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Biology > T8: Grey Matter > Flashcards

T8: Grey Matter Flashcards

1
Q

Reflex arc general stages

A

Rapid, involuntary response
Stimulus (environment change)
Receptor (detect stimulus)
Sensory neurone (ventral route)
Synapse
Relay neurone
Coordination (determine response)
Synapse
Motor neurone (dorsal route)
Effector (muscle/gland)
Response (action)

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2
Q

Nervous system subsections and their functions

A

Central (brain/spinal cord)
Peripheral (sensory/motor)
- somatic (voluntary/skeletal muscles)
- autonomic (involuntary smooth/cardiac muscle/glands)
— sympathetic (fight/flight)
— parasympathetic (rest/digest)

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3
Q

Nerve

A

Bundle of neurones wrapped in a protective coating

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4
Q

Neurone structure

A

Cell body: nucelus and other organelles
Dendrites: extensions that conduct impulses to cell body
Axon: transmit impulses away from cell body
- myelin sheath, Schwann cells, lipid, insulating layer, increase transmission speed, nodes of Ranvier)

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5
Q

3 types of neurone

A

Motor: cell body end of axon, relay - motor
Relay: cell body inside axon, sensory - motor
Sensory: cell body off axon, receptor - relay

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6
Q

Receptors

A

Detect stimuli
Convert energy source input —> electrical signals/nerve impulses
Cells that synapse sensory neurones
Part of a specialised sensory neurone

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7
Q

Name and describe 4 types of receptors

A

Chemoreceptors, chemical stimulae, taste, smell, blood conc
Mechanoreceptors, force stimulae, balance, touch, hearing
Photoreceptors, light stimulae, sight
Thermoreceptors, temperature stimulae

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8
Q

Spinal cord matter

A

Nerve cell bodies, grey matter
Axons and myelin sheaths, white matter

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9
Q

Iris light control mechanism

A

Autonomic nervous system
Strike retina photoreceptors
Nerve impulses —> optic nerve —> midbrain
Impulse —> midbrain —> parasympathetic Iris motor neurones
Circular muscles contract
Radial muscles relax
Smaller pupil, less light in

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10
Q

Compare the radial and circular muscles in the Iris

A

Antagonistic
Radial, sympathetic, contract, larger Iris
Circular, parasympathetic, contract, smaller Iris

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11
Q

Summation role

A

Control nerve pathways
Flexible responses
Integrate different electrical impulses —> coordinated response

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12
Q

What does the likelihood of a postsynaptic membrane depolarisation depend on

A

Type of synapse (inhibitory/excitatory)
Frequency of impulses
NOT the strength of the impulses
Spatial - several impulses from different neurones
Temporal - several impulses from one neurone

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13
Q

Compare excitatory and inhibitory synapses

A

Excitatory: more Na+ permeable, temporal/spatial, depolarisation +40mV
Inhibitory: less Na+ permeable, reduce AP likelihood, neurotransmitters open K+/Cl- channels in postsynaptic membrane, Cl- diffuse down conc grad into cell, K+ diffuse down conc grad out of cell, -90mV Hyperpolarisation

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14
Q

Synaptic process

A

AP arrives
Membrane depolarises
Ca2+ channels open and enter
Synaptic vesicles fuse to pre synaptic membrane
Neurotransmitters enter synaptic cleft via Exocytosis and diffuse across
Neurotransmitters bind to post synaptic membrane transmitters
Cation channel opens and Na+ eneters
Post synaptic membrane in depolarised
Initiates AP
Neurotransmitters released from receptor
Taken up by pre synaptic membrane/diffuse away to be broken down

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15
Q

Acetylcholine

A

First neurotransmitter discovered
Ca2+ facilitated diffusion into cytoplasm
Increase Ca2+ conc
Several impulses need to stimulate neurostramitter
Acetylcholine fuse to pre synaptic membrane and release via Exocytosis
Diffuse across synaptic cleft
Bind to complementary receptors
Receptor shape changes
Cation channels open
Membrane more permeable
Threshold met
AP generated
Reuptaken by pre synaptic membrane/broken down by acetylcholinesterase

