A-Level CIE Biology: 15 Coordination & Control

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Last updated 6:55 AM on 11/3/25
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100 Terms

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what is a hormone

chemical substance produced by an endocrine gland and carried by the blood.

  • chemicals which transmit information from one part of the organism to another and bring about a change.

  • they alter the activity of one or more specific target organs

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what do hormones control

functions that don’t need instant responses 

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what is the endocrine system

endocrine glands that produce hormones in animals collectively

<p>endocrine glands that produce hormones in animals collectively</p>
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gland

group of cells that produces and releases one or more substances (secretion)

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examples of cell-signalling molecules/hormones in blood

  • insulin

  • glucagon

  • ADH

  • adrenaline

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why do endocrine glands have a good blood supply

when they make hormones, they need to get the hormones into the bloodstream/blood plasma asap so they can travel around body to target organs and bring about response

<p>when they make hormones, they need to get the hormones into the bloodstream/blood plasma asap so they can travel around body to target organs and bring about response</p>
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what is needed for hormones

cells with receptors that the hormone can bind to either found on the csm or inside cells. they must be complementary to have an effect

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what hormones are peptides

insulin, glucagon and ADH

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features of peptide hormones

  • water-soluble so can’t cross pbl of csm 

  • bind to receptors on csm of target cells which activates second msngers to transfer signal thru cyto

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what hormones are steroids

testosterone, oestrogen, and progesterone

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features of steroid hormones

  • lipid-soluble and can cross pbl

  • bind to receptors in cyto of nucleus of target cells

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human nervous system: 2

  • central nervous system/cns - brain and spinal cord

  • peripheral nervous system/pns - all nerves in body

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what does the nervous system allow us to do and how

  • make sense of our surroundings nad respond to them and to coordinate and regulate body functions

  • info sent thru nervous system as nerve impulses which are electrical signals passing along nerve cells (neurones)

<ul><li><p>make sense of our surroundings nad respond to them and to coordinate and regulate body functions</p></li><li><p>info sent thru nervous system as nerve impulses which are electrical signals passing along nerve cells (neurones)</p></li></ul><p></p>
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nerve

bundle of neurones

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neurones function

coordinate the activity of sensory receptors (e.g. eye), decision making centres in the cns, and effectors such as muscles and glands.

<p>coordinate the activity of sensory receptors (e.g. eye), decision making centres in the cns, and effectors such as muscles and glands.</p>
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nervous system: parts, message, method, effectors, speed, duration

  • brains, spinal cord, nerves/neurones

  • electrical impulse

  • neurones

  • muscles or glands

  • very fast

  • short until electrical impulses stop

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endocrine system: parts, message, method, effectors, speed, duration

  • glands

  • chemical/hormone

  • bloodstream

  • target cells in specific tissues

  • slower

  • longer until hormone broken down

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axon

neurone’s long fibre

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how is an axon insulated

fatty sheath with small uninsulated sections along its length (nodes of Ranvier)

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what is the fatty sheath made of

myelin, substance made by specialised cells (schwann cells) when they wrap themselves around axon along its length

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what is the effect of the axon

electrical impulse doesn’t travel down whole axon but jumps from one node to the next

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why do electrical impulses jump

less time wasted transferring impulse from one cell to another 

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dendrites

cell bodies contain many extensions/dendrites that allow them to connect to many other neurones and receive impules from them forming a network for easy communication

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3 main types of neurone

sensory, relay, motor

<p>sensory, relay, motor</p>
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sensory function

carry impulses from receptors to cns/brainorspinalcord

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intermediate/relay neurone function

found entirely within cns and connect sensory and motor

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motor function

carry impulses from cns to effectors/muscles or glands

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are all neurones the same

no, each has slightly diff structure

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motor neurone structure: 3

  • large cell body at one end, that lies within spinal cord or brain

  • nucleus that is always in its cell body

  • many highly-branched dendrites extend from cell body, providing large sa for axon terminals of other neurones

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sensory neurones structure

  • same basic as motor but have cell body that branches off in middle of cell = may be near source of stimuli or in swelling of spinal nerve known as ganglion

