CHAPTER 6 - STIMULI AND RESPONSE, NERVOUS COORDINATION AND HOMEOSTASIS Flashcards
- survival and response - nervous communication - responses in plants - receptors - control of heart rate - neurones - synaptic transmission - muscle structure - muscle contraction - homeostasis basics - control of blood glucose concentration - diabetes and blood glucose concentration - the kidneys - controlling blood water potential
how do organisms respond to their external environment
- organisms increase their chances of survival by responding to chances in their EXTERNAL ENVIRONMENT
- ANIMALS can MOVE AWAY from HARMFUL ENV, like places that are too hot or too cold
- PLANTS cant move themselves, but they can CHANGE THE WAY THEY GROW IN AN ATTEMPT TO FIND MORE FAVOURABLE ENV CONDITIONS, ex seedlings growing in dark conditions can rapidly develop very long and thin stems to INCREASE their chances of finding light
how do organisms respond to changes in their internal environment
organisms also respond to changes in their internal environment to ensure that the conditions are always OPTIMAL for their metabolism (all the chemical reactions that go on inside them)
define the term ‘stimulus’
- any change in the INTERNAL or EXTERNAL environment
- ex, a change in temp, light intensity or pressure
what are the names of the 2 simple responses in simple mobile organisms
- simple mobile organisms, like woodlice, have SIMPLE RESPONSES to keep them in a FAVOURABLE ENV
- their response can either be TACTIC or KINETIC
what is the tactic response/taxis
- DIRECTIONAL MOVEMENT in response to a stimulus
- the DIRECTION of the STIMULUS affects the response
give a example of how taxis works in simple mobile organisms
- woodlice show a tactic response to LIGHT, they move AWAY from a light source
- this response helps them SURVIVE because it keeps them concealed under stones during the day, where they are safe from predators, and keeps them in damp conditions, THIS REDUCES WATER LOSS
what is the kinetic response/kinesis in simple mobile organisms
- NON DIRECTIONAL/RANDOM movement in response to a stimulus
- the INTENSITY of the STIMULUS affects the response
give an example of kinesis in simple mobile organisms
- woodlice show a KINETIC response to HUMIDITY
- in HIGH HUMIDITY, they MOVE SLOWLY AND TURN LESS OFTEN, so they stay where they are
- as the air gets DRIER, they MOVE FASTER AND TURN MORE OFTEN, so they MOVE INTO A NEW AREA
- this response helps woodlice move from DRIER AIR to MORE HUMID AIR and then stay put
- this IMPROVES their chances of SURVIVAL because it REDUCES THEIR WATER LOSS and HELPS TO KEEP THEM CONCEALED
what is positive taxis
- if an organism moves TOWARDS a stimulus its a positive taxis
what is negative taxis
- if an organism moves AWAY from a stimulus, its a negative taxis
what is a simple response
- simple responses are automatic responses to a stimulus, the organism does NOT choose to where move
what do animals have to do with information in order to respond to changes in the environment
- in order to respond to changes in the environment, an organism needs to PASS INFO between diff areas of its body
- in animals, some of this communication is carried out using nerve impulses
what is the role of receptors
- receptors DETECT STIMULI
- they can be cells or proteins on cell surface membranes
- there are many different types of receptors which detect diff stimuli, ex baroreceptors detect changes in blood pressure
- receptors are specific to one type of stimulus
what is the role of effectors
- cells that BRING ABOUT A RESPONSE TO A STIMULUS to PRODUCE AN EFFECT
- effectors include muscle cells and cells found in glands, like the pancreas
how do receptors and effectors communicate
- receptors communicate with effectors via the NERVOUS SYSTEM or the HORMONAL SYSTEM or sometimes BOTH
what are neurones
- nerve cells
- the nervous stem is made up of a complex network of NEURONES
what are sensory neurones and what is their role
- they transmit electrical impulses from receptors to the CNS (the brain and spinal cord)
what are motor neurones and what is their role
- they transmit electrical impulses from the CNS to effectors
what are relay neurones and what is their role
- they are also known as INTERMEDIATE/INTER/ASSOSCIATION NEURONES
- they transmit electrical impulses between SENSORY neurones and MOTOR neurones
how does nervous communication work
- a STIMULUS is DETECTED by RECEPTOR CELLS and an ELECTRICAL IMPULSE is sent along a SENSORY NEURONE
- when an ELECTRICAL IMPULSE reaches the END of a neurone, CHEMICALS called NEUROTRANSMITTERS take the info across the SYNAPSE GAP to the NEXT NEURONE, where ANOTHER electrical impulse is generated
- the CNS processes the info and sends impulses along MOTOR neurones to an EFFECTOR
give the chain of what is involved in nervous communication
stimulus -> receptors (sensory neurone) -> CNS (motor neurone) -> effectors -> response
give an example of nervous communication
- ex, when you see a friend waving to you and you wave back in response
- STIMULUS - you see a friend waving
- RECEPTORS - light receptors (photoreceptors) in your eyes detect the wave, the electrical impulse is carried by a SENSORY NEURONE to the CNS
- CNS - processes INFO and sends an electrical impulse along a MOTOR NEURONE
- EFFECTORS - MUSCLE cells are stimulated by the MOTOR neurone
- RESPONSE - muscles CONTRACT to make your arm wave
describe the nervous response
- when an ELECTRICAL IMPULSE reached the END of neurone, chemical messengers called NEUROTRANSMITTERS are SECRETED DIRECTLY ONTO CELLS, like muscle cells, so the nervous response is LOCALISED
- NEUROTRANSMITTERS are QUICKLY REMOVED once they have done their job, so the response is SHORT LIVED
- ELECTRICAL IMPULSES are really FAST, so the response is usually RAPID and this allows animals to react QUICKLY to stimuli
describe what takes place in simple reflexes
- a simple reflex is a RAPID, INVOLUNTARY response to a STIMULUS
- the pathway of communication goes through the SPINAL CORD but NOT through the CONSCIOUS PARTS of the BRAIN, so the RESPONSE happens AUTOMATICALLY
- because there is no time to respond, INFO travels really FAST from RECEPTORS -> EFFECTORS
- SIMPLE REFLEXES are PROTECTIVE, they help organisms to AVOID DAMAGE TO THE BODY as the response happens so quickly
what is the reflex arc
- the PATHWAY of NEURONES, LINKING RECEPTORS -> EFFECTORS in a SIMPLE REFLEX is called a REFLEX ARC
- 3 NEURONES involved - a sensory neurone, a relay neurone and a motor neurone
- stimulus -> receptors (sensory neurone) -> CNS (relay neurone in spinal cord) -> (motor neurone) -> effectors -> response
give a real life example of a simple reflex
- h=hand withdrawal response to heat
- STIMULUS - you touch a hot surface
