Topic 6 Flashcards
1
Q
Stimulus
A
-Detectable change in the environment
-detected by cells called receptors
2
Q
Nervous system structure
A
Central nervous system = brain and spinal cord
peripheral nervous system = receptors, sensory and motor neurones
3
Q
Simple reflex arc
A
Stimulus (touching hot object)
-> receptor
-> sensory neurone
-> coordinator (CNS / relay
neurone
-> motor neurone
-> effector (muscle)
-> response (contraction)
4
Q
Importance of simple reflexes
A
-Rapid - short pathway only three neurones & few synapses
-autonomic -conscious thought not involved - spinal cord coordination
-protect from harmful stimuli e.g., burning
5
Q
Tropism
A
-Response of plants to stimuli via growth
-can be positive (growing towards stimulus) or negative (growing away from stimulus)
-controlled by specific growth factors (IAA)
6
Q
Specific tropisms
A
Response to light -phototropism
response to gravity-gravitropism
response to water- hydrotropism
7
Q
Indoleacetic acid
A
-Type of auxin (plant hormone)
-controls cell elongation in shoots
-inhibits growth of cells in roots
-made in tips of roots / shoots
-can diffuse to other cells
8
Q
Phototropism in shoots
A
-Shoot tip produces IAA
-diffuses to other cells
-IAA accumulates on shaded side of shoot
-IAA stimulates cell elongation so plant bends towards light
-positive phototropism
9
Q
Phototropism in roots
A
-Root tip produces IAA
-IAA concentration increases on lower (darker) side
-IAA inhibits cell elongation
-root cells grow on lighter side
-root bends away from light
-negative phototropism
10
Q
Gravitropism in shoots
A
-Shoot tip produces IAA
-IAA diffuses from upper side to lower side of shoot in response to gravity
-IAA stimulates cell elongation
-so plant grows upwards
-negative gravitropism
11
Q
Gravitropism in roots
A
-Root tip produces IAA
-IAA accumulates on lower side of root in response to gravity
-IAA inhibits cell elongation
-root bends down towards gravity and anchors plant
-positive gravitropism
12
Q
Taxis
A
-Directional response by simple mobile organisms
-move towards favourable stimuli (positive taxis) or away from unfavourable stimuli (negative taxis)
13
Q
Kinesis
A
-When an organism changes its speed of movement and rate of change of direction in response to
a stimulus
-if an organism moves to a region of unfavourable stimuli it will increase rate of turning to return to origin
-if surrounded by negative stimuli, rate of turning decreases - move in straight line
14
Q
Receptors
A
-Responds to specific stimuli
-stimulation of receptor leads to establishment of a generator potential - causing a response
-pacinian corpuscle
-rods
-cones
15
Q
Pacinian corpuscle
A
Receptor responds to pressure changes
occur deep in skin mainly in fingers and feet
sensory neurone wrapped with layers of tissue
16
Q
Pacinian corpuscle structure
A
-Single sensory neurone wrapped around by layers of connective tissue each layer separated by a gel
-It has special stretch mediated Na+ channels which gets deformed when pressure is applied and causes depolarisation.
-Neurone also contains Schwann cells
17
Q
How pacinian corpuscle detects pressure
A
-When pressure is applied, stretch mediated sodium ion channels are deformed
-sodium ions diffuse into sensory neurone
-influx increases membrane potential - establishment of generator potential
18
Q
Rod cells
A
-Concentrated at periphery of retina
-contains rhodopsin pigment connected in groups to one bipolar cell (retinal convergence) - Spatial summation
- do not detect colour
19
Q
Cone cells
A
-Concentrated on the fovea
-fewer at periphery of retina
-3 types of cones containing different iodopsin pigments - red,green and blue
-one cone connects to one neurone - Temporal summation
- detect coloured light
20
Q
Rods and cones: describe differences in sensitivity to light
A
-Rods are more sensitive to light
-cones are less sensitive to light
21
Q
Rods and cones: describe differences in
visual acuity
A
-Cones give higher visual acuity
-rods have a lower visual acuity
22
Q
Visual acuity
A
-Ability to distinguish between separate sources of light
-a higher visual acuity means more detailed, focused vision
23
Q
Rods and cones: describe differences in
colour vision
A
-Rods allow monochromatic vision (black and white)
-cones allow colour vision
24
Q
Why rods have high sensitivity to light
A
-Rods are connected in groups to one bipolar cell
-retinal convergence
-spatial summation
-stimulation of each individual- cell alone is sub-threshold but because rods are connected in groups more likely threshold potential is reached
25
Why cones have low sensitivity to light
-One cone joins to one neurone
-no retinal convergence / spatial summation
-higher light intensity required to reach threshold potential
26
Why rods have low visual acuity
-Rods connected in groups to one bipolar cell
-retinal convergence
-spatial summation
-many rods only generate 1 impulse / action potential -> cannot distinguish between separate sources of light
27
Why cones have high visual acuity
-One cone joins to one neurone
-2 adjacent cones are stimulated, brain receives 2 impulses
-can distinguish between separate sources of light
28
Why rods have monochromatic vision
One type of rod cell
one pigment (rhodopsin)
29
Why cones give colour vision