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receptor cell

cell that responds to a stimulus. transducers. convert energy in one form (e.g. light/heat/sound) into energy in electrical impulse within sensory neurone

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where are receptor cells found

in sense organs (e.g. light receptor cells found in eye, chemoreceptors in taste buds)

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what are some receptors

specialised cells that detect a specific tyep of stimulus and infleunce the elcetrical activity of a sensory neurone (light and chemo eye and tongue)

others (e.g. touch) are just ends of sensory neurones themself

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what happens when receptor cells are stimulated. what if its weak/strong

depolarised

weak= not sufficiently depolarised and sensory neurone is not actviated to send impulses

strong=sensory neurone activated and transmits impulses to cns

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tongue surface. 

many small bumps called papillae covering surface of tongue, each covered in many taste buds which contain many chemoreceptors that are sensitive to chemicals in food and drinks bc covered with receptor proteins to detect diff chemis

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what do chemoreceptors in taste buds that detect salt (sodium chloride) respond directly to

sodium ions.

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if salt is present in food (dissolved in saliva) being eaten:

  • na+ diffuse thru highly selective channel proteins in csm of microvilli of chemoreceptor cells

  • leads to depolarisation of chemoreceptor cell memb

  • increase in + charge inside cell = receptor potential

  • if sufficient stimulation by na+ and sufficient depolarisation of membrane, the receptor potential becomes large enough to stimulate voltage-gated calcium ion channel proteins to open

  • as result, calcium ions enter the cyto of chemoreceptor cell and stimulate exocytosis of vesicles containing neurotransmitters from the basal membrane of the chemoreceptor

  • neurotransmitter stimulates an action potential in sensory neurone

  • sensory neurone then transmits an impulse to the brain

<ul><li><p>na+ diffuse thru highly selective channel proteins in csm of microvilli of chemoreceptor cells</p></li><li><p>leads to depolarisation of chemoreceptor cell memb</p></li><li><p>increase in + charge inside cell = receptor potential</p></li><li><p>if sufficient stimulation by na+ and sufficient depolarisation of membrane, the receptor potential becomes large enough to stimulate voltage-gated calcium ion channel proteins to open</p></li><li><p>as result, calcium ions enter the cyto of chemoreceptor cell and stimulate exocytosis of vesicles containing neurotransmitters from the basal membrane of the chemoreceptor</p></li><li><p>neurotransmitter stimulates an action potential in sensory neurone</p></li><li><p>sensory neurone then transmits an impulse to the brain</p></li></ul><p></p>
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when are receptors depolarised

when they are stimulated

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if stimulus is very weak/below certain threshold….

receptor cells wont be sufficiently depolarised and the sensory neurone will not be activated to send impulses

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if stimulus is strong enough to increase receptor potential above the threshold potential

then receptor will stimulate sensory neurone to send impulses 

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all-or-nothing principle

impulse only transmitted if initial stimulus is sufficient to increase membrane potential above threshold potential

<p>impulse only transmitted if initial stimulus is sufficient to increase membrane potential above threshold potential</p>
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with continued stimulation….

threshold levels in receptors often increase so that a greater stimulus is required before impulses sent along sensory neurones

<p>threshold levels in receptors often increase so that a greater stimulus is required before impulses sent along sensory neurones</p>
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neurones transmit ______ which travel v quickly along __________ from ____ to _____

electrical impulses, neurone cesm, one end to other

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are impulses flow of e-

no, they are known as action potentials and occur via very brief changes in distribution of electrical charge across csm.