- RECEPTORS - THERMORECEPTORS (HEAT receptors) in your skin detect the HEAT stimulus and a SENSORY NEURONE caries the impulse to the CNS
- CNS - a RELAY NEURONE in your SPINAL CORD carries the impulse to a MOTOR NEURONE
- EFFECTORS - the MOTOR NEURONE carries the impulse to muscle cells in your biceps
- RESPONSE - your biceps muscle contracts to pull you hand AWAY from the HEAT SOURCE and stop your hand from being damaged
what can override the reflex
- if there’s a RELAY NEURONE involved, in the simple reflex arc, then its possible to override the reflex
-ex, your brain could tell your hand to withstand the heat
do plants respond to stimuli or not
they do
what is the specific name for a plants response to stimuli
tropism
define and explain tropisms
- flowering plants, like animals, INCREASE their chances of survival by responding to changes in their environment
- a tropism is the response of a plant to a DIRECTIONAL STIMULUS (stimulus coming from a certain direction)
- plants respond to stimuli by REGULATING THEIR GROWTH
- a POSITIVE tropism is GROWTH TOWARDS THE STIMULUS
- a NEGATIVE tropism is GROWTH AWAY FROM THE STIMULUS
give examples of tropisms in plants
- they sense the DIRECTION of light and grow TOWARDS it to maximise light absorption for photosynthesis
- they can sense gravity, so their ROOTS and SHOOTS grow in the right DIRECTION
- climbing plants have a SENSE OF TOUCH, so they can find things to CLIMB and REACH THE SUNLIGHT
what is phototropism
- the growth of a plant IN RESPONSE TO LIGHT
- SHOOTS are POSITIVELY PHOTOTROPIC, grow TOWARDS light
- ROOTS are NEGATIVELY PHOTOTROPIC, grow AWAY from light
what is gravitropism
- the growth of a plant in RESPONSE TO GRAVITY
- SHOOTS are NEGATIVELY GRAVITROPIC, grow UPWARDS
- ROOTS are POSITIVELY GRAVITROPIC, grow DOWNWARDS
what are auxins
- plants RESPOND TO STIMULI using SPECIFIC GROWTH FACTORS
- these specific growth factors are HORMONE LIKE CHEMICALS that SPEED UP OR SLOW DOWN PLANT GROWTH
- plant GROWTH FACTORS are PRODUCED in the GROWING REGIONS OF THE PLANTS and they MOVE to where they are NEEDED in OTHER PARTS of the plant
what are the growing regions of the plant
- shoots
- root tips
explain how auxins work and how they move in the plants
- growth facts, AUXINS, are PRODUCED IN THE TIPS OF SHOOTS AND DIFFUSE BACKWARDS to STIMULATE THE CELL JUST BEHIND THE TIPS TO ELONGATE - this is where the CELL WALLS become LOOSE and STRETCHY, so the CELL GETS LONGER
- if the TIP of a SHOOT is REMOVED, NO AUXIN will be AVAILABLE and the SHOOT STOPS GROWING
- auxins STIMULATE GROWTH IN SHOOTS
- HIGH CONC INHIBIT GROWTHS IN THE ROOTS
are there other classes of growth factors and if so, how do they affect growth
- there are other classes of GF
- they affect growth in different ways
- ex, a GF called GIBBERELLIN stimulates FLOWERING and SEED GERMINATION
what is one of the tissues which can transport sugars around a plant
phloem
what is indoleacetic acid/IAA
- IAA is an important AUXIN that is PRODUCED in the TIPS of SHOOTS and ROOTS in FLOWERING PLANTS
- IAA is MOVED AROUND THE PLANT TO CONTROL TROPISMS
- IAA moves by DIFFUSION + ACTIVE TRANSPORT over SHORT DISTANCES
- IAA moves via the PHLOEM over LONG DISTANCES
- this ^ causes DIFFERENT PARTS of the plant having DIFFERENT CONCS of IAA
- the UNEVEN DISTRIBUTION of IAA means there’s UNEVEN GROWTH
explain and give an example of how IAA moves in phototropism
- IAA moved to the MORE SHADED PARTS of the SHOOTS and ROOTS, so there is UNEVEN GROWTH
- IAA CONC INCREASES on the SHADED SIDE -> CELLS ELONGATE and the SHOOTS BENDS TOWARDS THE LIGHT
- IAA CONC INCREASES on the SHADED SIDE -> growth is INHIBITED so the ROOT BENDS AWAY from the LIGHT
explain and give an example of how IAA moves in gravitropism
- IAA moved to the UNDERSIDE of SHOOTS and ROOTS, so there is UNEVEN GROWTH
- IAA CONC INCREASES on the LOWER SIDE -> CELLS ELONGATE so the SHOOT GROWS UPWARDS
- IAA CONC INCREASES on the LOWER SIDE -> GROWTH is INHIBITED so the ROOT GROWS DOWNWARDS
what are nervous impulses
- the electrical charges transmitted along a neurone
- they are created by the MOVEMENT of SODIUM and POTASSIUM IONS
explain the resting membrane potential
- in a neurones resting state (when its NOT being stimulated) the OUTSIDE of the MEMBRANE is POSITIVELY CHARGED, compared to the INSIDE
- this ^ is because there are MORE POSITIVE IONS OUTSIDE THE CELL THAN INSIDE, so the MEMBRANE is POLARISED (there is a DIFFERENCE IN CHARGE/POTENTIAL DIFFERENCE/VOLTAGE) ACROSS IT
- the VOLTAGE ACROSS the membrane when it is at REST is called the RESTING POTENTIAL, and its -70mV
how is the resting potential created and maintained
- by sodium-potassium pumps and potassium ion channels
- they are in a neurones membrane
describe what happens in the generator potential
- when a stimulus is detected, the cell membrane is EXCITED and becomes MORE PERMEABLE, allowing 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 the GENERATOR POTENTIAL
- a BIGGER stimulus excites the MEMBRANE MORE, causing a BIGGER MOVEMENT OF IONS and a BIGGER CHANGE IN POTENTIAL DIFFERENCE -> so a BIGGER GENERATOR POTENTIAL IS PRODUCED
describe what happens in an action potential
- if the GENERATOR POTENTIAL is BIG ENOUGH, it will TRIGGER AN ACTION POTENTIAL
- an AP is an ELECTRICAL IMPULSE ALONG A NEURONE
- an AP is only triggered if the GP reaches a certain level (THRESHOLD LEVEL)
- AP’s are all ONE SIZE, so the STRENGTH of the STIMULUS is measured by the FREQUENCY OF AP’S (the number of AP’s triggered during a certain time period)
- if the stimulus is TOO WEAK, the GP WONT REACH THE THRESHOLD and therefore there wont be any AP
what are pacinian corpuscles
- mechanoreceptors, detect mechanic stimuli like pressure and vibrations
- they are found in the skin
- they contain the END of a SENSORY NEURONE , this is called the SENSORY NEURONE ENDING
- the sensory nerve ending is wrapped in loads of LAYERS OF LAMELLAE (connective tissue)
what happens when a pacinian corpuscle is stimulated
- when a PC is stimulated, like by a tap on the arm for ex, the LAMELLAE ARE DEFORMED and PRESS ON THE SENSORY NERVE ENDING
- this ^ DEFORMS THE STRETCH MEDIATED SODIUM ION CHANNELS
- the channels OPEN and SODIUM IONS DIFFUSE INTO THE CELL -> this creates a GP
- if the GP reaches the THRESHOLD, it TRIGGERS AN AP
do pacinian corpuscles respond to other types of stimuli, apart from mechanical stimuli
- no
- PC’s only respond to mechanical stimuli, NOT to any other type of stimulus
- this an example of how RECEPTORS ONLY RESPOND TO SPECIFIC STIMULI
why are stretch mediated sodium ions called that
because they only open and let sodium ions pass through when they are STRETCHED
what is the effect of the stimulus being bigger
