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A Level Biology (SNAB) > Topic 8 > Flashcards

Topic 8 Flashcards

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1
Q

Neurone

A

Single cell that transmits nerve impulses, composed of a cell boxy, axon and dendrites

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2
Q

Nerve

A

A Complex Structure containing an axon bundle of many neurones

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3
Q

Breakdown of the Nervous System

A

Insert Diagram

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4
Q

Central Nervous System

A

Composed of the brain and Spinal cord

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5
Q

Peripheral Nervous System

A

Contains sensory and motor nerves which link into the CNS
Broken down into the:
- Autonomic Nervous System
- Somatic Nervous System

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6
Q

Autonomic Nervous System

A
  • involuntary actions
  • stimulates: smooth muscle, glands & cardiac muscle
    Broken down into the:
  • Sympathetic Nervous System
  • Parasympathetic Nervous System
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7
Q

Somatic Nervous System

A
  • Voluntary

- Stimulates skeletal muscle

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8
Q

Sympathetic Nervous System

A

Prepares ‘flight’ or ‘fight’ responses

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9
Q

Parasympathetic Nervous System

A

Rest & Digest

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10
Q

Motor Neurone

A

Insert Diagram

  • Cell body in CNS
  • Long Axon extends out to effectors
  • Many short dendrites
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11
Q

Sensory Neurone

A

Insert Diagram

  • Sensory cells -> CNS
  • long dendrons and axons
  • cell body in middle of neurone
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12
Q

Relay Neurone

A

Insert Diagram

  • mostly in CNS (transmits Action potential through)
  • large number of connections
  • Many short dendrites
  • one long axon
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13
Q

Myelin Sheath

A

Faster Action Potential (faster action potentials)

  • electrical insulator
  • comprised of schwann cells (lipid bilayer)
  • gaps between each S cells = nodes of Ranvier (sodium ion channels concentrated here)
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14
Q

Nodes of Ranvier

A

Site of depolarisation (Na+ channels)
- neurones cytoplasm conducts enough charge to depolarise next node
- impulse jumps from node to node
= saltatory conduction (v. fast)

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15
Q

Nervous System

A

Complex neurone network

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16
Q

Nervous pathway

A

Stimulus -> receptor -> sensory neurone -> CNS -> motor neurone -> effectors -> response

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17
Q

Eyes reaction to dim light

A

-> photoreceptors -> sensory neurone -> CNS processes info -> motor neurone -> Radial muscles in the Iris stimulated -> radial muscles contract (pupil dilates)

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18
Q

Eyes reaction to bright light

A

-> photoreceptors -> sensory neurone -> CNS processes info -> motor neurone -> Circular muscles in the Iris stimulated -> Circular muscles contract (pupil constricts)

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19
Q

Hormonal Systems

A

Comprised of Glands + hormones

  • hormones secreted when glands stimulated (via change in concentration of another substance or an electrical impulse)
  • hormones diffuse directly into the blood -> circulatory system transports
  • > diffuse out of the blood all over the body
  • > only bind to specefic receptors on membranes of target cells
  • > trigger response in target cells

E.g. Stimulus = low blood glucose concentration

  • receptor = pancreas cell’s receptors detect low levels
  • hormone = pancreas release glucagon
  • effector = target cells in liver detect glucagon; converts glycogen -> glucose
  • response = glucose released into blood
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20
Q

Gland

A

Cell group specialised to secrete a substance

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21
Q

Hormones

A

Chemical messengers

  • protein/peptides e.g. insulin
  • steroids e.g. progesterone
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22
Q

Nervous Communication

A

Electrical impulses -> faster response

  • localised response (neurone’s carry electrical impulses to specific cells)
  • short-lived responses (neurotransmitters usually quickly removed)
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23
Q

Hormonal Communication

A

Chemical -> slower response (speed of ‘blood’)

  • widespread response (target cells can be all over the body)
  • long-lived response (hormones break down very slowly)
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24
Q

Receptors

A

Specific to one stimulus

  • some = cells (e.g. photoreceptors)
  • others = proteins on cell surface membranes (e.g. glucose receptors)
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25
Q