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what are actiona potentials caused by

rapid movement of na+ and potassium ions across the membrane of the axon

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what happens in a resting axon (one that isnt transmitting inpulses)

the inside of axon always has slightly negative e- potential cmopared to outside

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what is the potential difference

-70mV (inside of axon has electrical potential 70mV lower than outside) ← resting potential

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4 factors in maintaining resting potential

  • sodium-potassium pumps in axon membrane

  • many large, neg charged mols (anions) inside axon

  • impermeability of axon membrane to ions

  • closure of voltage-gated channels (required for action potentials) in axon membrane

<ul><li><p>sodium-potassium pumps in axon membrane</p></li><li><p>many large, neg charged mols (anions) inside axon</p></li><li><p>impermeability of axon membrane to ions</p></li><li><p>closure of voltage-gated channels (required for action potentials) in axon membrane</p></li></ul><p></p>
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how does sodium-potassium pumps in axon membrane contribute to maintaining RP

  • pumps move na+ out of axon and k+ into axon

  • pump proteins use the energy from hydrolysis of ATP to continue moving ions against conc grads

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how do many large, neg charged mols (anions) inside axon contribute to maintaining RP

attracts K+ reducing change of them diffusing out of axon

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how does impermeability of axon membrane to ions contribute to RP

  • na+ cant diffuse through axon membrane when neurone is at rest

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how does closure of voltage-gated channels (required for action potentials) in axon membrane contribute to RP

  • stops na and k ions diffusing through axon membrane

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why are there channel proteins in axon membrane

allow na+ or k+ to pass through

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what does the open and close of the channel proteins depend on

electrical potential/voltage across axon membrane and are known as voltage-gated channel proteins (closed when axon memb at RP)

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what happens when action potential is stimulated (by receptor) in neurone: 10

  • na channel proteins in axon membrane open

  • na+ pass into axon dwon electrochemical gradient (greater conc of na+ outsiide axon than inside. inside of axon neg charged attracting pos charged na+)

  • reduces potential diff across axon mebrane as inside becomes less negative (depolarisation)

  • voltage-gated na channels open, allowing more na+ to enter so more depolarisation

  • positive feedback (small intial depolarisation leads to greater and greater lvls of depolarisation)

  • if potential diff reaches around -50mV (threshold value) many more channels open and many more na+ enter causing inside of axon to reach potential fo around +30mV

  • action potential generated

  • depolarisation of memb at site of first action potential causes current to flow to next section of axon memb, depolarising it and causing na+ voltage-gated hcannel proteins to open

    • flow of current is caused by diffusion of na+ along axong area of high conc to area of low conc

  • triggers production of another action potential in section of axon membrane and process continues

  • allows action potentials to begin at one end of an axon and then pass along entire length of axon membrane

<ul><li><p>na channel proteins in axon membrane open</p></li><li><p>na+ pass into axon dwon electrochemical gradient (greater conc of na+ outsiide axon than inside. inside of axon neg charged attracting pos charged na+)</p></li><li><p>reduces potential diff across axon mebrane as inside becomes less negative (depolarisation)</p></li><li><p>voltage-gated na channels open, allowing more na+ to enter so more depolarisation</p></li><li><p>positive feedback (small intial depolarisation leads to greater and greater lvls of depolarisation)</p></li><li><p>if potential diff reaches around -50mV (threshold value) many more channels open and many more na+ enter causing inside of axon to reach potential fo around +30mV</p></li><li><p>action potential generated</p></li><li><p>depolarisation of memb at site of first action potential causes current to flow to next section of axon memb, depolarising it and causing na+ voltage-gated hcannel proteins to open</p><ul><li><p>flow of current is caused by diffusion of na+ along axong area of high conc to area of low conc</p></li></ul></li><li><p>triggers production of another action potential in section of axon membrane and process continues</p></li><li><p>allows action potentials to begin at one end of an axon and then pass along entire length of axon membrane</p></li></ul><p></p>
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refractory period/repolarisation process 5

  • very shortly (1ms) after action potential in a section of axon memb is generate, all na+ voltage-gated channel proteins in section close, stopping any further na+ diffusing into axon

  • k+ voltage-gated channel proteins in this section of axon memb now open, allowing diffusion of k+ out of axon, down their conc grad

  • returns potential diff to normal (-70mv) a process known as repolarisation

    • actually short period of hyperpolarisation

    • potential diff across section of axon membrane briefly becomes more negative than the normal resting potential 

  • once resting potential close to being re-established, k+ ion voltage-gated channel proteins close