- the bigger the stimulus, ex the more pressure thats applied, the MORE SODIUM CHANNELS OPEN
- this creates a BIGGER GP, which is MORE LIKELY to REACH THE THRESHOLD and cause an AP
what are photoreceptors
receptors in your eye that detect light
describe how light is perceived by the eye
- light ENTERS the eye through the PUPIL is CONTROLLED BY THE MUSCLES OF THE IRIS
- light RAYS are FOCUSED by the LENS onto the RETINA, which lines the inside of the eye
- the RETINA contains the PHOTORECEPTOR CELLS
- the FOVEA is an area of the RETINA where there are LOTS OF PHOTORECEPTORS
- NERVE IMPULSES from the PHOTORECEPTOR CELLS are CARRIED from the RETINA -> BRAIN by the OPTIC NERVE
- the OPTIC NERVE is a BUNDLE OF NEURONES
- where the OPTIC NERVE LEAVES the EYE = THE BLIND SPOT as there are NO PHOTORECEPTOR CELLS and therefore its NOT SENSITIVE TO LIGHT
explain how photoreceptors work
- light enters the eye, hits the photoreceptors and is absorbed by LIGHT SENSITIVE OPTICAL PIGMENTS
- light BLEACHES the pigments and this causes a chemical change, which alters the MEMBRANE PERMEABILITY to SODIUM IONS
- a GEN POTENTIAL is CREATED and IF it reaches THRESHOLD, a NERVE IMPULSE is SENT ALONG A BIPOLAR NEURONE
- BIPOLAR NEURONES connect PHOTORECEPTORS to the OPTIC NERVE, which TAKES IMPULSES TO THE BRAIN
what are the 2 types of photoreceptors in the human eye
- rods
- cones
what are rods, explain their function
- mainly found in the PERIPHERAL PARTS OF THE RETINA
- contains different OPTICAL PIGMENTS than cones, which makes them sensitive to different WAVELENGTHS
- give information in BLACK AND WHITE/MONOCHROMATIC VISION
what are cones, explain their function
- mainly found PACKED TOGETHER in the FOVEA
- contains different OPTICAL PIGMENTS than rods, which makes them sensitive to different WAVELENGTHS
- cones give information in COLOUR/TRICHROMATIC VISION
- there are 3 TYPES OF CONES, each one contains a DIFFERENT OPTICAL PIGMENT
- there are : RED sensitive, GREEN sensitive and BLUE sensitive optical pigments
- when they are STIMULATED in DIFFERENT PROPORTIONS, you can see DIFFERENT COLOURS
explain and compare the sensitivity between rods and cones
RODS
- rod cells are VERY SENSITIVE to light, they work well in DIM LIGHT
- this is because MANY RODS join ONE BIPOLAR NEURONE, so MANY WEAK GEN POTENTIALS COMBINE to reach the THRESHOLD and TRIGGER AN AP
CONES
- LESS SENSITIVE than RODS, they work best in BRIGHT LIGHT
- this is because ONE CONE joins ONE BIPOLAR NEURONE, so it takes MORE LIGHT to REACH THE THRESHOLD and TRIGGER AN AP
explain and compare the visual acuity between rods and cones
- VA is the ability to tell apart points that are CLOSE TOGETHER
RODS
- give LOW VISUAL ACUITY because MANY RODS join the SAME BIPOLAR NEURONE, which means light from 2 points CLOSE TOGETHER cant be told apart
CONES
- give HIGH VISUAL ACUITY because CONES are CLOSE TOGETHER and ONE CONE joins ONE BIPOLAR NEURONE
- when LIGHT from 2 POINTS hits 2 CONES, 2 AP’S (one from each CONE) go to the BRAIN, so you can DISTINGUISH 2 POINTS THAT ARE CLOSE TOGETHER AS 2 SEPARATE POINTS
summarise rods
- MAINLY located in the PERIPHERAL PARTS of the RETINA
- give information in BLACK AND WHITE
- MANY rods join 1 BIPOLAR NEURONE
- HIGH SENSITIVITY to LIGHT
- give LOW VISUAL ACUITY
summarise cones
- MAINLY located in the FOVEA
- give info in COLOUR
- 1 CONE joins 1 BIPOLAR NEURONE
- LOW SENSITIVITY to LIGHT
- give HIGH VISUAL ACUITY
can you consciously control your heart rate or not?
- no
- it is controlled by a part if the NS called the ANS (autonomic nervous system)
what are the 2 different systems of the nervous system
- the CNS/central nervous system
- the PNS/peripheral nervous system
describe the CNS
- called the central nervous system
- made up of the BRAIN and SPINAL CORD
describe the PNS
- called the peripheral nervous system
- made of NEURONES that CONNECT the CNS to the REST OF THE BODY
- split into 2 different systems
what are the 2 systems the PNS is split into
- somatic nervous system
- autonomic nervous system
describe the functions of the somatic nervous system
- controls CONSCIOUS ACTIVITIES, like running or playing video games
describe the functions of the autonomic nervous system
- controls UNCONSCIOUS activities, like digestion
what 2 systems is the autonomic nervous system split into
- sympathetic nervous system
- parasympathetic nervous system
- they have OPPOSITE EFFECTS on the BODY
what is the function of the sympathetic nervous system
- the ‘fight or flight’ system
- gets the body ready for action
what is the function of the parasympathetic nervous system
- the ‘rest and digest’ system
- calms the body down
which nervous system is involved in the control of heart rate
the AUTONOMIC NERVOUS SYSTEM
what quality does heart/cardiac muscle have which allows it to contract and relax without receiving signals from nerves
- it is MYOGENIC
- means that it contracts and relaxes without receiving signals from nerves
- this pattern of contractions CONTROLS the REGULAR HEARTBEAT
how does the process of the control of heartbeat start
1) starts in the SAN (sinoatrial node), which is a small mass of tissue in the wall of the right atrium
2) the SAN is like a PACEMAKER, it sets the rhythm of the heartbeat by SENDING OUT REGULAR WAVES OF ELECTRICAL ACTIVITY TO THE ATRIAL WALLS
3) this ^ causes the RIGHT and LEFT ATRIA to CONTRACT AT THE SAME TIME
4) a BAND of NON CONDUCTING COLLAGES TISSUE PREVENTS THE WAVES OF ELECTRICAL ACTIVITY FROM BEING PASSED DIRECTLY FROM THE ATRIA -> VENTRICLES
5) instead, these waves of electrical activity are transferred from the SAN -> AVN (atrioventricular node)
6) the AVN is responsible for PASSING WAVES OF ELECTRICAL ACTIVITY ON THE BUNDLE OF HIS
7) but there is a SLIGHT DELAY BEFORE THE AVN REACTS, to make sure the ATRIA HAVE EMPTIED BEFORE THE VENTRICLES CONTRACT
8) the BUNDLE OF HIS - a group of MUSCLE FIBRES that are RESPONSIBLE FOR CONDUCTING THE WAVES OF ELECTRICAL ACTIVITY BETWEEN THE VENTRICLES TO THE APEX (BOTTOM) OF THE HEART
9) the BUNDLE SPLITS INTO FINER MUSCLE FIBRES in the RIGHT and LEFT VENTRICLE WALLS, called the PURKYNE TISSUE
10) the purkyne tissue CARRIES THE WAVES OF ELECTRICAL ACTIVITY INTO THE MUSCULAR WALLS OF THE RIGHT AND LEFT VENTRICLES, this causes them to CONTRACT SIMULTANEOUSLY from the BOTTOM UP
describe the communication between the heart and the brain
- the SAN generates ELECTRICAL IMPULSES which cause the CARDIAC MUSCLES TO CONTRACT
- the rate at which the SAN fires (heart rate) is UNCONSCIOUSLY CONTROLLED by a part of the BRAIN called the MEDULLA
- animals need to ALTER their HEART RATE to RESPOND TO INTERNAL STIMULI, like to prevent fainting due to low BP or to ensure the heart rate is high enough to supply the body with enough oxygen for ex
how is internal stimuli detected?
