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6 Stimuli & Homeostasis 🍄 AQA A-Level Biology - Coggle Diagram
6 Stimuli & Homeostasis 🍄 AQA A-Level Biology
Homeostasis
positive feedback
when one change occurs because of the stimulus in one direction which causes more changes to occur in the same direction
key words more
receptors
being complimentarily to proteins changing the tertiary structure of the receptors activating enzymes (kinase)
change in pH
causes ionic/hydrogen bonds to break so transcription factors cannot bind
stimuli --> receptors --> coordinators --> effectors --> response
negative feedback
counteracts any change in internal conditions to restore optimum conditions
Control of Blood Glucose Concentration
high blood glucose concentration- insulin
receptors in islets of Langerhan B cells detect increase in glucose which causes release of insulin into cappilaries. Insulin binds to receptor on target cell changing tertiary structure of receptor which causes protein channels in vesicles to fuse with cell surface membrane. More glucose diffuses via channel proteins and is either used in respiration to produce ATP or converted into glycogen to be stored in liver glycogenesis
low blood glucose concentration- glucaogon
receptors from alpha cells from islets of langerhan detect decrease in blood glucose which causes glucagon to bind to target cell receptors which causes
adenylate cyclase
to activate catalysing the conversion of ATP to
cAMP
and action of protein kinase which converts glycerol/amino acids to glucose glyconeogenesis or glycogenolysis
role of adrenaline
attaches to receptor on target cell and activates enzymes converting glycogen to glucose
Type 1 Diabetes
pancreas fails to create insulins so must regulate sugar intake, inject insulin if not can cause organ damage
Type 2 Diabetes
caused by overused insulin receptors so less sensitive to insulin, can be treated with changes diet & exercise
Control of Blood Water Concentration
osmoregulation
- control of the water potential of blood
hypothalamus osmoreceptors
detect drop in blood water potential which causes it to shrink as water moves out of osmoreceptor causing
posterior pituitary gland
to release
antidiuretic hormone ADH
which is secreted to blood and binds to surface of
collecting duct/distal convoluted tubule
activating enzyme phosphorylase causing vesicles called aquaporins to fuse with collecting duct cell surface membrane increasing the permeability to water reabsorption of water to blood reduce volume of urine and increase concentration
ultrafiltration
afferent arteriole is wider than efferent arteriole that leaves glomerulsus which creates a pressure gradient endothelium of cappilaries have small fenestrations in glomelurus which allows small molucules like glcusoe, amino acids, water, salts, ions and urea to pass through the basement membrane & epithelium of bowman's capsule/renal capsule and podocytes prevent large proteins from passing through
selective reabsroption
of glucose by co-transport from epithelial cells by actively transporting Na+ ions out of PCT which creates a low con of Na+ in PCT epithelial cell & water at proximal convoluted tubule
loop of henle
maintain a gradient of sodium ions in medulla as it acts as a
counter current multiplier
Na+ ions actively transported out of ascending limb using ATP creating a lower water potential in interstitial spaces ascending limb is impermeable to water so water can only move out of descending limb so water moves out by osmosis down water potential gradient out of descending limb lowest water potential at bottom of hairpin
Control of Heart Rate
myogenic stimulation of heart (without conscious thought) happens through the transmission of a wave of electrical activity
how do valves work?
when pressure is higher above than below valve opens, when pressure is higher below than above valve closes
sympathetic pathway
chemoreceptors detect change in pH/CO2 in blood this causes impulses to be sent to the medulla oblongata which sends MORE impulses to the SAN by sympathetic pathway to increase heart rate.
stimulation of heart
SAN produces wave of electrical activity/action potentials to atrial walls, the signal gets interrupted at the AVN and then conducts the signal to the ventricles down the Bundle of His in septum muscle to apex of heart splitting into Purkinje fibres, which goes the base up which allows the ventricles to empty pushing the blood into the aorta and pulmonary artery
parasympathetic pathway
baroreceptors detect rise in blood pressure, send impulses to medulla which sends more impulses to SAN by parasympathetic pathway reducing heart rate
saltatory conduction
myelin sheath allows electrical impulse to move quicker 'jumping' from node to node. Without this, impulses are slowed to the sarcollema
Receptors
Pacinian
corpuscle
retina rods
-
high visual sensitivity
because a many rod cells are connected to a single bipolar neurone which allows enough neurotransmitter to release to overcome the threshold and generate an action potential aka spatial summation (contains rhodopsin)
retina cones
high visual acuity
because each cone cell is connected to one bipolar neurone, so each cone cell sends a separate impulse to the brain.
low visual sensitivity
since temporal summation must occur to generate an action potential contains
iodopsin
3 different types- red, blue and green wavelengths high light intensity
stimulus
is a detectable change in the environment which can be detected by cells called receptors
spatial summation
- where multiple pre-synaptic neurones are connected to the same post-synaptic neurone to generate an action potential
temporal summation
-where multiple impulses are sent from a single pre-synaptic neurone in succession. This causes enough neurotransmitter to be released to synaptic cleft to pass threshold and generate an action potential.