    • K+ ion voltage-gated channel proteins then close and the na+ ion channel proteins in section of memb become responsive to depolarisation again

    • until occurs, section of the axon membrane is in a period of recovery and unresponsive

<ul><li><p>very shortly (1ms) after action potential in a section of axon memb is generate, all na+ voltage-gated channel proteins in section close, stopping any further na+ diffusing into axon</p></li><li><p>k+ voltage-gated channel proteins in this section of axon memb now open, allowing diffusion of k+ out of axon, down their conc grad</p></li><li><p>returns potential diff to normal (-70mv) a process known as repolarisation</p><ul><li><p>actually short period of hyperpolarisation</p></li><li><p>potential diff across section of axon membrane briefly becomes more negative than the normal resting potential&nbsp;</p></li></ul></li><li><p>once resting potential close to being re-established, k+ ion voltage-gated channel proteins close </p><ul><li><p>K+ ion voltage-gated channel proteins then close and the na+ ion channel proteins in section of memb become responsive to depolarisation again</p></li><li><p>until occurs, section of the axon membrane is in a period of recovery and unresponsive</p></li></ul></li></ul><p></p>
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add all the drug stuff***

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speed of conduction of impulse

how quickly impulse transmitted along neurone

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speed of conduction of impulse 2 main factors

  • presence/absence of myelin (myelin sheath on axon)

  • diameter of axon

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speed of conduction in unmyelinated neurones

very slow

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how does presence of myelin increase speed at which action pots can travel along neurone: 6

  • axon that are surrounded by myelin sheath, depolarisation (and action potentials that this would lead to) cant occur as myelin sheath stops diffusion of na+ and k+

  • action potentials only occur at nodes of ranvier (small uninsulated sections of axon)

  • local circuits of current that trigger depolarisation in next sections of axon memb exist between nodes of ranvier

  • action pots jump from one node to next

  • saltatory conduction

  • impulses travel much faster (50x) than unmyelinated axon of same diametr

<ul><li><p>axon that are surrounded by myelin sheath, depolarisation (and action potentials that this would lead to) cant occur as myelin sheath stops diffusion of na+ and k+</p></li><li><p>action potentials only occur at nodes of ranvier (small uninsulated sections of axon)</p></li><li><p>local circuits of current that trigger depolarisation in next sections of axon memb exist between nodes of ranvier</p></li><li><p>action pots jump from one node to next</p></li><li><p>saltatory conduction</p></li><li><p>impulses travel much faster (50x) than unmyelinated axon of same diametr</p></li></ul><p></p>
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saltatory conduction

knowt flashcard image
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why speed of conduction of impulse along neurones with thicker axons is greater than along those with thinner ones

  • thicker axons have axon membrane w greater s.a. over which diffusion of ions can occur

  • increases rate of diffusion of na+ and k+

  • increases rate at which depolarisation and action potentials can occur

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5 reasons why refractory period is important

  • ensures action potentials are discrete events, stopping them from merging into each other

  • ensures changes of memb potential are generated ahead (furhter along axon) rather than behind og action depolarisation as region behind is recovering from repolarisation that just occured

  • impulse can only travel in 1 direction, essential for successdful and efficient transmission of nerve impulses along neurone

  • minimum time between action potentials occuring at any one place along neurone

  • length of refractory period is key in determining the maximum frequency at which impulses can be transmitted along neurones between 500-1000 per second

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synaptic cleft

when two neurones meet they don;t actually come in physical contact with each other and a very small gap separates them (synaptic cleft)

<p>when two neurones meet they don;t actually come in physical contact with each other and a very small gap separates them (synaptic cleft) </p>
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synapse

ends of 2 neurones along synaptic cleft forming synapse

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synaptic transmission - basic mechanism

  • electrical impulses cant jump across synapses

  • when elcetrical impulse arrives at end of axon on presynaptic neurone, chem messengers called neurotransmitters released from vesicles at presynaptic memb

  • nts diffuse across synpatic cleft and bind temporarily w receptor mols on postsynaptic membrane