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16
Q

Resting potential

A

Inside more negative than outside cell
-70mV resting PD/polarisation
Na+ out via pump
K+ in via pump
Against conc grad (ATP/NRG)
Organic molecules too big to move
Cl- follows conc grad
K+ out via channel diffusion
PD pulls K+ back in
Conc/elec hard counteract
No net K+ movement
Electrochemical equilibrium

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17
Q

Action potential process

A

Depolarisation - VD Na+ channels open, Na+ flow into axon, PD threshold positive feedback, +40mV
Polarisation - VD Na+ channels close, VD K+ channels open, K+ leave axon, down EC gradient, -90mV
Hyperpolarisation - VD K+ channels close, K+ diffuse back into axon, restore resting potential

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18
Q

Compare nervous vs hormonal responses

A

Nervous - electrical impulses, nerves/neurones, fast, short term, use muscles, localised responses
Hormonal - chemicals/hormones, blood, slower, long term, only target cells can respond, widespread response

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19
Q

Refractory period

A

Partially depolarised membrane
Local current as Na+ goes to adjacent region
Wave of depolarisation passes along membrane
New AP can’t be generated for 5ms
VD channels close, RP restored, unidirectional travel

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20
Q

What varies impulse speed

A

Faster
Wider diameter
Myelination (insulated, depolarise nodes of Ranvier, circuit depolarises next node, AP triggered, saltatory conduction)

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21
Q

Photoreceptors generally

A

Retina
Rods: black and white, dim light
Cones: colour, bright light, fovea/centre
Photochemical pigments absorb light, chemical change

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22
Q

Photoreceptors structure

A

Light
Retina
Ganglion axon (lead to optic nerve)
Bipolar cells
Rod/cone cells
Inner segment
Outer segment (photoreceptor vesicles)
Choroid
Sclera

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23
Q

Photoreceptors in the dark

A

Na+ —> non specific cation channels —> outer segment
Na+ diffuse down conc grad —> inner segment
Pumps push Na+ back out cell
Na+ influx causes -40mV depolarisation
Trigger glutamine release
Bind to bipolar cells
Stop depolarisation

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24
Q

Photoreceptors in light

A

Light
Rhodopsin —> opsin + retinal
Opsin activates membrane bound reactions
Outer segment cations channels close
Na+ influx decreases
Inner segment pumps out Na+
Inside cell —> hyperpolarised
No glutamate released
Bipolar cells depolarise
Create AP

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25
Q

Plants nervous system

A

None
Use tropism, directional stimulus response
Positive/negative

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26
Q

Coleoptile

A

Protective sheath
Simple structure
Easily grown
Used for tropism investigation

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27
Q

What 3 things can be determined about phototropism from Coleoptile experiments

A

Need diffusion
Auxin elongates cells
Auxin made in tip

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28
Q

Cholodny-Went model

A

Auxins (eg. IAAs)
Transported by phloem
Bind to target cell receptors
Activate messenger signalling molecules
Control auxin regulated transcription genes
Synthesised proteins control cell expansion/division/replication
Cell wall acidified (pump moves H+ Into cell wall)
Expansion activated
Disrupt microfibrils/hemicellulose bonding
Polysaccharide slippage
Allow cell expansion

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29
Q

Phytochrome structure

A

Protein bonded to light absorbing pigment
2 non protein isomers
Pr/Phytochrome red (600nm)
Pfr/Phytochrome far red (730nm)

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30
Q

Phytochrome photoreversability

A

Inactive/night Pr
Far red light synthesised
Red light converted
Isotopes apart

Active/day Pfr
Red light synthesised
Far red light converted
Isotopes together
Rise fast in day
Decrease slowly at night

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31
Q

Germination

A

Seeds need light/optimum conditions
Red light triggers germination
Far red light inhibits it

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32
Q

Greening

A

Plant breaks through soil surface into daylight
Primary leaf development
Leaf unrolling/pigment production
Can inhibit internode elongation