- by PRESSURE and CHEMICAL RECEPTORS
PRESSURE
- called BARORECEPTORS
- they are in the AORTA and CAROTID ARTERIES
- stimulated by HIGH and LOW BP
CHEMICAL
- called CHEMORECEPTORS
- in the AORTA, CAROTID ARTERIES and in the MEDULLA
- monitor the OXYGEN LEVEL in the BLOOD and also CO2 and PH levels (as they are indicators of O2 level)
- ELECTRICAL IMPULSES from the RECEPTORS are sent to the MEDULLA along the SENSORY NEURONES
- the MEDULLA PROCESSES this INFO and SENDS IMPULSES to the SAN, along the SYMPATHETIC OR PARASYMPATHETIC NEURONES
explain how the control of heart rate responds to high BP
- BARORECEPTORS detect HIGH BP and send IMPULSES along SENSORY NEURONES -> MEDIULLA, which sends IMPULSES along PARASYMPATHETIC NEURONES
- they secrete ACETLYCHOLINE, which BINDS TO RECEPTORS on the SAN
- this causes the HEART RATE to SLOW DOWN, in order to REDUCE BP BACK TO NORMAL
explain how the control of heart rate responds to low BP
- BARORECEPTORS detected LOW BP and send IMPULSES along SENSORY NEURONES to the MEDULLA, which sends IMPULSES along the SYMPATHETIC NEURONES
- they secrete NORADRENALINE, which BINDS TO RECEPTORS on the SAN
- this causes the HEART RATE to SPEED UP, in order to INCREASE BP BACK TO NORMAL
explain how the control of heart rate responds to high blood O2/low CO2/high blood pH levels
- CHEMORECEPTORS detect CHEMICAL CHANGES in the BLOOD and SEND IMPULSES along SENSORY NEURONES to the MEDULLA, which SENDS IMPULSES along the PARASYMPATHETIC NEURONES
- they SECRETE ACETYLCHOLINE, which BINDS TO RECEPTORS ON THE SAN
- this causes the HEART RATE TO DECREASE, in order to RETUN O2,CO2 and PH LEVELS BACK TO NORMAL
explain how the control of heart rate responds to low blood O2/high CO2/low blood pH levels
- CHEMORECEPTORS detect CHEMICAL CHANGES in the BLOOD and SEND IMPULSES along the SYMPATHETIC NEURONES
- they secrete NORADRENALINE, which BINDS TO RECEPTORS on the SAN
- this causes the HEART RATE TO INCREASE, in order to RETURN OXYGEN, CO2 and pH LEVELS BACK TO NORMAL
what are nervous impulses
- ELECTRICAL CHARGES transmitted along a NEURONE
- they are CREATED by the MOVEMENT of SODIUM and POTASSIUM IONS
describe the resting membrane potential
- in a NEURONES RESTING STATE (when its NOT being stimulated), the OUTSIDE of the MEMBRANE is POSITIVELY CHARGED, compared to the INSIDE
- this ^ is because there are MORE POSITIVE IONS OUTSIDE the cell, than INSIDE
- so the MEMBRANE IS POLARISED, there is a DIFF IN CHARGE (called POTENTIAL DIFF/VOLTAGE) across it
- the VOLTAGE ACROSS THE MEMBRANE when its AT REST, is called the RESTING POTENTIAL
- the CHARGE of the RESTING POTENTIAL is about -70 mV
describe the movement of the SODIUM and POTASSIUM IONS
- the RESTING POTENTIAL is CREATED and MAINTAINED by the SODIUM-POTASSIUM PUMPS and POTASSIUM ION CHANNELS in a NEURONES MEMBRANE
- SODIUM-POTASSIUM PUMPS use ACTIVE TRANSPORT to MOVE 3 SODIUM IONS OUT OF THE NEURONE, for every 2 POTASSIUM IONS and ATP is NEEDED to do this
- POTASSIUM ION CHANNELS ALLOW FACILITATED DIFFUSION of POTASSIUM IONS OUT OF THE NEURONE, DOWN their CONC GRAD
1) the SP PUMPS MOVE SODIUM IONS OUT OF THE NEURONE, but the MEMBRANE is NOT PERMEABLE to SODIUM IONS, so they CAN NOT DIFFUSE BACK IN
2) this ^ creates a SODIUM ION ELECTROCHEMICAL GRADIENT (a conc grad of ions) as there are MORE POSITIVE SODIUM IONS OUTSIDE THE CELL, compared to the the INSIDE THE CELL
3) the SODIUM-POTASSIUM PUMPS also MOVE POTASSIUM IONS INTO THE NEURONE
4) when the cell is at REST, most POTASSIUM ION CHANNELS are OPEN, this means that the MEMBRANE IS PERMEABLE TO POTASSIUM IONS, so SOME DIFFUSE BACK OUT THROUGH POTASSIUM ION CHANNELS
even though positive ions are moving in and out of the cell, in total MORE POSITIVE IONS MOVE OUT OF THE CELL, THAN ENTER and this makes the OUTSIDE of the CELL POSITIVELY CHARGED COMPARED TO THE INSIDE
what is an action potential
- when a NEURONE is STIMULATED, OTHER ION CHANNELS in the CELL MEMBRANE (SODIUM ION CHANNELS) OPEN
- if the STIMULUS is BIG ENOUGH, it will TRIGGER A RAPID CHANGE IN POTENTIAL DIFFERENCE
- this ^ causes the CELL MEMBRANE to become DEPOLARISED (no longer polarised)
describe the process of an action potential
1) STIMULUS - this excited the NEURONE CELL MEMBRANE, this causes SODIUM ION CHANNELS TO OPEN
- the MEMBRANE becomes MORE PERMEABLE to SODIUM, so SODIUM IONS DIFFUSE INTO THE NEURONE DOWN THE SODIUM ION ELECTROCHEMICAL GRADIENT
- this ^ makes the INSIDE OF THE NEURONE LESS NEGATIVE
2) DEPOLARISATION - if the PD reaches the THRESHOLD (AROUND -55 mV), MORE SODIUM ION CHANNELS OPEN
- MORE SODIUM IONS DIFFUSE INTO THE NEURONE
3) REPOLARISATION - at a PD of around -30mV, the SODIUM ION CHANNELS CLOSE and POTASSIUM CHANNELS OPEN
- the MEMBRANE is MORE PERMEABLE to POTASSIUM, so POTASSIUM IONS DIFFUSE OUT OF THE NEURONE DOWN THE POTASSIUM ION CONC GRAD
- this starts to get the MEMBRANE back to its RESTING POTENTIAL
4) HYPERPOLARISATION - POTASSIUM ION CHANNELS are SLOW to CLOSE, so there is a slight ‘OVERSHOOT’, where TOO MANY POTASSIUM IONS DIFFUSE OUT OF THE NEURONE
- the PD becomes MORE NEGATAIVE than the RESTING POTENTIAL (less than -70 mV)
5) RESTING POTENTIAL - the ION CHANNELS ARE RESET
- the SODIUM-POTASSIUM PUMP RETURNS THE MEMBRANE TO ITS RESTING POTENTIAL BY PUMPING SODIUM IONS and POTASSIUM IONS IN, and this MAINTAINS THE RESTING POTENTIAL until the MEMBRANE IS EXCITED BY ANOTHER STIMULUS
describe the refractory period after an action potential
- after an AP, the NEURONE CELL MEMBRANE CANNOT BE EXCITED AGAIN STRAIGHT AWAY
- this ^ is because the ION CHANNELS are RECOVERING and they CANNOT BE MADE TO OPEN, SODIUM ION CHANNELS are CLOSED DURING REPOLARISATION and POTASSIUM ION CHANNELS are CLOSED during HYPERPOLARISATION
- this ^ period of RECOVERY is called the REFRACTORY PERIOD
- the refractory period acts as a TIME DELAY between ONE AP AND THE NEXT, this ensures that AP’S DO NOT OVERLAP, but instead PASS ALONG AS SEPARATE IMPULSES
- the refractory period also means that there is a LIMIT TO FREQUENCY AT WHICH NERVE IMPULSES CAN BE TRANSMITTED and that AP’S are UNIDIRECTIONAL (only travel in ONE direction)
describe what the wave of depolarisation
