOLARISED.
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ROD CELLS, IN THE DARK.
IN THE DARK, THE FOLLOWING OCCURS:
SODIUM IONS, ARE ACTIVELY PUMPED OUT OF THE ROD CELLS, GENERETING A CONCENTRATION GRADIENT.
SODIUM IONS DIFFUSE BACK DOWN THIS CONCENTRATION GRADIENT, INTO THE ROD CELL VIA SODIUM CHANNELS.
AT THIS STAGE, THERE IS LITTLE DIFFERENCE IN CHARGE BETWEEN THE OUTSIDE AND THE INSIDE OF THE THE ROD CELL, AND THE CELL IS SAID TO BE DEPOLARISED.
IN REALITY, THE INSID EOF THE CELL IS SLIGHTLY MORE NEGATIVE TO THE OUTSIDE.
THE DEPOLARISED ROD CELL RELEASES NEUROTRANSMITTERS WHICH DIFFUSE ACROSS A SYNAPSE TO A BIPOLAR NEURONE.
RATHER THAN INITIATING AN ACTION POTENTIAL IN THE BIPOLAR NEURONE, THIS NEUROTRANSMITTER INHIBITS THE GENERATION OF AN ACTION POTENTIAL, PREVENTING A NERVE IMPULSE FROM BEING SENT TO THE OPTIC NERVE.
THIS NEUROTRANSMITTER , IS SAID TO BE AN INHIBITORY NEUTRANSMITTER.
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ROD CELLS, IN THE LIGHT.
IN THE LIGHT, THE FOLLOWING OCCURS INSIDE ROD CELLS:
LIGHT BLEACHES RHODOPSZIN, CAUSING IT TO BREAK APART INTO RETINAL AND OPSIN.
THE BLEACHING OF RHODOPSIN, CAUSES THE SODIUM ION CHANNELS INTO THE CELL SURFACE MEMEBRANE OF THE ROD CELL TO CLOSE, PREVENTING SODIUM IONS FROM DIFFUSING BACK INTO THE ROD CELL.
THE ACTIVE TRANSPORT OF SODIUM IONS OUT OF THE CELL IS STILL TAKINH PLACE, SO SODIUM IONS ARE REMOVED FROM THE CELL BUT NOT ABLE TO RETURN.
THE LACK OF POSITIVELY CHARGED IONS ENTERING THE ROD CELL CAUSE SITS INTERIOR TO BECOME MORE NEGATIVE, UNTIL IT REACHED A HYPERPOLARISED STATE.
THE HYPERPOLARISED ROD CELL STOPS RELEASING AN INHIBITORY NEUROTRANSMITTER, SO THE GENERATION OF AN ACTION POTENTIAL IN THE NEIGHBOURING BIPOLAR NEURONE IS NO LONGER INHIBITED.
AN ACTION POTENTIAL IS GENERATED IN THE BIPOLAR NEURONE ATTACHED TO THE ROD CELL AND AN IMPULSE IS SENT TO THE OPTIC NERVE.
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HYPERPOLARISED.
A MEMBRANE THAT IS HYPERPOLARISED, HAS A MORE NEGATIVE POTENTIAL DIFFERENCE ACROSS IT THAN THE RESTING -70mV.
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PLANTS GROWING TOWARDS THE LIGHT.
GROWING TOWARDS LIGHT, MAXIMISES THE RATE OF PHOTOSYNTHESIS, AND THEREFORE GLUCOSE PRODUCTION.
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PLANTS, PRODUCING HAMRFUL OR FOUL-TASTING CHEMICALS.
PRODUCING HARMFUL, OR FOUL-TASTING CHEMICALS IN RESPONSE TO BEING EATEN BY A HERBIVORE REDUCES THE LIKLEHOOD OF BEING EATEN.
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PLANTS, ROOTS GROWING TOWARDS WATER, H2O.
ROOTS GROWING TOWARDS WATYER, H2O, MAXIMISES THE PLANTS ABILITY TO GAIN WATER, H2O.
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PLANTS RESPONSE TO STIMULI.
PLANTS CAN RESPONSE TO STIMULI, IN VARIOUS WAYS.
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ALTERING THEIR GROWTH.
ONE WAY PLANTS CAN RESPOND TO A STIMULI, IS TO ALTER THEIR GROWTH.
FOR EXAMPLE, A SEEDLING WILL BEND AND GROW TOWARDS THE LIGHT, BECAUSE THERE IS MORE GROWTH ON THE SHADED SIDE, THAN ON THE ILLUMINATED SIDE.
THIS TYPE OF DIRECTIONAL GROWTH REPSONSE, IS REFFERED TO AS A TROPISM.
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TROPISMS.
PHOTOTROPISM IS A GROWTH RESPONSE TO LIGHT.
GEOTROPISM, IS A GROWTH RESPONSE TO GRAVITY.
THE REPSONSE, TO GRAVITY IS ALSO KNOWN AS GRAVITROPISM.
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TROPISMS, POSITIVE OR NEGATIVE.
TROPISMS CAN BE POSITIVE OR NEGATIVE.
