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Biology > T8: Grey Matter > Flashcards

T8: Grey Matter Flashcards

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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
Plants nervous system
None Use tropism, directional stimulus response Positive/negative
26
Coleoptile
Protective sheath Simple structure Easily grown Used for tropism investigation
27
What 3 things can be determined about phototropism from Coleoptile experiments
Need diffusion Auxin elongates cells Auxin made in tip
28
Cholodny-Went model
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
29
Phytochrome structure
Protein bonded to light absorbing pigment 2 non protein isomers Pr/Phytochrome red (600nm) Pfr/Phytochrome far red (730nm)
30
Phytochrome photoreversability
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
31
Germination
Seeds need light/optimum conditions Red light triggers germination Far red light inhibits it
32
Greening
Plant breaks through soil surface into daylight Primary leaf development Leaf unrolling/pigment production Can inhibit internode elongation
33
Phytochrome mechanism
Light activates Phytochrome Activate signalling proteins Activate transcription factors Activates light regulated gene transcription
34
Flowering
Photoperiod: relative day/night period Pr:Pfr determines day/night length
35
Long vs short day plants
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
Name 7 features of the brain
Hypothalamus Cerebellum Medulla oblongata Frontal lobe Parietal love Temporal love Occipital love
37
Cerebellum
Back/base Balance/coordination
38
Hypothalamus
Centre/inner brain Thermoregulatory gland
39
Medulla oblongata
Brain stem Unconscious body processes
40
Frontal lobe
Front of cortex Decision making/reasoning
41
Parietal lobe
Top of cortex Orientation/movement/sensation/calculation/memory
42
Temporal lobe
Bottom of cortex Auditory/speech/sound/some memory
43
Occipital lobe
Back of cortex Visual processing
44
Animal testing for arguments
Utilitarianism Unethical to test on humans No alternatives Simialr genes Less developed pain response Need to test on whole organism not just cells
45
Animal testing against arguments
Consent/autonomy Genetically differ Human tissue/computer models Animal welfare Suffer/distressed Right to life Virtuosity
46
Absolutist
Always unacceotablw
47
Relativist
Justified in certain circumstances
48
Name 4 brain scans
MRI fMRI CT PET
49
MRI scans
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
fMRI
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
CT
X-rays Strength changes based on tissue density Thin image slice Structure not function Limited resolution Harmful X-rays Detect/monitor diseased tissue
52
PET
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
3 ways brain size increase without making more neurones in babies
More myelination Longer axons Synapse development
54
Describe how the visual system develops
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
Evidence for visual critical period
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
Habituation process
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
Learning
Relative behaviour/knowledge permanent change from Experince Synapse change Memory plasticity
58
Memory
Temporal/parietal lobes Hippocampus - long term Alter pattern of connection/strength of synapse
59
What causes Parkinson’s disease
Midbrain secretes dopamine Basal ganglia dopamine secreting neurones die Motor cortex receives less dopamine Loss of muscular movement
60
Parkinson’s disease symptoms
Muscle stiffness Muscle tremors Slow movement Poor balance Walking problems
61
Excess dopamine effect
Schizophrenia Treatment: Dopamine blocking receptors
62
Name 5 Parkinson’s treatments
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
Serotonin
Mood determination Brain stem neurones Lack associated with depression
64
Symptoms of depression
Low mood Loss of interest in hobbies Low energ Disrupted sleep Hopelessness Thoughts of death
65
Depression
Multi factorial condition Environmental factors Susceptibility genes (short 5-HTT presynaptic membrane serotonin uptake)
66
Treatments for depression
Selective serotonin reuptake inhibitors (SSRIs), inhibit synaptic cleft reuptake Monoamine oxidase inhibitors (MOAB), block serotonin enzymes
67
Drugs impact on synapses
Effect every stage of synaptic transmission Mimicry, stimulate APs Prevent neurotransmitters Block/open ion channels Inhibit breakdown enzyme
68
Ecstasy
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
MDMA side effects and risks
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
Nature vs nurture experiments (5)
New born baby abilities Animal experiments Damaged brain area studies Twin studies Cross cultural studies
71
Personalised medicine
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
Issues with personalised medicine
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
Genetic engineering
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
Vectors
Mechanism that carries the gene to another organism
75
Transgenic
Organism that has genetic material from another species
76
Genetically modifying animals
Low success injecting DNA into fertilised egg nucelus Use retroviruses
77
Plant vectors
Bacteria - agrobacterium, plasmid Gene gun - DNA covered gold bullet Viruses - insert DNA
78
Benefits of genetic engineering
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
Risks of genetic engineering
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

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