-3 types of cone cells with different optical pigments which absorb different
wavelengths of light
-red-sensitive, green-sensitive and blue sensitive cones
-stimulation of different proportions of cones gives greater range of colour perception
30
Myogenic
When a muscle (cardiac muscle) can contract and relax without receiving signals from nerves
31
Sinoatrial node
-Located in right atrium and is known as the pacemaker
-releases wave of depolarisation across the atria, causing muscles to contract
32
Atrioventricular node
-Located near the border of the right / left ventricle within atria
-releases another wave of depolarisation after a short delay when it detects the first
wave from the SAN
33
Bundle of His
Runs through septum
can conduct and pass the wave of depolarisation down the septum and Purkyne fibres in walls of ventricles
34
Purkyne fibres
In walls of ventricles
spread wave of depolarisation from AVN across bottom of the heart
the muscular walls of ventricles
contract from the bottom up
35
Role of non- conductive tissue
-Located between atria and ventricles
-prevents wave of depolarisation travelling down to ventricles
-causes slight delay in ventricles contracting so that ventricles fill before contraction
36
Importance of short delay between SAN and AVN waves of depolarisation
-Ensures enough time for atria to pump all blood into ventricles
-ventricle becomes full
37
Role of the medulla oblongata
-Controls heart rate via the autonomic nervous system
-uses sympathetic and parasympathetic nervous system to control SAN rhythm
38
Chemoreceptors
Located in carotid artery and aorta
responds to pH / CO2 conc. changes
39
Baroreceptors
Located in carotid artery and aorta
responds to pressure changes
40
Response to high blood pressure
-Baroreceptor detects high blood pressure
-impulse sent to medulla
-more impulses sent to SAN along parasympathetic neurones (releasing
noradrenaline)
-heart rate slowed
41
Response to low blood pressure
-Baroreceptor detects low blood pressure
-impulse sent to medulla
-more impulses sent to SAN along sympathetic neurones (releasing adrenaline)
-heart rate increases
42
Response to high blood pH
-Chemoreceptor detects low CO2 conc / high pH
-impulse sent to medulla
-more impulses sent to SAN along parasympathetic neurones (releasing
noradrenaline)
-heart rate slowed so less CO2
removed and pH lowers
43
Response to low blood pH
-Chemoreceptor detects high CO2
conc / low pH
-impulse sent to medulla
-more impulses sent to SAN along sympathetic neurones (releasing adrenaline)
-heart rate increases to deliver blood to heart to remove CO2
44
Structure of mylelinated neurone
Dendrites
Axon
Nucleus
Cell body
Myelin sheath
Schwann cells
Axon terminal
Node of ranvier
45
Resting potential
-The difference between electrical charge inside and outside the axon when a neuron
is not conducting an impulse
-more positive ions (Na+/K+) outside axon compared to inside
-inside the axon -70mV
46
How is resting potential established
-Sodium potassium pump actively transports 3 Na+ out of the axon, 2 K+ into the axon
-membrane more permeable to K+ (more channels and always open)
-K+ diffuses out down conc.gradient - facilitated diffusion
-membrane less permeable to Na+ (closed voltage gated Na+ channels)
-higher conc. Na+ outside
47
Action potential
-When the neurone's voltage increases beyond the -55mV threshold
-nervous impulse generated
-generated due to membrane becoming more permeable to Na+
48
Action potential: stimulus
-Voltage-gated Na+ channels open - membrane more permeable to Na+
-Na+ diffuse (facilitated) into neurone down conc. gradient
-voltage across membrane increases
49
Action potential: depolarisation
-When a threshold potential is reached, an action potential is generated
-more voltage-gated Na+ channels open
-Na+ move by facilitated diffusion down conc. gradient into axon
-potential inside becomes more positive
50
Action potential:repolarisation
-Na+ channels close, membrane less permeable it Na+
-K+ voltage-gated channels open, membrane more permeable to K+
-K+ diffuse out neuron down conc. gradient
-voltage rapidly decreases
51
Action potential: hyperpolarisation
-K+ channels slow to close -> overshoot in voltage
-too many K+ diffuse out of neurone
-potential difference decrease to -80mV
-sodium-potassium pump returns neurone to resting potential
52
Action potential graph
Draw and check kerboodle
53
All or nothing principle
-If depolarisation does not exceed -55 mV threshold, action potential is not produced
-any stimulus that does trigger depolarisation to -55mV will always peak at the same maximum voltage
54
Importance of all or nothing principle
-Makes sure animals only respond to large enough stimuli
-rather than responding to every small change in environment (overwhelming)
55
Refractory period
-After an action potential has been generated, the membrane enters a period where it cannot be stimulated
-because Na+ channels are recovering and cannot be opened
56
Importance of refractory period
-Ensures discrete impulses produced - action potentials separate and cannot be
generated immediately
-unidirectional - cannot generate action potential in refractory region
-limits number of impulse transmissions - prevent overwhelming
57
Factors affecting speed of conductance