- when an AP happens, some of the SODIUM IONS that ENTER THE NEURONE TO OPEN AND SODIUM IONS DIFFUSE INTO THAT PART
- this ^ CAUSES A WAVE OF DEPOLARISATION TO TRAVEL ALONG THE NEURONE
- the WAVE MOVES AWAY FROM THE PARTS OF THE MEMBRANE IN THE REFRACTORY PERIOD BECAUSE THESE PARTS CANT FIRE AN AP
explain the all or nothing principle
- once the threshold is reached, an AP will ALWAYS FIRE WITH THE SAME CHANGE IN VOLTAGE, no matter HOW BIG THE STIMULUS IS
- if the THRESHOLD ISNT REACHED, an AP WILL NOT FIRE
- this ^ is the ‘all or nothing’ nature of AP’s
- a BIGGER STIMULUS will not cause a bIGGER AP, but it WILL CAUSE THEM TO FIRE MORE FREQUENTLY
describe the structure of a myelinated motor neurone
- cell body has a nucleus in it and has dendrites coming out of it, which are extensions of the cell body that connect with other neurones
- the axon connects the cell body and the effector, and it is covered in myelin sheath which is made up of schwann cells
- the schwann cell has a nucleus
- between the schwann cells there are tiny patches of bare membrane called the nodes of ranvier
- then there is the axon terminal, which is connected to the effector
- the direction of the impulse is from the dendrites to the effector
what factors affect the speed of conduction of AP’s
- myelination
- axon diameter
- temperature
how does myelination affect the speed of conduction
- some neurones, including MANY MOTOR NEURONES, they have a MYLEIN SHEATH
- the MYLEIN SHEATH is an ELECTRICAL INSULATOR
- in the PNS, the SHEATH IS MADE OF a type of cell called a SCHWANN CELL
- BETWEEN the SCHWANN CELLS are tiny patches of BARE MEMBRANE called the NODES OF RANVIER
- SODIUM ION CHANNELS are CONCENTRATED at the NODES OF RANVIER
describe the process of saltatory conduction in MYLEINATED
- in a myelinated neurone, DEPOLARISATION only happens at the NODES OF RANVIER (because sodium ions can get through the membrane)
- the neurones CYTOPLASM conducts enough ELECTRICAL CHARGE to DEPOLARISE the NEXT NODE, so the IMPULSE ‘JUMPS’ FROM NODE TO NODE
- this ^ is called SALTATORY CONDUCTION and it is VERY FAST
describe conduction along a NON-MYLEINATED neurone
- they CAN NOT undergo SALTATORY CONDUCTION
- the IMPULSE TRAVELS AS A WAVE along the WHOLE LENGTH of the AXON MEMBRANE, so there is DEPOLARISATION ALONG THE WHOLE LENGTH OF THE MEMBRANE
- this is SLOWER than SALTATORY CONDUCTION, but it is still pretty quick
explain how axon diameter affects the speed of conduction
- AP’s are CONDUCTED QUICKER along axons with BIGGER DIAMETERS because there is LESS RESISTANCE TO THE FLOW OF IONS than in the CYTOPLASM of a SMALLER NEURONE
- with LESS RESISTANCE, DEPOLARISATION REACHES OTHER PARTS of the NEURONE CELL MEMBRANE QUICKER
explain how temperature affects the speed of conduction
- the SPEED OF CONDUCTION INCREASES AS THE TEMP INCREASES
- this ^ is because IONS DIFFUSE FASTER
- the SPEED ONLY INCREASES UNTIL 40 DEGREES CELSIUS, after that PROTEINS DENATURE AND SPEED DECREASES (the PUMPS and CHANNELS that MOVE IONS ACROSS THE MEMBRANE are PROTEINS, therefore they will also DENATURE AT HIGH TEMPS)
what are synapses
- the JUNCTION between a NEURONE and ANOTHER NEURONE
- OR the JUNCTION between a NEURONE and an EFFECTOR CELL, like a MUSCLE/TINY GLAND CELL
what is a synaptic cleft
- the TINY GAPS BETWEEN THE CELLS AT A SYNAPSE = SYNAPTIC CLEFT
what is the presynaptic neurone
- PRE = BEFORE, therefore the presynaptic neurone = THE ONE BEFORE THE SYNAPSE
- has a SWELLING called a SYNAPTIC KNOB, which contains SYNAPTIC VESICLES filled with CHEMICALS, called NEUROTRANSMITTERS
describe the effect of an action potential
1) when an AP reaches the END OF A NEURONE it causes NT’S to be RELEASED INTO THE SYNAPTIC CLEFT
2) the NT’S DIFFUSE ACROSS TO THE POSTSYNAPTIC MEMBRANE (the one AFTER the synapse) and BIND to SPECIFIC RECEPTORS
3) when NT’S BIND TO RECEPTORS, they MAY TRIGGER AN AP IN A NEURONE, cause MUSCLE CONTRACTION IN A MUSCLE CELL or CAUSE A HORMONES TO BE SECRETED FROM A GLAND CELL
4) because the RECEPTORS are ONLY on the POSTSYNAPTIC MEMBRANES, SYNAPSES ENSURE IMPULSES ARE UNIDIRECTIONAL (impulse can only travel in ONE DIRECTION)
5) NT’S are REMOVED FROM THE CLEFT, so the RESPONSE DOES NOT KEEP HAPPENING, they are taken BACK into the PRESYNAPTIC NEURONE R THEY ARE BROKEN DOWN BY ENZYMES AND the PRODUCTS are taken INTO THE NEURONE
what is acetylcholine
a NEUROTRANSMITTER
what specific receptors do acetylcholine bind to
CHOLINERGIC RECEPTORS
what is the name for synapses that use acetylcholine
CHOLINERGIC SYNAPSES
describe the entire process of how a nerve impulse is transmitted across a cholinergic synapse
1) ARRIVAL OF AN AP
- an AP arrives at the SYNAPTIC KNOB of the PRESYNAPTIC NEURONE
- the AP STIMULATES the VOLTAGE-GATED CALCIUM ION CHANNELS in the PRESYNAPTIC NEURONE TO OPEN
- CALCIUM IONS DIFFUSE INTO the SYNAPTIC KNOB
- (later, they are PUMPED OUT by ACTIVE TRANSPORT)
2) FUSION OF THE VESICLES
- the INFLUX of CALCIUM IONS into the SYNAPTIC KNOB causes the SYNAPTIC VESICLES TO FUSE WITH THE PRESYNAPTIC MEMBRANE
- the VESICLES RELEASE ACETYLCHOLINE into the SYNAPTIC CLEFT via EXOCYTOSIS
- (can only use influx for flowing INTO)
- (exocytosis is when a VESICLE IN A CELL MOVES TO THE CELL SURFACE MEMBRANE, FUSES WITH THE MEMBRANE AND RELEASES ITS CONTENTS OUTSIDE THE CEL)
3) DIFFUSION OF ACh
- ACh DIFFUSES ACROSS THE SYNAPTIC CLEFT and BINDS TO SPECIFIC CHOLINERGIC RECEPTORS on the POSTSYNAPTIC MEMBRANE, this causes SODIUM ION CHANNELS in the POSTSYNAPTIC MEMBRANE TO OPEN
- the INFLUX OF SODIUM IONS INTO the POSTSYNAPTIC MEMBRANE causes DEPOLARISATION
- an AP on the POSTSYNAPTIC MEMBRANE is GENERATED and if the THRESHOLD is REACHED
- ACh is REMOVED from the SYNAPTIC CLEFT, so the RESPONSE DOES NOT KEEP HAPPENING. it is BROKEN DOWN by ACETYLCHOLINESTERASE/AChE (enzyme) and the PRODUCTS are RE-ABSORBED by the PRESYNAPTIC NEURONE and USED TO MAKE MORE ACh
what are the 2 types of NT
- EXCITATORY
- INHIBITORY
- can also be BOTH
what are EXCITATORY NT’S and give an example of how they work
- they DEPOLARISE the POSTSYNAPTIC MEMBRANE, making it FIRE AN AP IF THRESHOLD IS RELEASED