POSITIVE TROPISMS, INVOLVE GROWTH TOWARDS A STIMULUS.
FOR EXAMPLE, POSITIVE PHOTOTROPISM IS A GROWTH RESPONSE TOWARDS LIGHT.
NEGATIVE TROPISMS, INVOLVE GROWTH AWAY FROM A STIMULUS.
FOR EXAMPLE, NEGATIVE GEOTROPISM IS A GROWTH RESPONSE AWAY FROM GRAVITY.
UPWARDS.
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PLANT GROWTH FACTORS.
THE PLANT GROWTH RESPONSES OF PLANTS RELY ON CHEMICAL SUBSTANCES THAT ARE RELEASED IN RESPONSE TO A STIMULUS.
THESE CHEMICAL GROWTH FACTORS, ACT IN A SIMILAR WAY TO THE HORMONES THAT ARE FOUND IN ANIMALS.
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PLANT GROWTH FACTORS, PRODUCTION.
GROWTH FACTORS ARE PRODUCED IN THE GROWING PARTS OF A PLANTS BEFORE MOVING FROM THE GROWING REGIONS TO OTHER TISSUES WHERE THEY REGULATE CELL GROWTH IN RESPONSE TO A DIRECT STIMULUS.
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AUXIN.
AUXIN IS A GROWTH FACTOR THAT STIMULATES CELL ELONGATION IN PLANT SHOOTS AND INHIBITS GROWTH IN CELLS IN PLANT ROOTS.
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GIBERELLINS.
STEM ELONGATION.
FLOWERING.
SEED GERMINATION.
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CYTOKININS.
CELL GROWTH AND DIVSION.
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ABSCISIC ACID, ABA.
LEAF LOSS.
SEED DORMANCY.
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ETHENE.
FRUIT RIPENING.
FLOWERING.
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WHAT IS INDOLEACETIC ACID, IAA?
INDOLEACETIC ACID, IAA, IS A TYPE OF AUXIN.
AUXINS ARE A GROUP OF PLANT GROWTH FACTORS THAT INFLUENCE MANY ASPECTS OF PLANT GROWTH.
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WHAT DOES INDOLEACETIC ACID, IAA, DO?
IT IS THOUGH THAT INDOLEACETIC ACID, IAA, BRINGS ABOUT PLANT RESPONSES SUCH AS PHOTOTROPISM BY ALTERING THE TRANSCRIPTION OF GENES INSIDE PLANT CELLS.
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INDOLEACETIC ACID, IAA, PRODUCTION.
INDOLEACETIC ACID, IAA, IS PRODUCED BY CELLS IN THE GROWING PARTS OF A PLANT, BEFORE IT IS REDISTRIBUTED TO OTHER PLANT TISSUES.
IAA, CAN BE TRANSPORTED FROM CELL TO CELL BY DIFFUSION AN DACTIVE TRANSPORT.
TRANSPORT OF IAA, OVER LONGER DISTANCES OCCURS IN THE PHLOEM.
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THE REDISTRIBUSTION OF INDOLEACETIC ACID, IAA.
THE REDISTRIBUTION, OF INDOLEACETIC ACID, IAA, IS AFFECTED BY ENVIRONMENTAL STIMULI, SUCH AS LIGHT AND GRAVITY, LEADING TO AN UNEVEN DISTRIBUTION OF INDOLEACETIC ACID, IAA, IN DIFFERENT PARTS OF THE PLANT.
THIS BRINGS ABOUT UNEVEN PLANT GROWTH.
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INDOLEACETIC ACID, IAA, IN PLANT SHOOTS.
LIGHT AFFECTS THE GROWTH OF PLANT SHOOTS, IN A RESPONSE, KNOWN AS PHOTOTROPISM.
THE CONCENTRATION OF INDOLEACETIC ACID, IAA, DETERMINES THERATE OF CELL ELONGATION WITHIN THE STEM.
A HIGER CONCENTRATION OF IAA, CAUSES AN INCREASE IN THE RATE OF ELONGATION.
IF THE CONCENTRATION OF IAA, IS NOT UNIFORM ACROSS THE STEM THEN UNEVEN CELL GROWTH CAN OCCUR.
WHEN LIGHT SHINES ON A STEM FROM SIDE, IAA IS TRANSPORTED FROM THE ILLUMINATED SIDE OF A SHOOT TO THE SHADED SIDE.
AN IAA, GRADIENT IS ESTABLISHED, WITH MORE ON THE SHADED AND LESS ON THE ILLUMINATED SIDE.
THE HIGHER CONCENTRATION, OF AUXIN ON THE SHADED SIDE OF THE SHOOT, CAUSES A FASTER RATE OF CELL ELONGATION, AND THE SHOOT BENDS TOWARDS THE LIGHT.
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INDOLEACETIC ACID, IAA, IN ROOTS.
ROOTS, RESPOND TO GRAVITY IN A RESPONSE KNWON AS GEOTROPISM.
IN ROOTS, IAA CONCENTRATION ALSO AFFECT CELL ELONGATION, BUT HIGHER CONCENTRATIONS RESULT IN A LOWER RATE OF CELL ELONGATION.
