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topic 9 continued (9.2-9.7) Flashcards

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1
Q

9.2 [chemical control in mammals]

What are hormones?

What are target cells?

A
  • Hormones are chemical messengers produced by endocrine glands and released into blood to be carried to receptors on target cells
  • hormones reach all cells, but only the cells with the complementary receptors for the hormone will respond = very specific
  • Target cells - cells in body which have specific receptors for that particular hormone
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2
Q

Difference between
endocrine glands and exocrine glands

A

Endocrine glands:

  • produce hormones
  • do not have ducts
  • release hormones directly into bloodstream
  • Effects last over a long period of time

Exocrine glands:

  • produce chemicals (eg enzymes)
  • release them along small tubes / ducts
  • which take them directly to where they are needed
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3
Q

endocrine system: Uses hormones for communication

Examples of endrocrine glands + the hormones they produce

A
  • Adrenal gland - Adrenaline
  • Pancrease - Insulin / glucagon
  • Testes - testosterone
  • Ovaries - oestrogen
  • Throid gland - thyroxin
  • pituitory gland - growth hormone, FSH/LH
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4
Q

Why is there a time lag between hormone production and response by an effector?

A

It takes time to:

● Produce hormone
● Transport hormone in the blood
● Cause required change to the target protein

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5
Q
  1. Why does the endocrine system interact closely with the nervous system?
  2. Release of hormones due to other chemical stimulus?
    (negative feedback system)
A

1.

  • some hormones are released as a result of direct stimulation of endocrine glands by nerves
  • eg adrenal medulla of the adrenal glands releases adrenaline when it’s stimulated by the sympathetic nervous system

2.

  • some hormones released in response to levels of another hormone/chemical in blood
  • secretion is controlled by a negative feedback system as it’s adjusted constantly to needs of the body
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6
Q

What are the 2 main mode of actions for hormones?

A
  1. Attach to receptor sites + trigger the release of a second messenger [adrenaline]
  2. Enter cells + bind directly to transcription factors [oestrogen]
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7
Q

Hormones’ mode of actions

  1. Attach to receptor sites + trigger the release of a second messenger
    - Adrenaline?
A
  • protein + peptide hormones are water soluble = cannot easily cross cell membrane = bind to receptor molecules on membrane outside target cell to triggers reactions inside to produce second messenger

Adrenaline:

  • Adrenaline is the first messenger
  • cAMP produced inside cell is the second messenger
  • cAMP activates enzymes to alter the metabolism of the cell
  • e.g. cAMP increases cellular respiration, contraction of muscle cells, relaxation of smooth muscle
  • allowing effects of adrenaline to show
  • cAMP = cyclic AMP
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8
Q

Hormones’ mode of actions

  1. Enter cells + bind directly to transcription factors
    (oestrogen)
A
  • Steroid hormones (eg oestrogen/ testosterone) are able to pass easily through cell membrane + enter cell (lipid soluble)
  • pass through the cell membrane + bind to a receptor inside the cell (act as internal messenger)
  • They form a hormone-receptor complex = which passes into the nucleus
  • +acts as a transcription factor to regulate gene expression switching sections of DNA on/off
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9
Q

9.3 [chemical control in plants]

External stimuli which plant respond to as they affect plant development

A
  • external stimuli affect plant’s development
  • They change levels of plant growth hormones
  • Light + gravity eg
  • The directional responses to these stimuli involve changes in growth = known as tropism
  • hormones only affect cells with the right receptors
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10
Q

Chemical control in plants occurs by which hormones?

