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Infection and response
Organisation
Cell biology
Biological molecules
Homeostasis and response
Responding to change (a2 only)
Energy transfers (a2 only)
The control of gene expression (a-level only)
Substance exchange
Bioenergetics
Genetic information & variation
Inheritance, variation and evolution
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1f industrialisation and the people: britain, c1783-1885
1c the tudors: england, 1485-1603
Britain & the wider world: 1745 -1901
Inter-war germany
World war one
2n revolution and dictatorship: russia, 1917-1953
World war two & the holocaust
1l the quest for political stability: germany, 1871-1991
The cold war
2j america: a nation divided, c1845-1877
Medieval period: 1066 -1509
The fight for female suffrage
2m wars and welfare: britain in transition, 1906-1957
2d religious conflict and the church in england, c1529-c1570
Britain: 1509 -1745
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24/06/2023
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8-5: Understanding how a nerve impulse (action potential) is conducted along an axon including changes in membrane permeability to sodium and potassium ions. . VOLTAGE (MV) (MEMBRANE POTENTIAL -70 . ACTION POTENTIAL 0 Na+ IONS IN THRESHOLD DEPOLARISATION 1 STIMULUS 1 REPOLARISATION 3 FAILED INITIATIONS K*IONS OUT 2 3 TIME (ms) 5 RESTING STATE REFRACTORY PERIOD 4 HYPERPOLARISATION -Resting potential Nerve cells are polarised in resting state: occurs as result of imbalance between sodium ions and potassium ions, gives inside of nerve cell negative charge in comparison to outside. Sodium ion pumps constantly and actively remove sodium ions from cell cytoplasm (across nerve cell membrane) Potassium ions diffuse out cell through ion channels, along conc gradient->experience electrostatic force attracting them back into cell as result of negative potential created. When forced on potassium ions balanced, there is no net movement: resting potential has been reached. Result of polarisation: difference in voltage across neurone membrane -> value of -70mV (resting potential) -Action potential • When stimulated, neurone cell membrane becomes depolarised. • Excitation of neurone cell triggered, causes sodium channel to open, making it more permeable to sodium ions, which will diffuse into neurone, making inside less negative. • Membrane potential becomes less and less negative, reaches threshold potential of -55mV. Triggers more sodium channels to open, eventually giving potential difference of +30mV -> end of depolarisation, start of repolarisation. -Repolarisation Achieved as result of sodium ion channels closing, potassium channels open. Potassium ions diffuse out of neurone...
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down concentration gradient, eventually restore resting potential. Closing of potassium ions slightly delayed, leads to hyperpolarisation -> when potential difference becomes greater than resting potential. Resting potential achieved with help of sodium-potassium pump, returns potential difference to value of -70mV. Short period when neurone membrane can't be excited as sodium ions enter recovery stage -> known as refractory period, ensures action potentials can pass in one direction only. • Action potential travels along neurone as wave of depolarisation, sodium ions move to adjacent resting region where they diffuse side ways, triggering change in potential difference -> stimulating another action potential. 8-7: Know the structure and function of synapses in nerve impulse transmission, including the role of neurotransmitters, including acetylcholine. -Synaptic transmission When action potential arrives at end of axon of presynaptic neurone, membrane becomes depolarised, causes voltage gated calcium ion channels to open. • Calcium ions diffuse into synaptic knob to move towards presynaptic membrane. • Calcium ions cause vesicles in synaptic knob to move towards presynaptic membrane where they fuse with it and release chemical messengers called neurotransmitters into synaptic cleft by exocytosis. • Neurotransmitter diffuse across synaptic cleft to bind with receptor molecules on post synaptic membrane -> causes associated sodium ion channels to open, allowing sodium to diffuse into postsynaptic cell. • If enough neurotransmitter molecules bind with receptors, then action potential is generated, travels down axon of postsynaptic neurone. Neurotransmitters broken down to prevent continued stimulation of postsynaptic neurone: enzyme that breaks wn acetylcholine is acetylcholinesterase. OPEN CALCIUM CHANNEL ACETYLCHOLINESTERASE OPEN ION CHANNEL 65 ACTION POTENTIALS RE-START, ALLOWING IMPULSE TO CONTINUE DOWN AXON OF POSTSYNAPTIC NEURONE 1. Action potential arrives, depolarising presynaptic membrane 2. Calcium ion channel proteins open. Calcium ions diffuse in 3. Presynaptic vesicles fuse with membrane 4. ACh released 5. ACh diffuses across synaptic cleft 6. ACh binds to receptor proteins 7. Receptor proteins open. Sodium ions diffuse through 8. Postsynaptic membrane is depolarised 9. ACh broken down into acetate and choline by acetylcholineterase 10. Choline recycled into ACh.