Nervous system receptors (resting state -> stimulus detected)

A

Resting state:

  • difference in charge between the internal and external of cell
  • voltage across membrane (making the receptor polarised) = potential difference
  • potential difference generated by ion pumps + channels

Stimulus detected:

  • permeability of cell membrane to ions is altered
  • changes potential difference
  • > bigger enough change triggers action potential (electrical impulse along neurone), but only if the threshold level reached
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26
Q

Potential difference

A

Voltage across a cell membrane

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27
Q

Photoreceptors

A

light receptors in the eye

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28
Q

Diagram of the eye

A

ngng

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29
Q

Pathway of light entering the eye

A
  1. Light enters via pupil (amount controlled by iris muscles)
  2. light rays focused by lens onto retina (lines inside of eye)
    - retina contains photoreceptors
  3. Fovea = area of retina with lots of photoreceptors
  4. Nerve impulses from the photoreceptors are carried from retina to the brain by optic nerve = neurone bundle
    - where the optic nerve leaves the eye = blind spot (no photoreceptors)
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30
Q

Effect of light hitting photoreceptor

A
  1. light enter eye -> hits photoreceptor & is absorbed by light-sensitive pigments
  2. light bleaches the pigment causing a chemical change
  3. triggers nerve impulse along bipolar neurone
    - bipolar neurones connect photoreceptors to optic nerve
    - light passes straight through the optic nerve & bipolar neurone to the photoreceptor which feeds it back
    - optic nerve -> brain
    (light -> photoreceptor; (EI) photoreceptor -> bipolar neurone -> optic nerve -> brain)
  4. Human eye = 2 potoreceptors
    - Rods = monochramatic; usually in peripheral part of retina
    - Cones = trichomatic; packed in fovea
    -> three types: R/G/B - sensitive
    -> stimulated in different proportions -> colours
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31
Q

Cone

A

ngng

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32
Q

Rod Cells

A

Contain light sensitive pigment = Rhodopsin

- rhodopsin = retinal + opsin (joined)

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33
Q

Rod Cells in the dark (no stimulation)

A
  1. Sodium ions (Na+) pumped out of cell using active transport
  2. Na+ diffuses back into the rod cell via open Na+ channels
  3. Inside cell becomes slightly -ve -> cell membrane = depolarised
  4. Triggers neurotransmitter release
  5. Neurotransmitters inhibit bipolar neurone
    - > no action potential fired, so no info is relayed
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34
Q

Rod Cells in the light (stimulated)

A
  1. light energy causes Rhodopsin to break down into Retinal + Opsin = bleaching (process)
  2. bleaching triggers Na+ channels to close
  3. Na+ actively transported out, and stopped from diffusing back in
  4. Na+ builds up outside the cell
    - makes the inside of the cell much more -ve (than outside)
    - cell membrane = hyperpolarised
  5. Hyperpolarised -> no neurotransmitter released by Rod cell
    - bipolar neurone is not inhibited
  6. Bipolar neurone depolarises
    - if change in potential difference reaches threshold
    - > action potential transmitted to the brain (via optic nerve)
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35
Q

Dendrite

A

An extension from the cell body that carried impulses to the cell body

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36
Q

Axon

A

An extension from the cell body that carries impulses away from the cell body

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37
Q

Neurone diagrams (Motor, Relay. Sensory)

A

INSERT DIAGRAMS

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38
Q

Neurone cell membranes

A

Resting state:

  • outside membrane is more positive compared to inside as more +ve ions there
  • > polarised
  • resting potential = -70mV
  • resting potential created + maintained by sodium-potassium pumps & potassium ion channels in neurone membrane
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39
Q