example
- ACh is an EXCITATORY NT (it binds to CHOLINERGIC RECEPTORS to cause an AP in the POSTSYNAPTIC MEMBRANE) at CHOLINERGIC SYNAPSES in the CNS and at NEUROMUSCULAR JUNCTIONS
what are INHIBITORY NT’S and give an example of how they work
- they HYPERPOLARISE the POSTSYNAPTIC MEMBRANE ( make the PD MORE NEGATIVE), PREVENTING it from FIRING AN AP
example
- GABA is an INHIBITORY NT, when it binds to its RECEPTORS it causes POTASSIUM ION CHANNELS TO OPEN on the POSTSYNAPTIC MEMBRANE, which HYPERPOLARISES the NEURONE
- ACh is an INHIBITORY NT at CHOLINERGIC SYNAPSES IN THE HEART, when it binds to RECEPTORS there it can cause POTASSIUM ION CHANNELS to OPEN on the POSTSYNAPTIC MEMBRANE which HYPERPOLARISES IT
what is an inhibitory synapse
a SYNAPSE where INHIBITORY NT’s are released from the PRESYNAPTIC MEMBRANE FOLLOWING AN AP is called an INHIBITORY SYNAPSE
what happens if the stimulus is weak
summation
what is summation
- only a SMALL AMOUNT OF NT will be RELEASED INTO THE SYNAPTIC CLEFT
- this may NOT BE ENOUGH to EXCITE THE POSTSYNAPTIC MEMBRANE to the THRESHOLD LEVEL and STIMULATE AN AP
- SUMMATION is where the EFFECT OF NT’S RELEASED FROM MANY NEURONES (or ONE NEURONE that is STIMULATED A LOT IN A SHORT PERIOD OF TIME) is ADDED TOGETHER
- it means SYNAPSES ACCURATELY PROCESS INFO, FINELY TUNING THE RESPONSE
what are the 2 types of summation
- SPATIAL SUMMATION
- TEMPORAL SUMMATION
explain SPATIAL summation
- SPATIAL SUMMATION is where 2 OR MORE PRESYNAPTIC NEURONES RELEASE THEIR NT’S AT THE SAME TIME OR ONTO THE SAME POSTSYNAPTIC NEURONE
- the SMALL AMOUNT of NT released from EACH OF THESE NEURONES can be ENOUGH ALTOGETHER TO REACH THE THRESHOLD in the POSTSYNAPTIC NEURONE and therefore TRIGGER AN AP
- (summation = where the SUM TOTAL of LOTS OF SMALLER IMPULSES TRIGGER AN AP)
what happens if the neurones release different types of NT’s in SPATIAL SUMMATION
- if SOME neurones release an INHIBITORY and then SOME release an EXCITATORY NT then it may result in NO AP (because the effects of the IN and EXC NT’S ‘CANCEL EACH OTHER OUT’)
explain TEMPORAL summation
- where 2 OR MORE NERVE IMPULSES ARRIVE IN QUICK SUCCESSION from the SAME PRESYNAPTIC NEURONE
- this ^ makes an AP MORE LIKELY because MORE NT IS RELEASED INTO THE SYNAPTIC CLEFT
- impulses have to FOLLOW EACH OTHER VERY QUICKLY, if not then the NT will be REMOVED FROM THE CLEFT BEFORE ITS REACHED A LEVEL HIGH ENOUGH TO TRIGGER AN AP
what type of NT’S can trigger an AP
EXCITATORY NT’S
what is a neuromuscular junction
- a NM junction is a SPECIALISED CHOLINERGIC SYNAPSE BETWEEN A MOTOR NEURONE AND A MUSCLE CELL
- a NM JUNCTION USE THE NT ACh, which bINDS TO CHOLINERGIC RECEPTORS, which are called NICOTINIC CHOLINERGIC RECEPTORS
explain how NM junctions work
- NM junctions work in basically the same way as CHOLINERGIC SYNAPSES, they both release ACh from VESICLES in the
PRESYNAPTIC MEMBRANE - the ACh then DIFFUSES ACROSS THE SYNAPTIC CELFT and BINDS TO CHOLINERGIC RECEPTORS on the POSTSYNAPTIC MEMBRANE, and this TRIGGERS AN AP if the THRESHOLD IS REACHED
- in BOTH types of SYNAPSE, ACh is BROKEN DOWN in the SYNAPTIC CLEFT by the ENZYME ACETYLCHOLINESTERASE (AChE)
what are the differences between 2 types of synapses at a NM junction
- the POSTSYNAPTIC MEMBRANE has LOTS OF FOLDS which FORM CLEFTS and these CLEFTS STORE AChE
- the POSTSYNAPTIC MEMBRANE has MORE RECEPTORS THAN OTHER SYNAPSES
- ACh is ALWAYS EXCITATORY, so when a MOTOR NEURONE FIRES AN AP, it NORMALLY TRIGGERS A RESPONSE IN A MUSCLE CELL. this is NOT ALWAYS THE CAUSE FOR A SYNAPSE BETWEEN 2 NEURONES
how does nicotine affect synaptic transmission
- some drugs are the SAME SHAPE as NT’S so they MIMIC THEIR ACTION AT RECEPTORS, THESE DRUGS ARE CALLED AGONISTS
- nicotine MIMICS ACh so BINDS TO NICOTINIC CHOLINERGIC RECEPTORS IN THE BRAIN
how does antagonists affect synaptic transmission
- some drug BLOCK RECEPTORS so they CAN NOT BE ACTIVATED BY NT’S, these drugs are called ANTAGONISTS
- this means FEWER RECEPTORS, IF ANY, CAN BE ACTIVATED
- CURARE BLOCKS THE EFFECTS OF ACh BY BLOCKING NICOTINIC CHOLINERGIC RECEPTORS AT NM JUNCTIONS, SO MUSCLE CELLS CAN NOT BE STIMULATED
- this results in THE MUSCLE BEING PARALYSED
how do drugs that inhibit enzymes which break down NT’S affect synaptic transmission
- some DRUGS INHIBIT THE ENZYME WHICH BREAKS DOWN NT’S (they stop it from working)
- this means there are MORE NT’S IN THE SYNAPTIC CLEFT TO BIND TO RECEPTORS AND THEY ARE THERE HERE FOR LONGER
- NERVE GASES STOP ACh from BEING BROKEN IN THE SYNAPTIC CLEFT
- this can LEAD TO LOSS OF MUSCLE CONTROL
how do drugs that stimulate the release of NT’S from the PRESYNAPTIC NEURONE affect synaptic transmission
- MORE RECEPTORS ARE ACTIVATED
- AMPHETAMINES force the NT DOPAMINE OUT OF THE SYNAPTIC VESICLES and INTO THE SYNAPTIC CLEFT
- this ^ INCREASES THE EFFECT OF DOPAMINE, it INCREASES ALERTNESS
how do drugs that inhibit the release of NT’s from the PRESYNAPTIC NEURONE affect synaptic transmission
- FEWER RECEPTORS ARE ACTIVATED
- OPIOIDS BLOCK CALCIUM ION CHANNELS in the PRESYNAPTIC NEURONE
- this ^ means FEWER VESICLES FUSE WITH THE LESS PRESYNAPTIC MEMBRANE, therefore LESS NT IS RELEASED
what are muscle cells
EFFECTORS as they CONTRACT in RESPONSE TO NERVOUS IMPULSES
what are the 3 types of muscle
- SMOOTH MUSCLE
- CARDIAC MUSCLE
- SKELETAL MUSCLE
describe smooth muscle
- CONTRACTS WITHOUT CONTRACTS WITHOUT CONSCIOUS CONTROL
- found in the WALLS OF INTERNAL ORGANS (apart from the heart), like the stomach, intestine and blood vessels
describe cardiac muscle
- CONTRACTS WITHOUT CONSCIOUS CONTROL, like smooth muscle
- ONLY FOUND IN THE HEART
describe skeletal muscle
- also called striated, striped or voluntary muscle is the TYPE OF MUSCLE YOU USE TO MOVE, like biceps and triceps which move the lower arm
what is the role of SKELETAL muscle
- SK muscles are ATTACHED TO BONES VIA TENDONS
- LIGAMENTS ( bands of strong connective tissue) ATTACH BONES TO OTHER BONES, which HOLDS THEM TOGETHER
- PAIRS OF SK MUSCLES CONTRACT AND RELAX to MOVE BONES AT A JOINT
- THE BONES OF THE SKELETON are INCOMPRESSIBLE/RIGID so they ACT AS LEVERS, which gives the MUSCLES SOMETHING TO PULL AGAINST