-Myelination (increases speed)
-axon diameter (increases speed)
-temperature (increases speed)
58
How myelination affects speed
-With myelination - depolarisation occurs at Nodes of Ranvier only -> saltatory
conduction
-impulse jumps from node-node
-in non-myelinated neurones, depolarisation occurs along full length of axon - slower
59
How axon diameter affects speed
Increases speed of conductance
Less leakage of ions
60
How temperature affects speed
-Increases speed of conductance
-increases rate of movement of ions as more kinetic energy (active transport/diffusion)
-higher rate of respiration as enzyme activity faster so ATP is produced faster - active transport faster
-diffusion of neurotransmitters is faster due to more kinetic energy
61
Saltatory conduction
-Gaps between myelin sheath are nodes of Ranvier
-action potential can "jump" from node to node via saltatory conduction - action potential travels faster as depolarisation across whole length of axon not required
62
Synapse
-Gaps between end of axon of one neurone and dendrite of another
-impulses are transmitted as neurotransmitters
-pre synaptic neurone, synaptic cleft and post synaptic neurone
63
Role of calcium ions in synaptic transmission
-Depolarisation of the pre- synaptic knob opens voltage gated Ca2+ channels and Ca2+ diffuses into synaptic knob.
-stimulates vesicles containing neurotransmitter to fuse with membrane and release neurotransmitter into the synaptic cleft via exocytosis
64
Why are synapses unidirectional
-Receptors only present on the post-synaptic membrane
-enzymes in synaptic cleft break down excess-unbound neurotransmitter
- concentration gradient of neurotransmitters established from pre-post synaptic neurone
-neurotransmitter only released from the pre-synaptic neurone
65
Cholinergic synapse
-The neurotransmitter is acetylcholine
-enzyme breaking down acetylcholine = acetylcholine-esterase
-breaks down acetylcholine to acetate and choline to be recycled in the pre synaptic neurone in which ATP produced by mitochondria is used.
- Ach binds to receptors on sodium ion channels in the membrane of post synaptic neurone.
66
Summation
-Rapid build-up of neurotransmitters in the synapse to help generate an action potential by 2 methods:
-spatial or temporal
-required because some action potentials do not result in sufficient concentrations of
neurotransmitters released to generate a new action potential
67
Spatial summation
Many different neurones collectively trigger a new action potential by combining the
neurotransmitter they release to exceed the threshold value e.g., retinal convergence for rod cells
68
Temporal summation
When one neurone releases neurotransmitters repeatedly over a short period of time to exceed the threshold value e.g., 1 cone cell signalling 1
image to the brain
69
Inhibitory synapses
-Causes chloride ions (Cl-) to move into post-synaptic neurone and K+ to move out
-makes membrane hyper polarise(more negative) so less likely an action potential will be propagated
70
Neuromuscular junction
-Synapse that occurs between a motor neurone and a muscle
-similar to synaptic junction
71
Compare the NMJ with a cholinergic synapse (4 difference and 1similatity)
NMJ
-Unidirectional - neurotransmitter receptors only on post-synaptic membrane
-Only excitatory
-Connects motor neurones to muscle
-end point tor action potential
-Ach binds to receptors on muscle fibre
Cholinergic synapse:
-Unidirectional - neurotransmitter receptors only on post-synaptic membrane
-excitatory or inhibitory
-connects two neurones (sensory/motor/relay)
-New action potential generated in next neurone
-Ach binds to receptors on post-synaptic membrane
72
Myofibril
-Made up of fused cells that share nuclei/cytoplasm (sarcoplasm) and many mitochondria
-millions of myofibrils make up muscle fibre - bringing about movement
- two key proteins - myosin and actin that forms sarcomere
73
Ultra structure of myofibril
Draw and check kerboodle
H zone - only myosin
A band - H Zone + overlap of actin and myosin
I band - only actin filaments
Z line to another z line is one sarcomere
74
Role of Ca2+ in sliding filament theory
-Ca2+ enter from sarcoplasmic reticulum and causes tropomyosin to change shape
-myosin heads attach to exposed binding sites on actin forming actin-myosin cross bridge
-this is at an angle that creates tension leading to the actin being pulled along and in doing so the ADP attached is released
-ATP molecule attaches to myosin head which causes it to detach from the binding site
-ATP hydrolysed by ATPase on myosin which provides energy for myosin heads to return to its normal position
75
Role of tropomyosin in sliding filament
theory
-Tropomyosin covers binding site on actin filament
-Ca2+ bind to tropomyosin on actin so it changes shape
-exposes binding site
-allows myosin to bind to actin, forming cross bridge
76
Role of ATP in myofibril contraction
-Hydrolysis of ATP -> ADP + Pi releases energy
-movement of myosin heads pulls actin - power stroke
-ATP binds to myosin head causing it to detach, breaking cross bridge
-myosin heads recocked
-active transport of Ca2+ back to sarcoplasmic reticulum
77
Role of myosin in myofibril contraction
-Myosin heads (with ADP attached) attach to binding sites on actin.