Neurone Cell Membrane + Stimulation ->

A
  1. Stimulus
    - excites neurone cell membrane -> Na+ channels open
    - Na+ diffuse in down the Na+ electochemical gradient
    - > inside neurone is less -Ve than external to it
  2. Depolarisation
  • triggered if potential difference reaches threshold = -55mV
  • > more Na+ channels open -> more Na+ diffuses in
  1. Repolarisation
    - potential difference = + 30 mV
    - > Na+ channels close
    - > K+ channels open
    - > membrane becomes more K+ permeable
    - > K+ diffuses out down K+ concentration gradient
    - starts to restore membrane to resting potential
  2. Hyperpolarisation
    - K+ channels = slow to close -> slight ‘overshoot’
    -> too many K+ diffuse out
    - Potential difference = more -ve than resting potential
    = -75mV
  3. Resting Potential
    - ion channels reset
    - Sodium-pottasium pump returns membrane to resting potential (maintained until next excitation)

note: after action potential cell membrane cannot be excited

40
Q

How does an action potential move along neurone

A

As a ‘wave’ of depolarisation

  1. Action potential happens -> some Na+ diffuse (in) sideways
  2. causes Na+ channels in next region to open -> Na+ diffuse into that part
  3. -> wave of depolarisation travels along neurone
  4. Wave moves away from regions in refractory period (as they have no ability to fire an action potential)

INSERT DIAGRAM

41
Q

Refractory period

A

Acts as a time delay between one action potential and the next

  • prevents action potential overlap
  • pass along as discrete (separate) impulses
  • make’s sure action potentials are unidirectional
42
Q

Bigger Stimulus =

A

More frequent impulses

Action Potentials always fire with the same change in voltage (when threshold reached)
- bigger impulse triggers more frequent impulses of the same charge

43
Q

Local Anesthetics affect on Na+ movement

A

Stops pain in localised area

  • binds to Na+ channels in neurone membranes
  • > membranes cannot depolarise
  • stops action potential from being conducted
  • > stops info about pain reaching the brain
44
Q

Synapse

A

Junction between neurones

  • tiny gap between cells at a synapse = synaptic cleft
  • synaptic knob = swelling at pre-synaptic neurone which contains synaptic vesicles (containing neurotransmitters)
  • AP reaches end of a neurone -> neurotransmitters release into cleft
  • > diffuse across to post-synaptic membrane -> binds to receptors
  • binding to receptor can trigger action potential, muscle contraction or secretion (neurone, effector, gland)
  • receptors only on post-synaptic membrane (AP = unidirectional)
  • neurotransmitters reabsorbed by pre-synapse or broken down via an enzyme and the products absorbed by the neurone
  • > stops prolonging of the response
45
Q

Synapse Diagram

A

INSERT DIAGRAM

46
Q

Nerve Impulse Transmission

A
  1. Action Potential reaches synaptic knob
    - AP stimulates voltage-gated calcium ion channels to open
    - calcium ions diffuse into pre-synaptic knob
  2. Ca+ influx triggers synaptic vesicles to move to pre-synaptic membrane
    - vesicles fuse with membrane
    - > neurotransmitters released into the synaptic cleft via exocytosis
  3. Neurotransmitters diffuse across synaptic cleft
    - > bind to specefic receptors in post-synaptic membrane
    - sodium ion channels in post-synaptic membrane opne
    - sodium influx into post-synapse cause the membrane to depolarise
    - > AP generated if threshold reached on the membrane
    - neurotransmitters removed from the synaptic cleft (uptaken by pre-synaptic knob) to prevent continued excitation
47
Q

Synaptic Divergence

A

One neurone connects to many neurones, dispersing information to different parts of the body

48
Q

Synaptic Convergence

A

Many neurones connect to one neurone, amplifying information

49
Q

Weak Stimulus

A

Triggers small neurotransmitter release

- may not be enough to excite postsynaptic membrane & trigger an action potential

50
Q

Summation

A

Effect of neurotransmitter release from many neurones or one continuously stimulated, which are added together

51
Q

Tropism

A

Response of a plant to a directional stimulus (via regulating their growth)

52
Q

Positive Tropism

A

Growth towards

53
Q

Negative Tropism

A

Growth Away

54
Q

Phototropism

A

Response to light

  • shoots = positively phototropic
  • roots = negatively phototropic
55
Q

Geotropism

A

Response to gravity

  • shoots = negatively geotropic
  • roots = positively geotropic
56
Q

Growth Factors

A

Plant have no nervous system
So a response to stimuli is controlled by growth factors which speed/slow plant growth
- producing in ‘growing’ regions e.g. leaves/shoot tips
- migrate to where they are needed in other plant regions

