3.6 Organisms respond to changes in their internal and external environments (A-level only) Flashcards
(108 cards)
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 (e.g. 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
INSERT IMAGE HERE
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
INSERT IMAGE HERE
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
INSERT IMAGE HERE
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)
- 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
- one cone connects to one neurone
- 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 neurones only generate one 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 the **medulla**
* **more impulses** sent to **SAN** via **parasympathetic neurones** (releasing **acetylcholine**)
* fewer impulses from SAN
* heart rate slowed
41
Response to low blood pressure
* **Baroreceptor** detects low blood pressure
* impulse sent to the **medulla**
* **more impulses** sent to **SAN** along **sympathetic neurones** (releasing **noradrenaline**)
* 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 **acetylcholine**)
* heart rate slowed so less CO2 was 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 **acetylcholine**)
* heart rate increases to deliver blood to heart to remove CO2
44
Structure of myelinated
motor neurone
INSERT IMAGE HERE
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 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
INSERT IMAGE HERE
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
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**
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** 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
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
| INSERT IMAGE HERE
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
| INSERT IMAGE HERE
69
Inhibitory synapses
* Causes **chloride ions (Cl-)** to move into post-synaptic neurone and K+ to move out
* makes membrane **hyperpolarise** (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
INSERT IMAGE HERE
72
Myofibril
* Made up of **fused cells** that **share nuclei/cytoplasm** (sarcoplasm) and **many mitochondria**
* millions of muscle fibres make myofibrils – bringing about movement
73
Ultrastructure of myofibril
INSERT IMAGE HERE
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**
* activates **ATPase** on myosin
* ATP hydrolysed so energy for myosin heads to be **recocked**
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
79
Slow-twitch muscle fibres
* Specialised for **slow**, **sustained contractions** (endurance)
* lots of **myoglobin**
* **many mitochondri**a – 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
Negative feedback
* When there is a **deviation from normal values** and restorative systems are put in place to return this back to the **original level**
* involves the **nervous system** and **hormones**
83
Islets 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
84
Alpha cells
* Located in the **islets of Langerhans**
* release **glucagon**
* when detect blood glucose concentration is **too low**
85
Beta cells
* Located in the **islets of Langerhans**
* release **insulin**
* when detect blood glucose concentration is **too high**
86
Factors affecting blood glucose concentration
* Eating food containing **carbohydrates** → glucose absorbed from the intestine to the blood
* **exercise** → increases rate of respiration, using glucose
87
Action of insulin
* Binds to **specific receptors** on membranes of **liver cells**
* increases **permeability** of cell membrane (**GLUT-4 channels** fuse with membrane)
* glucose can enter from blood by **facilitated diffusion**
* activation of enzymes in liver for **glycogenesis**
* rate of **respiration increases**
88
Action of glucagon
* Binds to **specific receptors** on membranes of **liver cells**
* activates enzymes for **glycogenolysis**
* activates enzymes for **gluconeogenesis**
* rate of **respiration decreases**
* blood glucose concentration increases
89
Role of adrenaline
* Secreted by **adrenal glands** above the kidney for fight or flight.
* activates **secretion of glucagon**
* **glycogenolysis** and **gluconeogenesis**
* works via **secondary messenger model**
90
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
91
Glycogenolysis
* **Hydrolysis** of **glycogen** back into glucose
* occurs due to the action of **glucagon** to increase blood glucose concentration
92
Glycogenesis
* Process of **glucose** being **converted to glycogen** when blood glucose is higher than normal
* caused by **insulin** to lower blood glucose concentration
93
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
94
Second messenger model process
* **Adrenaline/glucagon** bind to **specific complementary receptors** on the cell membrane
* activate **adenylate cyclase**
* converts **ATP** to **cyclic AMP** (secondary messenger)
* cAMP activates **protein kinase A** (enzyme)
* protein kinase A activates a **cascade** to break down glycogen to glucose **(glycogenolysis)**
95
Diabetes
* A disease when blood glucose concentration cannot be controlled naturally
96
Type 1 diabetes
* Due to body being **unable to produce insulin**
* starts in **childhood**
* **autoimmune disease** where **beta cells** attacked
* treated using **insulin injections**
97
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**
98
Osmoregulation
* Process of **controlling the water potential** of the blood
* controlled by hormones e.g. **antidiuretic hormone** (affects distal convoluted tubule and collecting duct)
99
Nephron
* The structure in the kidney where **blood is filtered**, and useful substances are **reabsorbed** into the blood
100
Nephron structure
INSERT IMAGE HERE
101
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
102
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 cells into intercellular space to create a **concentration gradient**
* glucose can diffuse into the blood again
103
Counter current multiplier mechanism
* Describes how to **maintain a gradient** of Na+ in **medulla** by the **loop of Henle**.
* Na+ **actively transported** out **ascending limb** to medulla to **lower water potential**
* water moves **out descending limb** + DCT + collecting duct by **osmosis** due to this water potential gradient
104
Reabsorbtion 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
105
Role of hypothalamus in
osmoregulation
* Contains **osmoreceptors** which detect changes in **water potential**
* produces **ADH**
* when blood has low water potential, osmoreceptors **shrink** and **stimulate more ADH** to be made so more released from the pituitary gland
106
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.
107
Role of pituitary gland in osmoregulation
* ADH moves to the pituitary gland from the hypothalamus
* **releases ADH** into capillaries
* travels through blood → kidney
| INSERT IMAGE HERE
108
Synapse structure
INSERT IMAGE HERE