-form actin-myosin cross bridge
-power stroke - myosin heads move pulling actin
-requires ATP to release energy
-ATP binds to myosin head to break cross bridge so myosin heads can move further along
actin
78
Phosphocreatine
-A chemical which is stored in muscles
-when ATP concentration is low, this can rapidly regenerate ATP from ADP by providing a Pi group.
-for continued muscle contraction
-restored when muscle is relaxed from atp
79
Slow-twitch muscle fibres
-Specialised for slow, sustained contractions (endurance)
-lots of myoglobin
-many mitochondria - high rate aerobic respiration to release ATP
-many capillaries - supply high concentrations of glucose/O2 & prevent build-up of lactic acid
-e.g. thighs / calf
80
Fast-twitch muscle fibres
-Specialised in producing rapid, intense contractions of short duration
-glycogen -> hydrolysed to glucose -> glycolysis
-higher concentration of enzymes involved in anaerobic respiration - fast glycolysis
-phosphocreatine store
-e.g., eyelids/biceps
81
Homeostasis
-Maintenance of constant internal environment via
physiological control systems
-control temperature, blood pH, blood glucose concentration and water potential within
limits
82
Islet of langerhans
-Region in the pancreas containing cells involved in detecting changes in blood glucose levels
-contains endocrine cells (alpha cells and beta cells) which release hormones to restore blood glucose levels
83
Alpha cells
-Located in the islets of Langerhans
-release glucagon
-when detect blood glucose concentration is too low
84
Beta cells
-Located in the islets of
Langerhans
-release insulin
-when detect blood glucose
concentration is too high
85
Factors affecting blood glucose concentration
Eating food containing carbohydrates -> glucose
absorbed from the intestine to the blood
exercise -> increases rate of respiration, using glucose
86
Action of insulin
-Binds to specific receptors on membranes of liver cells
-increases permeability of cell membrane (GLUT-4 channels fuse with membrane) as it stimulates intracellular chemical which causes vesicles containing glucose channel proteins to fuse with the membrane
-glucose can enter from blood by facilitated diffusion
-activation of enzymes in liver for glycogenesis
-rate of respiration increases
87
Action of glucagon
-Binds to specific receptors on membranes of liver cells
-activates enzymes for glycogenolysis - second messenger model
-activates enzymes for gluconeogenesis - adrenaline
-rate of respiration decreases
-blood glucose concentration increases
88
Role of adrenaline
-Secreted by adrenal glands above the kidney when glucose concentration is too low (exercising)
-activates secretion of glucagon
-glycogenolysis and gluconeogenesis
-works via secondary messenger model
89
Gluconeogenesis
-Creating glucose from non- carbohydrate stores in liver e.g. amino acids -> glucose
-occurs when all glycogen has been hydrolysed and body requires more glucose
-initiate by glucagon when blood glucose concentrations are low
90
Glycogenolysis
-Hydrolysis of glycogen back into glucose
-occurs due to the action of glucagon to increase blood glucose concentration
91
Glycogenesis
-Process of glucose being converted to glycogen when blood glucose is higher than normal
-caused by insulin to lower blood glucose concentration
92
What is a second messenger model
-Stimulation of a molecule (usually an enzyme) which can then stimulate more molecules to bring about desired response
-adrenaline and glucagon demonstrate this because they cause glycogenolysis to occur inside the cell when binding to receptors on the outside
93
Second messenger model process
-Adrenaline/glucagon bind to specific complementary receptors on the cell membrane
-activate adenyl cyclase for glucagon and protein g for adrenaline
-converts ATP to cyclic AMP (secondary messenger)
-cAMP activates protein kinase A(enzyme)
-protein kinase A causes break down glycogen to glucose (glycogenolysis)
94
Diabetes
A disease when blood glucose concentration cannot be controlled naturally
95
Type 1 diabetes
-Due to body being unable to
produce insulin
-starts in childhood
-autoimmune disease where
beta cells attacked
-treated using insulin injections
96
Type 2 diabetes
-Due to receptors in target cells
losing responsiveness to insulin
-usually develops due to obesity
and poor diet
-treated by controlling diet and
increasing exercise with insulin
injections
97
Osmoregulation
-Process of controlling the water potential of the blood
-controlled by hormones e.g., antidiuretic hormone (affects distal convoluted tubule and collecting duct)