33
Q

Phytochrome mechanism

A

Light activates Phytochrome
Activate signalling proteins
Activate transcription factors
Activates light regulated gene transcription

34
Q

Flowering

A

Photoperiod: relative day/night period
Pr:Pfr determines day/night length

35
Q

Long vs short day plants

A

Long, flower when darkness is less than 12 hours, Pfr needed
Short, flower when darkness is more than 12 hours, Pr needed, Pfr inhibits flowering

36
Q

Name 7 features of the brain

A

Hypothalamus
Cerebellum
Medulla oblongata
Frontal lobe
Parietal love
Temporal love
Occipital love

37
Q

Cerebellum

A

Back/base
Balance/coordination

38
Q

Hypothalamus

A

Centre/inner brain
Thermoregulatory gland

39
Q

Medulla oblongata

A

Brain stem
Unconscious body processes

40
Q

Frontal lobe

A

Front of cortex
Decision making/reasoning

41
Q

Parietal lobe

A

Top of cortex
Orientation/movement/sensation/calculation/memory

42
Q

Temporal lobe

A

Bottom of cortex
Auditory/speech/sound/some memory

43
Q

Occipital lobe

A

Back of cortex
Visual processing

44
Q

Animal testing for arguments

A

Utilitarianism
Unethical to test on humans
No alternatives
Simialr genes
Less developed pain response
Need to test on whole organism not just cells

45
Q

Animal testing against arguments

A

Consent/autonomy
Genetically differ
Human tissue/computer models
Animal welfare
Suffer/distressed
Right to life
Virtuosity

46
Q

Absolutist

A

Always unacceotablw

47
Q

Relativist

A

Justified in certain circumstances

48
Q

Name 4 brain scans

A

MRI
fMRI
CT
PET

49
Q

MRI scans

A

Mag field + radio waves
Detect soft tissue
Monitor H2
Interact w waves
Release NRG
3D imaging
Diagnose tumours/strokes
Finely detailed images
Better resolution than CT

50
Q

fMRI

A

O2 uptake to brain regions
Deoxyhaemaglobin absorbs radio waves
Oxyhaemaglobin doesn’t
More brain activity = more oxyhaemaglobin = less signal
Negative imaging
Sequence of events
Shows function/process

51
Q

CT

A

X-rays
Strength changes based on tissue density
Thin image slice
Structure not function
Limited resolution
Harmful X-rays
Detect/monitor diseased tissue

52
Q

PET

A

Inject with short life isotopes
Bind to receptors
Emit positrons
Collide with tissue electrons —> gamma
More rays = more blood flow = more activity
Image conversion
Show change in activity
Once/twice a year
Expensive

53
Q

3 ways brain size increase without making more neurones in babies

A

More myelination
Longer axons
Synapse development

54
Q

Describe how the visual system develops

A

Retinal neurone axons synapse to thalamus
Thalamus neurones grow towards visual cortex in occipital lobe
Both eyes must be stimulated during critical period
Synapses used during critical period are strengthened and become permanent
Lost synapses can’t be reformed
Ocular dominance columns (alternate receiving stimuli, genetically determined)

55
Q

Evidence for visual critical period

A

Medical observations
Light vs dark
Monocular deprivation
- Hubel and Wiesel
- Stitched one kitten/monkey eye
- After 3 months, blind in that eye
- Smaller ocular dominance columns in stitched eye
- Unstitched eye has larger ocular dominance columns than usual
- Same test on adults, no blindness/change

56
Q

Habituation process

A

New experiences
New neurone connections
New synapses
Pathway stores memory
Hypocampus
Learn stimulus isn’t a threat
Fewer Ca2+
Fewer neurotransmitters
Less chance of AP
No longer react/react as fast to stimuli
Sensitisation is the converse

57
Q

Learning

A

Relative behaviour/knowledge permanent change from Experince
Synapse change
Memory plasticity

58
Q

Memory

A

Temporal/parietal lobes
Hippocampus - long term
Alter pattern of connection/strength of synapse