  • stimulates postsynaptic neurone to generate elec impulse that then travels down axon to postsynaptic neurone

  • nts destroyed/recycled to prevent continued stimulation of 2nd neurone which cld cause repeated impulses to be sent

<ul><li><p>electrical impulses cant jump across synapses</p></li><li><p>when elcetrical impulse arrives at end of axon on presynaptic neurone, chem messengers called neurotransmitters released from vesicles at presynaptic memb</p></li><li><p>nts diffuse across synpatic cleft and bind temporarily w receptor mols on postsynaptic membrane</p></li><li><p>stimulates postsynaptic neurone to generate elec impulse that then travels down axon to postsynaptic neurone</p></li><li><p>nts destroyed/recycled to prevent continued stimulation of 2nd neurone which cld cause repeated impulses to be sent</p></li></ul><p></p>
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process of synaptic transmission w ACh - detailed mch

  • arrival of action potential at presynaptic memb causes depolarisation of memb

  • stimulates voltage-gated ca2+ channel proteins to open

  • ca2+ diffuse down elcetrochemical gradient from tissue fluid surrounding synapse (high conc of ca2+) into cytoplasm of presynaptic neurone (low conc of ca2+)

  • stimulates ACh containing vesicles to fuse w presynaptic memb releasing ACh mols into synaptic cleft

  • ACh mols diffuse across synaptic cleft and temp bind to receptor proteins in postsynaptic memb

  • causes conformational change in receptor proteins which open, allowing na+ to diffuse down electrochemical gradient into cyto of postsynaptic neurone

  • na+ cause depolarisation of postsynaptic memb, re-starting electrical impulse that can now continue down axon of postsynaptic neurone

  • orevent na+ channels from staying permanently open and to stop permanent depolarisation of postsynaptic memb, ACh mols broken down and recycled

  • enzyme acetylcholinesterase catalyses hydrolysis of ACh mols into acetate and choline

  • choline absorbed back into presynaptic memb and reacts w acetyl coA to form ACh and packaged into presynaptic vesicles ready to be used when another action potential arrives

<ul><li><p>arrival of action potential at presynaptic memb causes depolarisation of memb</p></li><li><p>stimulates voltage-gated ca2+ channel proteins to open</p></li><li><p>ca2+ diffuse down elcetrochemical gradient from tissue fluid surrounding synapse (high conc of ca2+) into cytoplasm of presynaptic neurone (low conc of ca2+)</p></li><li><p>stimulates ACh containing vesicles to fuse w presynaptic memb releasing ACh mols into synaptic cleft</p></li><li><p>ACh mols diffuse across synaptic cleft and temp bind to receptor proteins in postsynaptic memb</p></li><li><p>causes conformational change in receptor proteins which open, allowing na+ to diffuse down electrochemical gradient into cyto of postsynaptic neurone</p></li><li><p>na+ cause depolarisation of postsynaptic memb, re-starting electrical impulse that can now continue down axon of postsynaptic neurone</p></li><li><p>orevent na+ channels from staying permanently open and to stop permanent depolarisation of postsynaptic memb, ACh mols broken down and recycled</p></li><li><p>enzyme acetylcholinesterase catalyses hydrolysis of ACh mols into acetate and choline</p></li><li><p>choline absorbed back into presynaptic memb and reacts w acetyl coA to form ACh and packaged into presynaptic vesicles ready to be used when another action potential arrives</p></li></ul><p></p>
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how many diff nts

40+ 

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acetylcholine

ACh, key nt used thru nervous system

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cholinergic synapses

synapses that use nt ACh

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when does striated muscle contract

when it receives an impulse from a motor neurone via the neuromuscular junction

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why do calcium ions diffuse into the neurone

when impulse travelling along axon of motor neurone arrives at presynaptic membrqane, action potential causes this

<p>when impulse travelling along axon of motor neurone arrives at presynaptic membrqane, action potential causes this</p>
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steps before muscle contraction/sliding filament model can begin

  • inward diffusion of ca2+ ions stimulates vesicles containing nt acetylcholine to fuse w presynaptic memb