what are antagonistic pairs
- MUSCLES that WORK TOGETHER TO MOVE A BONE are called ANTAGONISTIC PAIRS
- the CONTRACTING MUSCLE is called the AGONIST and the RELAXING MUSCLE is called the ANTAGONIST
explain antagonistic pairs with the example of biceps and triceps
- the bones of your LOWER ARM are attached to a BICEPS MUSCLE and a TRICEPS MUSCLE by TENDONS
- the BICEPS and TRICEPS WORK TOGETHER TO MOVE YOUR ARM, WHILE ONE CONTRACTS THE OTHER RELAXES
BICEPS
- when your BICEP CONTRACTS, your TRICEP RELAXES
- this PULLS THE BONE, so your ARM BENDS/FLEXES at the ELBOW
- here, the BICEPS IS THE AGONIST and the TRICEPS IS THE ANTAGONIST
TRICEPS
- when your TRICEPS CONTRACT, YOUR BICEPS RELAXES
- this PULLS THE BONE so your arm STRAIGHTENS/EXTENDS at the ELBLOW
- here, the TRICEPS IS THE AGONIST and the BICEPS is the ANTAGONIST
why do muscles work in pairs
- because they can only PULL when they CONTRACT, they can not PUSH
describe the structure of skeletal muscle
- SK muscle is made up of LARGE BUNDLES of LONG CELLS called MUSCLE FIBRES
- the CELL MEMBRANE of MUSCLE FIBRE CELLS is called the SARCOLEMMA
- bits of the SARCOLEMMA FOLD INWARDS ACROSS THE MUSCLE FIBRE and STICK INTO THE SARCOPLASM (a muscle cells cytoplasm)
- these folds are called TRANSVERSE TUBULES and they HELP TO SPREAD ELECTRICAL IMPULSES THROUGHOUT THE SARCOPLASM, so they REACH ALL PARTS OF THE MUSCLE FIBRE
- a NETWORK OF INTERNAL MEMBRANES called the SARCOPLASMIC RETICULUM runs through the SARCOPLASM
- the SARCOPLASMIC RETICULUM STORES and RELEASES CALCIUM IONS, which are needed for MUSCLE CONTRACTION
- MUSCLE FIBRES have LOTS OF MITOCHONDRIA to PROVIDE ATP, which is NEEDED FOR MUSCLE CONTRACTION
- they are MULTINUCLEATE (contains many nuclei) and have lots of LONG CYLINDRICAL ORGANELLES called MYOFIBRILS
- MYOFIBRILS are made up of PROTEINS and are HIGHLY SPECIALISED for CONTRACTION
explain the structure of myofibrils
- they contain BUNDLES OF THICK AND THIN MYOFILAMENTS that MOVE PAST EACH OTHER TO MAKE MUSCLES CONTRACT
- the THICK MYOFILAMENTS are made of the PROTEIN MYOSIN
- the THIN MYOFILAMENTS are made of the PROTEIN ACTIN
- if a MYOFIBRIL is looked at under a ELECTRON MICROSCOPE, you will see a PATTERN OF ALTERNATING DARK AND LIGHT BANDS
- DARK BANDS contain the THICK MYOSIN FILAMENTS and SOME OVERLAPPING THIN ACTIN FILAMENTS = these are called A BANDS
- LIGHT BANDS ONLY CONTAIN THIN ACTIN FILAMENTS = these are called I BANDS
- a MYOFIBRIL is made up of MANY SHORT UNITS, called SARCOMERES
- the END OF EACH SARCOMERE is marked with a Z LINE
- in the MIDDLE of the MYOSIN FILAMENTS there is a M LINE
- around the M LINE is the H ZONE, which ONLY CONTAINS MYOSIN FILAMENTS
explain the sliding filament theory
- this theory explains MUSCLE CONTRACTION
- this is where MYOSIN and ACTIN FILAMENTS SLIDE OVER ONE ANOTHER to make the SARCOMERES CONTRACT, the MYOFILAMENTS THEMSELVES DONT CONTRACT
- the SIMULTANEOUS CONTRACTION of LOTS OF SARCOMERES means the MYOFIBRILS and MUSCLE FIBRES CONTRACT
- SARCOMERES RETURN TO THEIR ORIGINAL LENGTH as the MUSCLE RELAXES
what does muscle contraction involve, basic
- myosin
- actin filaments
what are myosin filaments
myosin filaments have GLOBULAR HEADS that are HINGED, so they can MOVE BACK AND FORTH
- each myosin HEAD has a BINDING SITE FOR ACTIN
- each myosin HEAD has a BINDING SITE FOR ATP
what are actin filaments
- they have BINDING SITES for MYOSIN HEADS, this is called ACTIN-MYOSIN BINDING SITES
- another PROTEIN called TROPOMYOSIN is found BETWEEN ACTIN FILAMENTS, it helps MYOFILAMENTS MOVE PAST EACH OTHER
describe the binding sites in resting muscles
- for MYOSIN and ACTIN FILAMENTS to SLIDE PAST EACH OTHER, the MYOSIN HEAD needs to BIND TO the ACTIN-MYOSIN BINDING SITE on the ACTIN FILAMENT
- in a RESTING/UNSTIMULATED MUSCLE the ACTIN-MYOSIN BINDING SITE IS BLOCKED BY TROPOMYOSIN, which means that MYOFILAMENTS can NOT SLIDE PAST EACH OTHER because the MYOSIN HEADS CAN NOT BIND TO THE ACTIN FILAMENTS
explain the process of muscle contraction
ARRIVAL OF AN AP
- when an AP from a MOTOR NEURONE STIMULATES A MUSCLE CELL, IT DEPOLARISES THE SARCOLEMMA
- DEPOLARISATION SPREADS DOWN the T TUBULES TO THE SARCOPLASMIC RETICULUM, this causes the SARCOPLASMIC RETICULUM to RELEASE STORED CALCIUM IONS into the SARCOPLASM
- this INFLUX OF CALCIUM IONS into the SARCOPLASM TRIGGERS MUSCLE CONTRACTION
- CALCIUM IONS BIND TO A PROTEIN ATTACHED TO TROPOMYOSIN, this causes the PROTEIN TO CHANGE SHAPE
- this PULLS THE ATTACHED TROPOMYOSIN OUT OF THE ACTIN-MYOSIN BINDING SITE ON THE ACTIN FILAMENT
- this ^ EXPOSES THE BINDING SITE, WHICH ALLOWS THE MYOSIN HEAD TO BIND, the BOND FORMED WHEN A MYSOSIN HEAD BINDS TO AN ACTIN FILAMENT is called an ACTIN-MYOSIN CROSS BRIDGE
MOVEMENT OF THE ACTIN FILAMENT
- CALCIUM IONS also ACTIVATE the ENZYME ATP HYDROLASE, which HYDROLYSES ATP INTO ADP+Pi, to PROVIDE ENERGY NEEDED FOR MUSCLE CONTRACTION
- the ENERGY RELEASED FROM ATP causes the MYSOIN HEAD TO BEND, which PULLS THE ACTIN FILAMENT ALONG in a ROWING ACTION
BREAKING OF THE CROSS BRIDGE
- ANOTHER ATP MOLECULE PROVIDES THE ENERGY NEEDED TO BREAK THE ACTIN MYOSIN CROSS BRIDGE, so the MYOSIN HEAD DETACHES from the ACTIN FILAMENT AFTER ITS MOVED
- the MYOSIN HEAD then RETUNS TO ITS STARTING POSITION and REATTACHES TO A DIFFERENT BINDING SITE, FURTHER ALONG the ACTIN FILAMENT
- a NEW ACTIN-MYOSIN BRIDGE IS FORMED and THE CYCLE IS REPEATED (attach, move, detach, reattach to a new binding site)
- many actin myosin bridges FORM and BREAK VERY RAPIDLY, PULLING THE ACTIN FILAMENT ALONG - which SHORTENS THE SARCOMERE and this CAUSES THE MUSCLE TO CONTRACT
- this cycle continues as long as CALCIUM IONS ARE PRESENT
RETURN TO RESTING STATE
- when the MUSCLE STOPS BEING STIMULATED, the CALCIUM IONS LEAVE THEIR BINDING SITES and they are MOVED BY ACTIVE TRANSPORT BACK INTO THE SARCOPLASMIC RETICULUM, this causes the TROPOMYOSIN MOLECULES TO MOVE BACK SO THEY BLOCK THE ACTIN MYOSIN BINDING SITES AGAIN
- muscles ARE NOT CONTRACTED because NO MYOSIN HEADS ARE ATTACHED TO ACTIN FILAMENTS, so there are no actin myosin cross bridges