57
Q

Auxins

A

A growth factor that stimulates shoot growth by cell elongation

  • triggers cell walls to loosen + stretch -> cells elongate
  • a high concentration in the roots, inhibits growth
58
Q

Gibberellins

A

A growth factor that stimulates flowering + seed germentation

59
Q

Cytokinins

A

A growth factor that stimulates cell division & differentiation

60
Q

Ethene

A

A growth factor that stimulates fruit ripening & flowering

61
Q

Abscisic Acid (ABA)

A

A growth factor that is involved in the falling of leaves

62
Q

Indoleacetic Acid (IAA)

A

A type of Auxin that is produced in the tips of flowering plants
- enters nucleus of a cell and regulates gene transcription in relation to cell elongation & growth
- moved around plant to control tropisms
–> via active transport & diffusion across short distances
–> via the phloem for long distances
- different parts of the plant have different amounts
- uneven distribution results in uneven growth for each region
E.g. Phototropism
- IAA moves to shaded shoot region
-> Tip bends towards light
E.g. Geotropism
- IAA moves to underside of shoots/roots
-> shoot grows up; root downwards

63
Q

Photoreceptors (in plants)

A

= Phytochromes

  • found particuarly in leaves, seeds, roots & stem
  • control range of responses e.g. season dependent flowering (short/long day related)
64
Q

Phytochromes

A

Light absorbing molecules that exist in two states

  • Pr = red light of 660nm
  • Pfr = far-red light of 730nm
  • converts from one state to another when exposed:
  • -> Pr -> Pfr = quick conversion when exposed to red light
  • -> Pfr -> Pr = quick conversion when exposed to far red light
  • -> Pfr -> Pr = slow conversion in darkness

Daylight contains more red light than far red light
- more Pr is converted into Pfr than Pfr into Pr
- amount of each = light dependent; so varies from season to season due to length of the day/night
- differing amounts control the response to light, and as such regulate gene transcription
E.g. flowering
- some plants = high Pfr stimulated flowering (short nights e.g. summer -> Pfr build up)

65
Q

Cerebrum

A

Largest part of the brain

  • divided into halves = cerbral hemispheres (left & right)
  • has a thin outer layer which is highly folded (large SA) = cerebral cortex
  • deals with vision, learning, thinking, emotions & movement
  • comprised of 4 lobes: Occipital, parietal, temporal and frontal
  • -> back cortex = vision
  • -> front cortex = thinking
66
Q

Hypothamalus

A

Just beneath middle part of the brain (temporal lobe)

  • automatically maintains thermoregulation
  • produces hormones which control the pituitary gland (below the hypothalamus)
67
Q

Medulla Oblongata

A

The base of the brain; just above the spinal cord

- automatically controls breathing + heart rate

68
Q

Cerebellum

A

Underneath the cerebrum

  • comprised of a folded cortex
  • coordinates movement + balance
69
Q

Diagram of the Brain

A

INSERT DIAGRAM

70
Q

Computed Tomography (CT)

A

X-rays are used to produce cross-sectional images which look up at the brain from below
- dense structures absorb more radiation and show up as a lighter colour

Shows major structure, but not the function of them
- but by highlighting a diseased/damaged area this can be linked to a loss of function

Diagnose medical problems

  • blood = different density, shows up with a lighter colour
  • highlight bleeding, extent & location
  • which blood vessels are damaged -> likely effect on function

Danger

  • x-rays can cause mutations in the DNA
  • low risk from one CT scanner (danger only in continual exposure)
71
Q

Magnetic Resonance Imaging (MRI)

A

Utilises magnetic field and radio waves to produce cross-sectional images of the brain looking down from above

  • higher quality images than CT as can show the difference between soft tissues/different tissue types
  • overall better resolution with clear difference (normal/abnormal)
  • no functional imaging

Tumour cells show up lighter and respond differently than healthy cells

  • size + location (exact)
  • best approach + guess effect on function
72
Q

Functional Magnetic Resonance Imaging (fMRI)