    • ACh released diffuses across neuromuscular junction and binds to receptor proteins on sarcolemma (surface memb of muscle fibre cell)

    • stimulates ion channels in sarcolemma to open, allowing na+ to diffuse in

    • depolarises sarcolemma generating action potential that passes down t-tubules towards centre of muscle fibre

  • action potentials cause voltaged-gated ca2+ ion channel proteins in membs of sarcoplasmic reticulum (whcih lie v close to t tubules) to open

    • ca2+ ions diffuse out of sarcoplasmic reticulum (SR) and into sarcoplasm surrounding myofibrils

    • ca2+ ions bind to troponin mols stimulating them to change shape

    • causes troponin and tropomyosin proteins to change position on thin (actin) filaments

    • myosin binding sites exposed to actin mols

<ul><li><p>inward diffusion of ca2+ ions stimulates vesicles containing nt acetylcholine to fuse w presynaptic memb</p><ul><li><p>ACh released diffuses across neuromuscular junction and binds to receptor proteins on sarcolemma (surface memb of muscle fibre cell)</p></li><li><p>stimulates ion channels in sarcolemma to open, allowing na+ to diffuse in</p></li><li><p>depolarises sarcolemma generating action potential that passes down t-tubules towards centre of muscle fibre</p></li></ul></li><li><p>action potentials cause voltaged-gated ca2+ ion channel proteins in membs of sarcoplasmic reticulum (whcih lie v close to t tubules) to open</p><ul><li><p>ca2+ ions diffuse out of sarcoplasmic reticulum (SR) and into sarcoplasm surrounding myofibrils</p></li><li><p>ca2+ ions bind to troponin mols stimulating them to change shape</p></li><li><p>causes troponin and tropomyosin proteins to change position on thin (actin) filaments</p></li><li><p>myosin binding sites exposed to actin mols</p></li></ul></li></ul><p></p>
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how myofibrrils within muscle fibres stimulated to contract

knowt flashcard image
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striated muscle

makes up muscles in body attached to skeleton (striated=striped/streaky) made of muscle fibres

<p>makes up muscles in body attached to skeleton (striated=striped/streaky) made of muscle fibres</p>
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3 muscle fibre features that make it a highly specialised cell like unit

  • each contains an organised arragnement of contractile proteins in cytoplasm

  • each surrounded by csm

  • each contains many nuclei which is why nto usually referred to as cedlls

<ul><li><p>each contains an organised arragnement of contractile proteins in cytoplasm</p></li><li><p>each surrounded by csm</p></li><li><p>each contains many nuclei which is why nto usually referred to as cedlls</p></li></ul><p></p>
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diff parts of muscle fibres w diff names to equivalent parts

  • csm = sarcolemma

  • cyto = sarcoplasm

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what does sarcoplasm contain and why

  • mitoch for carrying out aerobic resp to generate atp required for muscle contraction

  • myofibrils (bundles of actin and myosin filaments) which slide past each other during muscle contraction

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myofibrils: qhere, what, how

  • located in sarcoplasm

  • made up of 2 types of protein filament:

    • thick made of myosin

    • thin made of actin

  • arranged in particular order creating diff types of band and line

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6 parts of myofibril + description

  • h band - only thick myosin fils present

  • i band - only thin actin fils present

  • a band - contain areas where only myosin fils are present and areas where myosin and actin fils overlap

  • m line - attachment for myosin fils

  • z line - attachment for actin fils

  • sarcomere - section of myofibril between 2 z lines

<ul><li><p>h band - only thick myosin fils present</p></li><li><p>i band - only thin actin fils present</p></li><li><p>a band - contain areas where only myosin fils are present and areas where myosin and actin fils overlap</p></li><li><p>m line - attachment for myosin fils</p></li><li><p>z line - attachment for actin fils</p></li><li><p>sarcomere - section of myofibril between 2 z lines</p></li></ul><p></p>
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3 features of thick filaments (made of myosin mols)

  • fibrous protein mols w globular head

  • fibrous part of mysoin mols anchors mol into thick filament

  • in thick filament many myosin mols like next to each other with their globular heads all pointing away from the M line