98
Nephron
The structure in the kidney
where blood is filtered, and
useful substances are
reabsorbed into the blood
99
Nephron structure
1. Glomerulus and bowman’s capsule :- made of specialised cells called podocytes, capillary made of endothelium.
filters small solutes from the blood
2. Proximal convoluted tubule: - lined with epithelial cells and surrounded by many capillaries.
reabsorbs ions, water, and nutrients; removes toxins and adjusts filtrate pH
3. Descending loop of Henle:
allow water to pass from the filtrate into the interstitial fluid
4. Ascending loop of Henle:
reabsorbs Na+ and CI- from the filtrate into the interstitial fluid
5. Distal convoluted tubule:
selectively secretes and absorbs different ions to maintain blood pH and electrolyte balance
6. Collecting duct:
reabsorbs solutes and water from the filtrate
100
Formation of glomerular filtrate
-Diameter of efferent arteriole is smaller than afferent arteriole
-build-up of hydrostatic pressure
-water/glucose / ions squeezed out capillary into Bowman's capsule through pores in capillary endothelium, basement membrane and podocytes
-large proteins too large to pass
101
Reabsorption of glucose by PCT
-Co-transport mechanism
-walls made of microvilli epithelial cells to provide large surface area for diffusion of glucose into cells from PCT
-sodium actively transported out epithelial cells into intercellular space to create a concentration gradient
-Na+ now diffuses down concentration gradient from lumen to epithelial cells via co transport protein and this brings glucose along
-glucose diffuses into blood by facilitated diffusion
102
Counter current multiplier mechanism or Reabsorption of water
-Describes how to maintain a gradient of Na+ in medulla by the loop of Henle.
-Na+ actively transported out ascending limb(lots of mitochondria)to medulla to lower water potential
-water moves out descending limb + DCT + collecting duct by osmosis due to this water potential gradient
103
Reabsorption of water by DCT/collecting duct
-Water moves out of DCT and
collecting duct by osmosis
down a water potential gradient
-controlled by ADH which
changes the permeability of
membranes to water
104
Role of hypothalamus in osmoregulation
-Contains osmoreceptors which
detect changes in water
potential
-produces ADH which then passes to posterior pituitary gland from where its secreted into capillaries
-when blood has low water
potential, osmoreceptors shrink
and stimulate more ADH to be
made so more released.
105
Anti-diuretic hormone
-Produced by hypothalamus,
released by pituitary gland
-affects permeability of walls of
collecting duct & DCT to water
-more ADH means more aquaporins fuse with walls so more water is reabsorbed back to blood- urine more concentrated.
106
Role of pituitary gland in osmoregulation
-ADH moves to the pituitary
gland from the hypothalamus
-releases ADH into capillaries
-travels through blood -> kidney
107
Synapse structure
Look at notes
108
What happens to parts of sarcomere when muscle contracts
H zone narrows or shortens
I band narrows or shortens
A band stays constant
Z line come closer
Overall sarcomere shortens
109
What are the three main proteins involved in sliding filament theory
Myosin - made of two proteins - one is fibrous protein which makes up the tail and the other is a globular protein which makes the bulbous head
Actin - globular protein which twist to form a helical shape
Tropomyosin - long thin thread that wounds around actin filament.
110
What happens during muscle relaxation
Nervous stimulation ceases and calcium ions are actively transported back into the endoplasmic reticulum using energy from hydrolysis of atp
Causing tropomyosin to change shape and block binding sites of chin again therefore myosin head cannot bind and muscle relaxes
The antagonistic muscles now pulls actin out from between myosin