A

Shows change in brain activity from above

  • more oxygenated blood -> active areas (lights up red in colour on screen)
  • the molecules in more oxygenated blood return a stronger signal to the scanner

fMRI = detailed, high resolution image of structure
with the function illustrated by the the scanner picking up blood flow when action performed
- seizures -> area working abnormally, cause, treatment

73
Q

Positron Emission Tomography (PET)

A

Radioactive tracer introduced to body which is absorbed by the tissues

  • scanner detects tracer radioactivity and builds up a map
  • different tracers utilised to determine different function e.g. radioactively traced glucose for glucose metabolism
  • PET = very detailed; structure + function in real time
  • unusually active/inactive parts compared to a ‘normal’ brain
74
Q

Habituation

A

Learned behaviours
- unimportant stimulus is repeated over time which we learn to ignore (reduced response)
- this ensures energy is not wasted + focus on survival needs
E.g. Prairie dogs do not produce alarm call for humans as they’ve learnt they are no threat
- fewer electrical impulses sent to effectors
1. reduced exposure -> reduced Ca+ which enters pre-synaptic knob
2. Decreased influx -> less neurotransmitters released
3. Fewer Na+ channels in postsynaptic membrane open -> reduced chance of threshold being reached
4. Fewer signals sent to the effector

75
Q

Visual Cortex

A

Area of the cerebral cortex that is at the back of the brain and is comprised of Ocular Dominance Columns (ODC)

  • receives + processes visual information from either the left or the right eye
  • neurones grouped together in columns = ODC
  • -> info from right eye -> right ODC
  • -> left eye -> left ODC
  • columns = same size and arranged in alternating pattern across the visual cortex
76
Q

Critical Period

A

A period in baby mammals where visual stimulation organises the neurones

  • baby mammals are born with lots of neurones in the visual cortex, which require visual stimulation to be organised
  • proper organisation -> elimination of unnecessary synapses
  1. Synapses that receive visual stimulation and pass nerve impulses onto visual cortex are retained
  2. synapses that receive no visual stimulation and do not pass on information are removed
  3. If there is no stimulation of the eye during the critical period the visual cortex does not develop properly and many synapse are destroyed (can cause blindness)
77
Q

Animal use in medical research (Against)

A
  • Animals are biologically different so the drugs tested will produce different effects
  • Pain + distress to animals
  • alternatives: cultures of human cells + computer models that can predict effects
  • animal rights
78
Q

Animal use in medical research (For)

A
  • Similar enough biologically, and have produced lots of medical breakthroughs e.g. antibiotics, insulin, organ transports
  • only used when necessary, and struct rules are in place
  • only way to study side effects on whole body as cultures + models are not a true representation as there is no interaction
  • Only method to study behaviour
  • human have (more) rights (tenative)
79
Q

Parkinson’s Disease

A

A brain disorder that affects motor skills as neurones in regions for movement control are destroyed

  • neurotransmitter dopamine is reduced (corresponding producers destroyed) -> less in synaptic cleft
  • less binds to receptors triggering fewer Na+ channels in the postsynaptic membrane to open meaning less likelihood of depolarisation
  • fewer action potentials are produced
  • symptoms: tremors + slow movement
80
Q

Depression

A

A mental health disorder linked to low-levels of Serotonin (neurotransmitter)

  • serotonin is utilised in parts of the brain that control mood
  • antidepressants increase serotonin in the brain
    e. g. SSRI’s and SNRI’s
81
Q

SSRI’s

A

Selective Serotonin Reuptake Inhibitors

  • Increases serotonin presence in synaptic cleft
  • more likely to be received by receptors on post synaptic membrane
82
Q

SNRI’s

A

Serotonin-Noradrenaline Reuptake Inhibitors

83
Q

L-Dopa

A

Utilised to treat the symptoms of Parkinson’s disease

  • the structure is very similar to dopamine, but it can cross the blood-brain barrier whereas dopamine cannot
  • absorbed into brain where it is converted into dopamine (via enzyme Dopa-decarboxylase)
  • > higher dopamine levels, meaning more nerve impulses can be transmitted in affected areas, and subsequently more control over movement
84
Q

Dopa-decarboxylase

A

an enzyme used to convert L-Dopa to dopamine

85
Q

MDMA

A

Otherwise known as Ecstascy, it can increase serotonin by inhibiting reuptake (binds + blocks reuptake proteins on the pre-synaptic membrane)

  • also triggers increased serotonin release
  • serotonin levels stay high & cause depolarisation of the post-synaptic membrane
  • > effect = mood elevation
  • long term use leads to habituation and subsequent neurone damage
86
Q

Human Genome Project

A

A 13 year project that identified all of the genes found in human DNA, which was then stored in databases and used to identify genes and subsequent proteins involved with diseases.