when pupil
dilates
the circular muscles relax and the radial muscles contract. when the pupil
constricts
the radial muscles relax and the circular muscles contract
Survival & Response
role of IAA indoleacetic acid
reflex arch
stimulus ---> sensory neurone --> relay neurone --> motor neurone --> effector muscle/gland --> response
taxes
directional movement away from unfavourable environment
kineses
nondirectional random movement away from unfavourable environment
Nervous Coordination
what increases speed of action potentials?
saltatory conduction myelination, axon diameter the wider the less leakage of ions, temperature faster diffusion of enzymes and thus more ATP
Resting Potential
1. Carrier protein 3Na+ out and 2K+ in at sodium potassium pump. 2. Membrane more permeable to K+ since there are more K+ channel proteins. 3. Higher con. of K+ diffusing out than Na+ diffusing in so membrane is polarised -70mV becomes more negative neurone membrane.
Action Potentials
1. Na+ voltage-gated channels open Na+ diffuse into axon. This increases voltage so depolarisation threshold potential. 2. As voltage increase more Na+ channels open. 3. At a point, voltage-gated Na+ channels close, and membrane is repolarised. 4. K+ channel opens K+ diffuse out of neurons but this goes on for too long which is called hyperpolarisation., 5. Then in the refractory period it comes back to resting potential -70mV.
spatial summation
- many different neurones attaching to one post-synaptic neurone, causing more Na+ channels to open by combining neurotransmitter to release generating action potential
temporal summation
- one neurone releases one neurotransmitter repeatedly until enough neurotransmitter is release to trigger action potential
Synapse
1. An action potential arrives at pre-synaptic knob which depolarises the pre-synaptic membrane. 2. This stimulates voltage-gated Ca channels to open so Ca ions diffuse into pre-synaptic knob. 3. Vesicles containing neurotransmitters (
acetylecholine
) fuse with pre-synaptic membrane which releases the neurotransmitter into synaptic cleft. 4. Neurotransmitters diffuse down con gradient to post-synaptic membrane and bind to complimentary receptors. 5. This causes Na+ channels on post-synaptic membrane widen causing Na+ ions to move from synaptic cleft to post-synaptic neurone which depolarises membrane and could generate an action potential if above threshold. 6. Neurotransmitters broken down by enzymes (
acetylcholine esterase
-
acetate + choline
), recycled and reuptaken by pre-synaptic membrane.
Why do neurotransmitters only travel in one direction?
Because the neurotransmitters are only found in vesicles in the pre-synaptic knob and the complimentary receptors are only on the post-synaptic neurone so they can only bind to that side.
Inhibitory Synapse
- cause Cl- ions to move into postsynaptic neurone and K+ ions move out of postsynaptic neurone which makes the membrane more negative causing hyperpolarisation which makes it unlikely for an action potential to be generated -80mV
Cholinergic Synapse
1. Action potential depolarises pre-synaptic membrane. 2. Voltage-gates Ca+ channels open Ca+ diffuse into pre-synaptic knob 3. Vesicles containing acetylcholine fuse with pre-synaptic membrane and are released (exocytosis) 4. Acetylchloine diffuses across synaptic cleft and binds to receptors on post-synaptic knob. 5. This stimulates Na+ channels to open and Na+ to diffuse into post-synaptic knob depolarising the post-synaptic membrane.
Contraction of Skeletal Muscles
Sliding Filament Model
- 1. when an action potential reaches a muscle it stimulates Ca ions to be released 2.This causes tropomyosin to move and reveal myosin binding sites on actin 3. This results in myosin heads making actionomyosin bridges which causes ADP + Pi to be released. 4. A new ATP molecule can bind to myosin head causing it to change shape slightly so it is no longer complimentary to actin binding site so it detaches. 5. In the sarcoplasm ATPase hydrolyses ATP (caused by release of Ca ions) which causes the myosin head to move back to the original position (this is called a powerstroke)
Neuromuscular Junctions
- connects motor neurone to muscle fibre which have acetylcholine/neurotransmitters receptors triggering the muscles to contract.
Differences & Similarities between Cholinergic Synapse, and Neuromuscular junction
- both are unidirectional, both are excitatory but a cholinergic synapse can also be inhibitory, connects two neurons vs connects motor neurone and effector muscle, an action potential is created in the next neurone vs end point, acetylcholine receptors on post-synaptic membrane vs on muscle fibres.
Slow Twitch Fibres
ex. calf muscle, marathon runners.
structural features - contains a large supply of myoglobin (O2 store) and a rich blood supply, and many mitochondria
for long-term aerobic respiration.
Fast Twitch Fibres
ex. biceps
structural features- thicker, a large store of glycogen, more myosin filaments, a store of phosphocreatine to help make ATP from ADP and a large amount of enzymes to help with anaerobic respiration
contract faster to provide short powerful bursts of contractions.
in anaerobic respiration phosphocreatine
stored in muscles to rapidly regenerate ATP from ADP to meet demand