59
Q

What causes Parkinson’s disease

A

Midbrain secretes dopamine
Basal ganglia dopamine secreting neurones die
Motor cortex receives less dopamine
Loss of muscular movement

60
Q

Parkinson’s disease symptoms

A

Muscle stiffness
Muscle tremors
Slow movement
Poor balance
Walking problems

61
Q

Excess dopamine effect

A

Schizophrenia
Treatment: Dopamine blocking receptors

62
Q

Name 5 Parkinson’s treatments

A

Dopamine can’t pass blood-brain barrier
Slow dopamine loss - selegiline, inhibit MAOB (dopamine enzyme), increase availability
Treating symptoms - L-dopa, dopamine precursor, pass blood-brain barrier, converted
Dopamine antagonists - mimic dopamine structure, bind to receptors, trigger APs
Gene therapy - modify, increase production, deep stages
Deep brain stimulation - treat symptoms, medication reduction

63
Q

Serotonin

A

Mood determination
Brain stem neurones
Lack associated with depression

64
Q

Symptoms of depression

A

Low mood
Loss of interest in hobbies
Low energ
Disrupted sleep
Hopelessness
Thoughts of death

65
Q

Depression

A

Multi factorial condition
Environmental factors
Susceptibility genes (short 5-HTT presynaptic membrane serotonin uptake)

66
Q

Treatments for depression

A

Selective serotonin reuptake inhibitors (SSRIs), inhibit synaptic cleft reuptake
Monoamine oxidase inhibitors (MOAB), block serotonin enzymes

67
Q

Drugs impact on synapses

A

Effect every stage of synaptic transmission
Mimicry, stimulate APs
Prevent neurotransmitters
Block/open ion channels
Inhibit breakdown enzyme

68
Q

Ecstasy

A

MDMA
Thinking/mood memory
Increase serotonin conc in synaptic cleft
Bind to serotonin cytoplasm transporter molecules
Prevent synaptic cleft removal
More serotonin into synaptic cleft

69
Q

MDMA side effects and risks

A

Short term, change behaviour/brain chemistry
Long term, change behaviour/brain structure/insomnia/depression
Altered perceptions
Anxiety
Clouded thinking
Agitation
Disturbed behaviour
Sweating
Dry mouth
Increased heart rate
Fatigue
Muscle spasms
Hyperthermia
Kidney failure
Withdrawal symptoms

70
Q

Nature vs nurture experiments (5)

A

New born baby abilities
Animal experiments
Damaged brain area studies
Twin studies
Cross cultural studies

71
Q

Personalised medicine

A

Targeted drugs for different genotypes
Human genome project (HGP)
DNA/mRNA sequences, gene expression and protein structure stored in a database
Sequences compared using data retrieval/analysis

72
Q

Issues with personalised medicine

A

Increased research cost, only available to the wealthy
Use data for corporate discriminate
Some patients may be refused as it might not work
Distressing that only option might fail

73
Q

Genetic engineering

A

Restriction nucleases cut DNA in organism with desired characteristic
DNA inserted into a bacteria cell
Ligase joins DNA to that of bacteria
Bacteria cell multiplied in fermenter

74
Q

Vectors

A

Mechanism that carries the gene to another organism

75
Q

Transgenic

A

Organism that has genetic material from another species

76
Q

Genetically modifying animals

A

Low success injecting DNA into fertilised egg nucelus
Use retroviruses

77
Q

Plant vectors

A

Bacteria - agrobacterium, plasmid
Gene gun - DNA covered gold bullet
Viruses - insert DNA

78
Q

Benefits of genetic engineering

A

Higher crop yield/nutrition, reduce famine/malnutrition
Pest resistant crops, lower production/environmental cost
Industrial enzymes cost effectively made by GMOs
Treat disease with human proteins by GMOs not animal proteins, reduce allergy risk
Plant GMO vaccines, not refrigerated, more accessible

79
Q

Risks of genetic engineering

A

Long term health impacts of GMO foods
Pest resistance, more pesticides needed
GMO monocultures, bad for biodiversity
Moral objection to changing plants for human benefit

Biology (8 decks)

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