  • allowed for development of new drugs that targeted identified genes e.g. an enzyme that helps cancer cells spread throughout the body
  • highlighted common genetic variations
  • -> highlighted drugs that were less effective on these variations
  • -> drugs tailored to people with these variations (personalised medicine + treatment)
87
Q

Issues presented by genome sequencing

A
  • specific genetic variations result in increased research cost, so the resultant drugs will be more expensive, which could lead to a two-tier health surface only the wealthy can afford
  • refused expensive drug due to lack of genetic compatibility even if its the only drug available (last hope)
  • info could be used by others: employers & insurers could unfairly discriminate e.g increase life-insurance premium
  • psychologically damaging (in knowing the drug is unlikely to work, especially if only hope)
  • gene patenting (one of the original leaders of the human genome project attempted to do so when the project was first started)
88
Q

Genetically Modified Organisms

A

Organisms that have had their DNA altered for a specific purpose e.g. drug production or to increase yield

89
Q

Genetically Modified Microorganism (Drug Production)

A
  • gene for protein isolated using restriction enzymes
  • gene copied using PCR
  • copies inserted into plasmids (vector)
  • plasmids inserted into microorganism
  • grown in large containers so they divide -> produce lots of the protein
  • protein then purified -> used for drug
    e. g. Insulin for type 1 diabetes, or blood clotting factors for haemophiliacs
90
Q

Genetically Modified Plants (Drug Production)

A
  • gene for protein inserted into bacterium
  • infects plant cell
  • bacterium inserts itself into plant cell DNA -> genetically modified
  • plant cell grown into adult plant -> whole plant contains copy of gene
  • protein produced purified from plant tissues
    e. g. insulin + cholera vaccine

note: GMO’s used in agriculture -> herbicide resistant + high-yield
- potential for cross-breeding (environmental impact)

91
Q

Genetically Modified Animals (Drug Production)

A
  • gene inserted into nucleus of a fertilised animal egg cell
  • egg cell implanted into adult animal -> every cell contains gene copy
  • protein purified from milk of the animal
    e. g. antithrombin (blood clotting disorder) utilised in GMO goats
92
Q

Benefits of GMO’s

A
  1. Crops -> higher yield; more nutritious
    - reduced] risk of famine + malnutrition
  2. pest resistance
    - fewer pesticides needed
    - reduces cost -> cheaper food
    - reduced environmental problems
  3. Industry + enzymes: GMO’s -> larger quantities
  4. disorders treated with human proteins
    - safer + more effective
    e. g. cow insulin can cause allergic reactions
  5. vaccines produced in plant tissue
    - no refrigeration
    - available for more people (more remote areas)
  6. plant + animal drug production = cheap
    - reproduced using conventional farming methods
93
Q

Risks of GMO’s

A
  1. transmission f genetic material
    - herbicide resistant crops interbred with wild plants -> superweeds
    - drug crops interbred (unnecessary drugs consumed -> potential impact on effectiveness)
  2. long term impacts with unforseen consequences
  3. wrong to GM animals for human benefit
94
Q

Sodium-Potasium pump

A

Works via active transport

  • three Na+ taken out of neurone for every two K+ that move in
  • requires ATP
  • membrane is not permeable to Na+ so it cannot diffuse back in which creates a sodium ion electrochemical gradient
  • K+ can diffuse back in (via facilitated diffusion)
  • outside = more +ve charge
95
Q

Pottasium ion channel (neurone membrane)

A

Facilitated diffusion of K+ out of neurone

- down concentration gradient

A Level Biology (SNAB) (10 decks)

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