T8: Grey Matter Flashcards
Reflex arc general stages
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)
Nervous system subsections and their functions
Central (brain/spinal cord)
Peripheral (sensory/motor)
- somatic (voluntary/skeletal muscles)
- autonomic (involuntary smooth/cardiac muscle/glands)
— sympathetic (fight/flight)
— parasympathetic (rest/digest)
Nerve
Bundle of neurones wrapped in a protective coating
Neurone structure
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)
3 types of neurone
Motor: cell body end of axon, relay - motor
Relay: cell body inside axon, sensory - motor
Sensory: cell body off axon, receptor - relay
Receptors
Detect stimuli
Convert energy source input —> electrical signals/nerve impulses
Cells that synapse sensory neurones
Part of a specialised sensory neurone
Name and describe 4 types of receptors
Chemoreceptors, chemical stimulae, taste, smell, blood conc
Mechanoreceptors, force stimulae, balance, touch, hearing
Photoreceptors, light stimulae, sight
Thermoreceptors, temperature stimulae
Spinal cord matter
Nerve cell bodies, grey matter
Axons and myelin sheaths, white matter
Iris light control mechanism
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
Compare the radial and circular muscles in the Iris
Antagonistic
Radial, sympathetic, contract, larger Iris
Circular, parasympathetic, contract, smaller Iris
Summation role
Control nerve pathways
Flexible responses
Integrate different electrical impulses —> coordinated response
What does the likelihood of a postsynaptic membrane depolarisation depend on
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
Compare excitatory and inhibitory synapses
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
Synaptic process
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
Acetylcholine
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
Resting potential
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
Action potential process
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
Compare nervous vs hormonal responses
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
Refractory period
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
What varies impulse speed
Faster
Wider diameter
Myelination (insulated, depolarise nodes of Ranvier, circuit depolarises next node, AP triggered, saltatory conduction)
Photoreceptors generally
Retina
Rods: black and white, dim light
Cones: colour, bright light, fovea/centre
Photochemical pigments absorb light, chemical change
Photoreceptors structure
Light
Retina
Ganglion axon (lead to optic nerve)
Bipolar cells
Rod/cone cells
Inner segment
Outer segment (photoreceptor vesicles)
Choroid
Sclera
Photoreceptors in the dark
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
Photoreceptors in light
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
Plants nervous system
None
Use tropism, directional stimulus response
Positive/negative
Coleoptile
Protective sheath
Simple structure
Easily grown
Used for tropism investigation
What 3 things can be determined about phototropism from Coleoptile experiments
Need diffusion
Auxin elongates cells
Auxin made in tip
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
Phytochrome structure
Protein bonded to light absorbing pigment
2 non protein isomers
Pr/Phytochrome red (600nm)
Pfr/Phytochrome far red (730nm)
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
Germination
Seeds need light/optimum conditions
Red light triggers germination
Far red light inhibits it
Greening
Plant breaks through soil surface into daylight
Primary leaf development
Leaf unrolling/pigment production
Can inhibit internode elongation
Phytochrome mechanism
Light activates Phytochrome
Activate signalling proteins
Activate transcription factors
Activates light regulated gene transcription
Flowering
Photoperiod: relative day/night period
Pr:Pfr determines day/night length
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
Name 7 features of the brain
Hypothalamus
Cerebellum
Medulla oblongata
Frontal lobe
Parietal love
Temporal love
Occipital love
Cerebellum
Back/base
Balance/coordination
Hypothalamus
Centre/inner brain
Thermoregulatory gland
Medulla oblongata
Brain stem
Unconscious body processes
Frontal lobe
Front of cortex
Decision making/reasoning
Parietal lobe
Top of cortex
Orientation/movement/sensation/calculation/memory
Temporal lobe
Bottom of cortex
Auditory/speech/sound/some memory
Occipital lobe
Back of cortex
Visual processing
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
Animal testing against arguments
Consent/autonomy
Genetically differ
Human tissue/computer models
Animal welfare
Suffer/distressed
Right to life
Virtuosity
Absolutist
Always unacceotablw
Relativist
Justified in certain circumstances
Name 4 brain scans
MRI
fMRI
CT
PET
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
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
CT
X-rays
Strength changes based on tissue density
Thin image slice
Structure not function
Limited resolution
Harmful X-rays
Detect/monitor diseased tissue
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
3 ways brain size increase without making more neurones in babies
More myelination
Longer axons
Synapse development
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)
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
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
Learning
Relative behaviour/knowledge permanent change from Experince
Synapse change
Memory plasticity
Memory
Temporal/parietal lobes
Hippocampus - long term
Alter pattern of connection/strength of synapse
What causes Parkinson’s disease
Midbrain secretes dopamine
Basal ganglia dopamine secreting neurones die
Motor cortex receives less dopamine
Loss of muscular movement
Parkinson’s disease symptoms
Muscle stiffness
Muscle tremors
Slow movement
Poor balance
Walking problems
Excess dopamine effect
Schizophrenia
Treatment: Dopamine blocking receptors
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
Serotonin
Mood determination
Brain stem neurones
Lack associated with depression
Symptoms of depression
Low mood
Loss of interest in hobbies
Low energ
Disrupted sleep
Hopelessness
Thoughts of death
Depression
Multi factorial condition
Environmental factors
Susceptibility genes (short 5-HTT presynaptic membrane serotonin uptake)
Treatments for depression
Selective serotonin reuptake inhibitors (SSRIs), inhibit synaptic cleft reuptake
Monoamine oxidase inhibitors (MOAB), block serotonin enzymes
Drugs impact on synapses
Effect every stage of synaptic transmission
Mimicry, stimulate APs
Prevent neurotransmitters
Block/open ion channels
Inhibit breakdown enzyme
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
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
Nature vs nurture experiments (5)
New born baby abilities
Animal experiments
Damaged brain area studies
Twin studies
Cross cultural studies
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
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
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
Vectors
Mechanism that carries the gene to another organism
Transgenic
Organism that has genetic material from another species
Genetically modifying animals
Low success injecting DNA into fertilised egg nucelus
Use retroviruses
Plant vectors
Bacteria - agrobacterium, plasmid
Gene gun - DNA covered gold bullet
Viruses - insert DNA
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
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