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5 features of thin filaments (made of actin mols)

  • globular protein mols

  • many actin mols link tg to form chain

  • 2 actin chains twist tg to form 1 thin filament

  • fibrous protein (tropomyosin) twisted around 2w actin chains

  • another protein known as troponin is attached to actin chains at regular intervals

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how does sliding filament model of muscle coontraction occur -detailed:

  • action potential arrives at neuromuscular junction

  • ca2+ released from sarcoplasmic rfeticulum

  • ca2+ bind to troponin mols stimulating shape change

  • troponin and tropomyosin proteins change position on actin (thin) filaments

  • myosin binding sites exposed on actin mols

  • glob heads of myosin mols bind with these sites, forming cross-bridges between 2 types of filament

  • myosin heads move and pull the actin filaments towards the centre of the sarcomere causing the muscle to contract a very small distance

  • atp hydrolysis occurs at myosin heads, providing energyt required for myosin heads to release actin filaments

  • myosin heads move back to og positions and bind tfo new binding sites on actin fils closer to z disc

  • myosin heads move again pulling actin fils even closer to centre of sarcomere causing it to shorten once more and pulling z discs closer together

  • myosin heads hydrolyse atp once more to detach again

  • as long as troponin and tropomysoin not blocking myosin-binding sites and muscle has a supply of atp process repeats until muscle fully contracted

<ul><li><p>action potential arrives at neuromuscular junction</p></li><li><p>ca2+ released from sarcoplasmic rfeticulum</p></li><li><p>ca2+ bind to troponin mols stimulating shape change</p></li><li><p>troponin and tropomyosin proteins change position on actin (thin) filaments</p></li><li><p>myosin binding sites exposed on actin mols</p></li><li><p>glob heads of myosin mols bind with these sites, forming cross-bridges between 2 types of filament</p></li><li><p>myosin heads move and pull the actin filaments towards the centre of the sarcomere causing the muscle to contract a very small distance</p></li><li><p>atp hydrolysis occurs at myosin heads, providing energyt required for myosin heads to release actin filaments</p></li><li><p>myosin heads move back to og positions and bind tfo new binding sites on actin fils closer to z disc</p></li><li><p>myosin heads move again pulling actin fils even closer to centre of sarcomere causing it to shorten once more and pulling z discs closer together</p></li><li><p>myosin heads hydrolyse atp once more to detach again</p></li><li><p>as long as troponin and tropomysoin not blocking myosin-binding sites and muscle has a supply of atp process repeats until muscle fully contracted</p></li></ul><p></p>
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what happens during muscle contraction

sarcomeres within myofibrils shnorten as the z discs are pulled closer together

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venus flytrap

carnivorous plant that can gain nitrogen compounds by trappind and digesting small animals, mainly insects.

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structure of venus flytrap

  • the specialised leaf divided into two lobes on either side of midrib

  • inside of lobes is red and has nectar secreting glands on edges to attract insects

  • each llobe has 3 stiff sensory hairs that detech gtouch

  • if insect touchnes one hair action potential generated which causes 2 lobes to fold along midrib capturing insect

<ul><li><p>the specialised leaf divided into two lobes on either side of midrib</p></li><li><p>inside of lobes is red and has nectar secreting glands on edges to attract insects</p></li><li><p>each llobe has 3 stiff sensory hairs that detech gtouch </p></li><li><p>if insect touchnes one hair action potential generated which causes 2 lobes to fold along midrib capturing insect</p></li></ul><p></p>
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how is the closure of the trap achieved

when sensory hairs are touched repeatedly, generating an action potential as follows:

  1. insect lands on leaf and touches sensory hairs

  2. ca2+ ion channels in cells at base of hair open

  3. ca2+ flows in and generates receptor potential

  4. if 2 of the sensory hairs are stimulated at the same time or one hair twice within 30s an action potential occurs and is propagated across cells of trap (if no repeat stim then trap resets to beginning so plant doesnt waste energy if insect not present)

