Year 13 Flashcards
(39 cards)
Resting potential
Sodium potassium pump transports 3 sodium ions out of the axon and 2 potassium ions into the axon.
Active transport – against a concentration gradient.
Concentration of sodium ions outside the cell increases.
Potassium ions diffuse out of the axon
The sodium ion gate is closed. The sodium ions cannot diffuse into the axon. Positive charge on the outside of the axon
Action potential
Sodium ion channel protein opens.
Sodium ions diffuse into the axon along the concentration gradient. Potassium ion channel protein closes.
Inside of the axon becomes positively charged.
Outside of the axon becomes less positive (-) charged.
Repolarisation
Potassium ion channels open
Potassium ions diffuse out of axon
Sodium ion channels close.
More positively charged outside axon.
Sodium ions actively transported outside the axon.
Pacinian corpuscle
Increase pressure deforms stretch mediated sodium on channels Sodium channels open
Sodium ions flow in
Depolarisation
Leads to a generator potential
Rod cells
Rhodopsin breaks down when light shines on it. Rhodopsin → retinal + opsin
Results in a series of reactions
Generator potential being produced.
ATP is needed to re-synthesise rhodopsin.
Synapses
Action potential reaches end of sensory neurone. Na+ enters the axon.
Calcium ion channels in the presynaptic membrane open allowing calcium ions to diffuse into the presynaptic knob.
Ca2+ ions cause vesicles containing acetylcholine to fuse with the presynaptic membrane.
Neurotransmitter is released into the synapse.
Acetylcholine diffuses across the synapse.
Binds to the receptor proteins on post synaptic membrane –
Causes sodium ion channels to open on post synaptic membrane.
Sodium ions enter relay neurone.
Action potential generated at next Node of Ranvier.
Acetylcholinesterase breaks down acetylcholine which leaves the receptor protein. Acetyl and choline diffuse across the synapse.
Acetyl and choline reabsorbed into the presynaptic knob
Condense to form acetylcholine.
Muscle contraction
Action potential arrives in the muscle cell membrane.
Actin potential travels down a T tubule.
Action potential causes calcium ions to be released from the ER in the muscle cell. Calcium ions bind to the troponin
Tropomyosin to move and reveal the myosin binding sties.
Myosin head binds to the actin to form an actinomyosin bridge.
Myosin moves in power stroke
Myosin pulls the actin.
ADP is released from the myosin head.
Attachment of ATP to the myosin head causes actinomyosin bridge to break
ATP is hydrolysed
Energy released used to ‘recock’ the myosin head.
Calcium ions reabsorbed into the ER of the muscle cell by active transport
Myosin binding sites are hidden preventing myosin binding to the actin.
Control of the cardiac cycle
SAN sends wave of electrical activity over the atria
Atria contract
Non-conducting tissue prevents impulses reaching the ventricles AVN delays impulse blood leaves atria into ventricles
AVN sends wave of electrical impulses down Bundle of His or Purkyne fibres Ventricles contract from base up sending blood into arteries
Increasing heart rate due to increased respiration
Rate of respiration increases in muscles
Chemoreceptors detect rise in CO2 / H+ / acidity / carbonic acid / fall in pH Receptors in aortic arch or carotid bodies
Send impulses to cardioaccelerator centre in medulla
Increased frequency of impulses to SAN
Along sympathetic nervous system to SAN
Release of noradrenaline increase impulses frequency from SAN
Reducing heart rate due to increase blood pressure
Pressure receptors or baroreceptors detect increase in blood pressure Baroreceptors in aortic arch or carotid arteries
Send impulses to cardioinhibitory centre in medulla
Increased frequency of impulses to SAN
Along parasympathetic nervous system
Release of acetylcholine decreases frequency of impulses from SAN;
Phototropism in stems
Shoot tip produces IAA
IAA diffuses down the stem equally
Light causes IAA to move away from the light to the shaded side IAA causes cells to elongate on the shaded side
Cells on the shaded side grow longer