- the ACTIN FILAMENTS SLIDE BACK TO THEIR RELAXED POSITION, which LENGTHENS THE SARCOMERE
what are the 3 ways in which ATP is continually generated so exercise can be continued
- aerobic respiration
- anaerobic respration
- ATP-phosphocreatine (PCR) system
explain how aerobic respiration continually generates ATP
- most ATP is generated via OXIDATIVE PHOSPHORYLATION in the cells MITOCHONDRIA
- aerobic respiration only works when OXYGEN IS AVAILABLE, so its good for long periods of low intensity exercise
explain how anaerobic respiration continually generates ATP
- ATP is made rapidly by GLYCOLYSIS
- the END PRODUCT of GLYCOLYSIS is PYRUVATE, which is CONVERTED to LACTATE by LACTATE FERMENTATION
- LACTATE can QUICKLY BUILD UP IN THE MUSCLES and cause MUSCLE FATIGUE
- anaerobic respiration is GOOD for SHORT PERIODS of hard exercise, like a 400m sprint
explain how ATP phosphocreatine system continually generates ATP
- ATP is made by PHOSPHORYLATING ADP, ADDING A PHOSPHATE GROUP TAKEN FROM PCr
- the equation is : ADP +PCr -> ATP +Cr (creatine)
- PCr is STORED INSIDE CELLS and the ATP-PCr SYSTEM GENERATES ATP VERY QUICKLY
- PCr RUBS OUT AFTER A FEW SECONDS, so it is used during SHORT BURSTS OF VIGOROUS EXERCISE, like a tennis serve
- ATP-PCr system is ANAEROBIC (doesnt need oxygen) and its ALACTIC (it DOES NOT form ANY LACTATE)
- some of the CREATINE gets BROKEN DOWN into CREATININE, which is REMOVED from the BODY VIA THE KIDNEYS
- CREATININE LEVELS CAN BE HIGHER in PEOPLE WHO EXERCISE REGULARLY AND THOSE WITH A HIGHER MUSCLE MASS
- HIGH CREATININE LEVELS MAY ALSO INDICATE KIDNEY DAMAGE
what are the 2 types of muscle fibres that skeletal muscles are made up of
- slow twitch
- fast twitch
describe the properties of slow twitch muscle fibres
- slow twitch muscle fires CONTRACT SLOWLY and can WORK FOR A LONG TIME WITHOUT GETTING TIRED, this makes them good for ENDURANCE ACTIVITIES like long distance running
- high proportions of slow twitch muscles are found in the muscles you use for POSTURE, like the muscles in the BACK and CALVES
- ENERGY is RELEASED SLOWLY through AEROBIC RESPIRATION in SLOW TWITCH MUSCLE FIBRES
- they have LOTS OF MITOCHONDRIA and BLOOD VESSELS to SUPPLY THE MUSCLES WITH OXYGEN
- the MITOCHONDRIA are MAINLY FOUND NEAR TO THE EDGE OF MUSCLE FIBRES, so that there is a SHORT DIFFUSION PATHWAY FOR OXYGEN FROM THE BLOOD VESSELS TO THE MITOCHONDRIA
- SLOW TWITCH MUSCLE FIBRES ARE ALSO RICH IN MYOGLOBIN, a red coloured protein that STORES OXYGEN so they are reddish in colour
describe the properties of fast twitch muscle fibres
- fast twitch muscle fibres CONTRACT VERY QUICKLY but also GET TIRED QUICKLY
- this makes them GOOD FOR SHORT BURSTS of SPEED and POWDER, like sprinting and eye movement
- high proportions of fast twitch muscle fibres are found in muscles you use for FAST MOVEMENT, like in the legs, arms and eyes
- ENERGY is RELEASED QUICKLY through ANAEROBIC RESPIRATION using GLYCOGEN in FAST TWITCH MUSCLE FIBRES
- they also have stores for PCr so that ENERGY CAN BE GENERATED VERY QUICKLY WHEN NEEDED
- fast twitch muscle fibres have FEW MITOCHONDRIA or BLOOD VESSELS
- they DO NOT have much MYOGLOBIN EITHER, so they cannot STORE MUCH OXYGEN, which gives them MORE OF A WHITISH COLOUR
define and explain homeostasis
- changes in your EXTERNAL ENV which can affect your INTERNAL ENV (the blood and tissue fluid that surrounds your cells)
- homeostasis is the maintenance of a STABLE INTERNAL ENV
- it involves control systems that keep your INTERNAL env roughly CONSTANT, within certain limits
- this means your INTERNAL ENV is kept in a state of DYNAMIC EQUILIBRIUM (fluctuating around a normal level)
- keeping your INTERNAL ENV STABLE is VITAL FOR CELLS TO FUNCTION NORMALLY and STOP THEM FROM BEING DAMAGED
explain the importance of homeostasis
- its very important to maintain the right CORE BODY TEMP and BLOOD pH
- this is because temp and pH AFFECT ENZYME ACTIVITY and ENZYMES CONTROL THE RATE OF METABOLIC REACTIONS (chemical reactions in living cells)
- it is also important to maintain the right BLOOD GLUCOSE CONC as CELLS NEED GLUCOSE FOR ENERGY and BLOOD GLUCOSE CONC affects the WP OF BLOOD
explain the importance of TEMPERATURE in maintaining homeostasis
- the RATE OF METABOLIC REACTIONS INCREASES when TEMP INCREASES
- MORE HEAT = MORE KINETIC ENERGY = MOLECULES MOVE FASTER, this makes SUBSTRATE MOLECULES MORE LIKELY to COLLIDE WITH ENZYMES ACTIVE SITES
- the ENERGY of these COLLISIONS also INCREASES, which means each collision is MORE LIKELY to result in a REACTION
- but if the TEMP GETS TOO HIGH, over 40 degrees, the REACTION EVENTUALLY STOPS
- the RISE IN TEMP makes the ENZYMES MOLECULES VIBRATE MORE
- if the TEMP GOES ABOVE a CERTAIN LEVEL, this VIBRATION BREAKS SOME OF THE HYDROGEN BONDS that HOLDS THE ENZYME IN ITS 3D SHAPE
- the ACTIVE SITE CHANGES SHAPE and the ENZYME AND SUBSTRATE NO LONGER FIT TOGETHER, at this point the ENZYME = DENATURED and it NO LONGER FUNCTIONS AS A CATALYST
- of body temp is TOO LOW, the ENZYME ACTIVITY IS REDUCED which SLOWS THE RATE OF METABOLIC REACTIONS
- the HIGHEST RATE OF ENZYME ACTIVITY HAPPENS AT THEIR OPTIMUM TEMP, around 37 degrees celsius in humans
explain the importance of pH in maintaining homeostasis
- if BLOOD Ph is too HIGH or too LOW (too alkaline or too acidic) ENZYMES BECOME DENATURED
- the IONIC BONDS and HYDROGEN BONDS that HOLD THEM IN THEIR 3D SHAPE ARE BROKEN, so the SHAPE OF THE ENZYMES ACTIVE SITE IS CHANGED and it NO LONGER WORKS AS A CATALYST
- the HIGHEST RATE OF ENZYME ACTIVITY happens at their OPTIMUM pH, so this is when METABOLIC REACTIONS ARE FASTEST
- the OPTIMUM pH is around 7/NEUTRAL, but some enzymes found in the stomach work best at a low pH
how is pH calculated
pH = -log^10 [H+]
explain the importance of blood glucose concentration in maintaining homeostasis
- if blood glucose conc is TOO HIGH, the WP of BLOOD is REDUCED TO A POINT WHERE WATER MOLECULES DIFFUSE OUT OF CELLS INTO THE BLOOD VIA OSMOSIS
- this ^ can cause the cells to shrivel up and die
- if blood glucose conc is TOO LOW, cells are UNABLE TO CARRY OUT NORMAL ACTIVITIES because there is NOT ENOUGH GLUCOSE FOR RESPIRATION TO PROVIDE ENERGY