  5. cells at base of trap change shape and trap closes (sealing requires ongoing activation of sensory hairs which happen when prey continue to move inside closed trap)

  6. further stim causes ca2+ to enter gland cells where they stimulate exocytosis of vesicles containing digestive enzymes

  7. trap stays closed for up to week so prey is digested and nutrients absorbed

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receptor potential

change in membrane potential that occurs in a receptor cell due to an initial stimulation; if this reaches a threshold then it can result in an action potential

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plant hormones/plant growth regulators

responsible for most communication within plangts

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auxin

type of plant growth regulator that influences many aspects of growth including elongation growth which determines the overall length of roots and shoots

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principle chemical in group of auxins made by plants

IAA (indole 3-acetic acid) → auxin

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when is IAA synthesized

growing tips of roots and shoots (i.e. in meristems where cells divide)

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3 stages where growth in meristems occur:

  • cell divisions by mitosis

  • cell elongation by absorption of water

  • cell differentiation 

iaa controls growth by elongation

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how is growth controlled by elongation

  • auxin molecule bind to receptor protein on csm

  • auxin stimulates atpase proton pumps to pump h+ from cyto to cell wall across csm

  • acidifies cell wall (lowers pH)

  • activates proteins (expansins) which loosen bonds between cellulose microfibs

  • at same time k+ channels stims to open

  • this leads to increase in k+ conc in cyto which decreases wp of cyto

  • cell absorbs water by osmosis (water enters thru aquaporins)

  • increased internal pressure of cell, causing cell wall to stretch (possible bc expansin)

  • cell elongates

<ul><li><p>auxin molecule bind to receptor protein on csm</p></li><li><p>auxin stimulates atpase proton pumps to pump h+ from cyto to cell wall across csm</p></li><li><p>acidifies cell wall (lowers pH)</p></li><li><p>activates proteins (expansins) which loosen bonds between cellulose microfibs</p></li><li><p>at same time k+ channels stims to open</p></li><li><p>this leads to increase in k+ conc in cyto which decreases wp of cyto</p></li><li><p>cell absorbs water by osmosis (water enters thru aquaporins)</p></li><li><p>increased internal pressure of cell, causing cell wall to stretch (possible bc expansin) </p></li><li><p>cell elongates</p></li></ul><p></p>
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gibberellins

type of plant growth regulator involved in controlling seed germination and stem elongation.

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what state is barley seed in when shed fcrom parent plant

dormancy (contains very little water and is metabolically inactive) so can survive harsh conditions until theyre right for successful germination (e.g. cold winter→ spring)

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what 3 things do barley seed contains:

  • embryo - grow into new plant when seed germinates

  • endosperm - starch-containing energy store surrounding embryo

  • aleurone layer - protein-rich layer on the outer edge of endosperm

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what happens to barley seeds when conditions are right

  • barley seed starts to absorb water to begin germination

  • this stims embryo to produce gibberellins

  • gibberellin mols diffuse into aleurone layer and stim cells there to synth enzyme amylase

    • in barley seeds, it has been shown that gibberellin does this by regulating genes involved in synthesis of amylase causing increase in transcription of mRNA coding for amylase

  • amylase hydrolyses starch mols in endosperm, producing soluble maltose mols

  • maltose converted to glucose and transported to embryo

  • glucose can be respired by embryo, providing embryo w energy needed for it to grow

<ul><li><p>barley seed starts to absorb water to begin germination</p></li><li><p>this stims embryo to produce gibberellins</p></li><li><p>gibberellin mols diffuse into aleurone layer and stim cells there to synth enzyme amylase</p><ul><li><p>in barley seeds, it has been shown that gibberellin does this by regulating genes involved in synthesis of amylase causing increase in transcription of mRNA coding for amylase</p></li></ul></li><li><p>amylase hydrolyses starch mols in endosperm, producing soluble maltose mols</p></li><li><p>maltose converted to glucose and transported to embryo</p></li><li><p>glucose can be respired by embryo, providing embryo w energy needed for it to grow</p></li></ul><p></p>
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gibberellin stimulation

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