NOTE, THAT THIS IS THE OPPOSITE AFFECT, TO THAT OF IAA ONN SHOOT CELLS.
IAA, IS TRANSPORTED, TO THE LOWER SIDE OF THE PLANT ROOTS.
THE RESULTING HIGH CONCENTRATION OF AUXIN, AT THE LOWER SIDE OF THE ROOTS, INHIBITS CELL ELONGATION.
AS A RESULT, THE LOWER SIDE GROWS AT A SLOWER RATE THAN THE UPPER SIDE OF THE ROOT, CAUSING THE ROOT TO BEND DOWNWARDS.
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WHAT IS THE FLOWERING, IN PLANTS CONTROLLED BY?
FLOWERING IN PLANTA, IS CONTROLLED BY THE STIMULUS OF NIGHT LENGTH.
NIGHTS ARE SHORTER DURING, THE SPRING AND THE SUMMER, AND LONGER IN THE AUTUMN AND WINTER.
SOME PLANTS, FLOWER WHEN NIGHTS ARE SHORT, AND SOME FLOWER WHEN NIGHT ARE LONG.
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NIGHT, REACHING A CERTAIN LENGTH.
WHEN THE NIGHTS, REACH A CERTAIN LENGTH, GENES THAT CONTROL FLOWERING MAY BE SWITCHED ON OR OFF, LEADING TO THE ACTIVATION OR INHIBITION OF FLOWERING.
GENES, THAT ARE SWITCHED ARE ON ARE EXPRESSED, LEADING TO THE PRODUCTION OF THE POLYPEPTIDES, FOR WHICH THEY CODE, WHILE GENES THAT ARE SWITCHED OFF ARE NOT EXPRESSED, SO THE POLYPEPETIDES FOR WHICH THEY CODE ARE NOT PRODUCED.
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THE LENGTH OF THE NIGHT, DETECTION.
THE LENGTH OF THE NIGHT, CAN BE DETECTED BY A PLANT, BECAUSE IT DETERMINED THE QUANTITIES OF DIFFERENT FORMS OF A PIGMENT, CALLED PHYTOCHTOME IN THE LEAF.
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PHYTOCHROME, PIGMENT.
THE PHYTOCHTIME PIGMENT, EXISTS IN TWO,2, FORMS.
PR, IS THE INACTIVE FORM OF PHYTOCHROME, IT ABSORBS LIGHT FROM THE RED PART OF THE SPECTRUM.
WAVELENGTH, 660 nm.
PFR, IS THE ACTIVE FORM OF PHYTOCHROME.
IT ABSORBS LIGHT FROM THE FAR RED PART OF THE SPECTRUM.
WAVELENGTH, 730 nm.
ABSORPTION OF DIFFERENT WAVELENGTHS OF LIGHT CAUSES A REVERSIBLE CONVERSION, BETWEEN PR AND PFR, FORMS OF PHYTOCHTOME.
WHEN PR ABSORTBS RED LIGHT, 660nm, IT IS CONVERTED INTO PFR.
WHEN PFR ABSORBS FAR RED LIGHT, 730nm, IT IS CONVERTED BACK INTO PR.
IN THR ABSCENCE OF RED LIGHT, THE UNSTABLE PFR GRADUALLY CONVERTS BACK INTO PR.
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DURING THE DAY.
DURING THE DAY, THE LEVELS OF PFR RISE.
SUNLIGHT CONTAISN MORE WAVELENGTHS AT 660nm, THAN 730nm, SO THE CONVERTSION FROM PR, TO PFR, OCCURS MORE RAPIDLY IN THE DAYTIME THAN THE CONVERSION OF PFR, TO PR.
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DURING THE NIGHT.
DURING THE NIGHT, THE LEVELS OF PR RISE.
RED LIGHT WAVELENGTHS ARE NOT AVAILABLE IN THE DARKNESS, AND PFR, CONVERTS SLOWLY BACK TO PR.
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LONG DAY PLANTS.
LONG DAY PLANTS FLOWER WHEN THE NIGHTS ARE SHORT, FOR EXAMPLE IN THE SUMMER.
WHEN NIGHTS ARE NIGHT, THE DAY LENGTH IS LONGER, HENCE THE TERM 'LONG DAY PLANTS.".
IN LONG DAY PLANTS HIGH LEVELS OF THE ACTIVE FORM OF PHTOCHROME, ACTIVATE FLOWERING.
FLOWERING OCCURS, DUE TO THE FOLLOWING PROCESS,
DAYS ARE LONG SO PR, IS CONVERTED TO PFR, AT A GREATER RATE, THAN PFR, IS CONVERTED TO PR.
THE ACTIVE FORM OF PHYTOCHROME, PFR, IS PRESETN AT HIGH LEVELS.
HIGH PFR LEVELS, ACTIVATE FLOWERING,
PFR ACTIVATES EXPRESSION OF GENES THAT STIMULATE FLOWERING.
THE ACTIVE GENE IS TRANSCRIBES, AND TRANSLATED.
THE RESULTING PROTEIN CAUSES FLOWERS TO BE PRODUCED RATHER THAN STEM AND LEAVES.