The stem grows towards the light
Gravitropism in roots
Root tip produces IAA
Gravity causes IAA to concentrate in the lower side of the root IAA inhibits elongation of cells on lower side
Root grows downwards/towards gravity
Kinesis
Response to a changing stimulus
Movement is random/not directional
Rate of turning changes
Taxis
Directional response to a directional stimulus Animal moves towards or away from the stimulus
Glycolysis
Glycolysis takes place in cytoplasm
Glucose phosphorylated
Provides activation energy
Phosphorylated glucose hydrolysed to form 2 triose phosphate Triose phosphate oxidised by removal of hydrogen
Hydrogen transferred to NAD to form NADH
2 pyruvate molecules made
Substrate level phosphorylation produces 2 ATP
Links reaction
Pyruvate is decarboxylated to form acetyl
Hydrogen is removed and attached to NAD to form NADH Acetyl is bound to Coenzyme A
Kerbs cycle
Occurs in the mitochondria
Pyruvate enters the mitochondria by active transport
Acetyl coenzyme A delivers acetyl
Acetyl combines with a 4-carbon molecule
A 6-carbon molecule is formed
Coenzyme A is released to pick up more acetyl
The 6-carbon molecule is decarboxylated and oxidised twice
2 NAD are reduced/NADH is produced
To form a 4-carbon molecule
The 4-carbon molecule is oxidised
Reduced NAD is produced/NADH is produced
Reduced FAD is produced/FADH is produced
A molecule of ATP is made by substrate level phosphorylation
The 4-carbon molecule is rearranged to make the original 4-carbon molecule
Oxidative phosphorylation
Krebs cycle / link reaction produces reduced NAD and reduced FAD Electrons released from NADH and FADH
Electrons pass along electron transport chain
Through series of redox reactions
Energy is released from electrons Protons/H+ move into intermembrane space Protons/H+ diffuse through ATP synthase
To form ATP from ADP and Pi
Glucagon
Glucagon is made in alpha cells of islet of Langerhans Released into blood
Glucagon binds to specific receptor.
On target cell - muscles and liver
Activation of adenylate cyclase
ATP converted to cyclic AMP
cAMP activates protein kinase
Protein kinase hydrolysis glycogen to form glucose (glycogenolysis) Facilitated diffusion of glucose out of target cells
Increases blood glucose levels
Insulin
Insulin made in β cells of islet of Langerhans Released into blood
Insulin binds to specific receptors
On target cells – muscle and liver
Vesicles containing glucose channel proteins fuse with cell membrane Increased facilitated diffusion of glucose into target cell
Decrease blood glucose level
Ultra filtration- kidney
High blood pressure created in glomerulus
Due to contraction of left ventricle wall
Small molecules pass through basement membrane Proteins/large molecules too large to go through membrane Podocytes encourage transfer of molecules
Selective reabsorption
Glucose/amino acids co-transported
Carrier protein transports sodium ion along with glucose/amino acid
Into cytoplasm of proximal convoluted tubule cell down concentration gradient of sodium ions
Low concentration of sodium ions maintained by active transport of sodium ions out of cell by sodium potassium pump
Facilitated diffusion of glucose/amino acids into blood though a channel protein
Absorption of water in loop of Henle
Sodium ions actively transported out of ascending limb Chloride ions diffuse out to create sodium chloride Creates low water potential in medulla/tissue fluid Creates water potential gradient
Water moves by osmosis out of descending limb and is absorbed into capillaries
Volume of water in nephron is reduced
Water balance
Decreased water potential of blood (lack of water, increased sweating, solutes in diet)
Detected by osmoreceptors in hypothalamus
Increased impulses to pituitary gland
Pituitary releases more ADH
ADH binds to specific receptors on target cell – distil convoluted tubule Vesicles containing aquaporins fuse with cell membrane
Increases permeability of cell membrane to water
More water reabsorbed into the blood
By osmosis down water potential gradient
Water potential of blood increases