A
  • auxins
    (cell elongation, apical dominance, root growth)
  • cytokinins
    (promote lateral bud growth)
  • gibberellins
    (stimulate elongation of cells, growth of fruit + breaking dormancy in seeds)
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11
Q

Auxins

  1. Cell elongation

auxins affect ability of cell wall to stretch

A
  • auxins synthesised in meristem + diffuse down plant
  • auxins bind to receptors on cell surface membrane
  • This activates hydrogen ion pumping into the cell wall space
  • H+ ions lower the pH to 5 = optimum for enzymes to break bonds between cellulose microfibrils
  • makes microfibrils able to slide
  • = cell walls are flexible + can stretch
  • = water can enter by osmosis
  • = allowing cell elongation to occur

eventually enzymes destroy auxins so elongation will stop

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12
Q

Auxins

  1. Root growth
A
  • Auxins are actively transported down the plant towards roots (from shoots in meristem to roots)
  • the more auxins transported down the stem, the more root growth
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13
Q

Auxins

  1. Apical dominance
    (supression of lateral buds)
A
  • where 1 lead shoot grows bigger + faster then the others
  • High auxins levels from dominant shoot inhibits lateral bud growth
  • When this shoot grows further away, the inhibition from auxins is reduced
  • so cytokinin dominance occurs there (promote lateral bud growth)
  • is meristem shoot is removed, source of auxins is removed = cytokinin is dominant = lateral buds grow
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14
Q

Tropisms?
2 types?

A
  • Tropisms are directional growth responses to specific enviornmental cues
  • auxins play major role in these
  1. Phototropism (light)
  2. Gravitropism (gravity)
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15
Q

Phototropism in plant shoots?
Phototropism in plant roots?

A

Plant shoots:

  • grow / bends towards light unilaterally
  • positive phototropism
  • auxins move to the shaded side and promote elongation towards light

Plant roots:

  • grow / bends away from light
  • negative phototropism
  • auxins move to the light side and promote elongation away from light towards shade
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16
Q

Gravitropism in plant shoots?
Gravitropism in plant roots?

A

Plant shoots:

  • Grow against gravity
  • Auxins move down plant to promote elongation
  • Negative gravitropism

Plant roots:

  • Grows in direction of gravity
  • Positive gravitropism
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17
Q

Gibberelllins?
how do they stimulate germination?

A

Gibberellins - seed germination / breaking dormancy in seeds

To stimulate germination..

  • Seed absorbs water + swells = activates the embryo
  • The activated embryo secretes gibberellins
  • Gibberellins diffuse to the aleurone layer
  • Aleurone layer produces amylase
  • Amylase diffuses to the endosperm layer + breaks down starch (carbs food store of endosperm) into glucose
  • products released from endosperm are used by embryo to make new cells + germinate
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18
Q

Cytokinins?

A
  • Cytokinins are growth stimulants that promote cell division in apical meristems/ lateral bud development
  • +work synergistically with ethene to promote abscission of leaves
  • high levels of cytokinin keep leaves healthy + alive
  • when cytokinins levels fall = leaf dries + falls
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19
Q

Apical dominance of auxins + cytokinins

A
  • 1 shoot grows bigger + faster than others = has high auxins
  • Auxins inhibit lateral bud growth
  • When this shoot grows away = inhibition reduced
  • cytokinins promote lateral bud growth
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20
Q

Plant hormones often interact with each other = can be synergistically or antagonistically

  1. Antagonism?
A
  • when 2 hormones have opposite effects + the balance between them determines response
  • Antagonistic actions of Cytokinins + Auxins on apical dominance = they interact antagonistically
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21
Q
  1. Synergy
A
  • when 2 hormones work together, complimenting eachother
  • giving greater response together
  • Auxins + gibberellins work together synergistically in the growth of stems
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22
Q

CORE PRACTICAL 14:
Investigate the effect of gibberellin on the production of
amylase in germinating cereals using a starch agar assay

A

??

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23
Q

How phytochrome controls flowering

A

phytochrome is a plant pigment that reacts with different types of light + affects the responses of plants

  • 2 forms of phytochrome pigments are pr + pfr
  • red light (from sunlight) converts pr→ pfr
  • far red light (in dark) converts pfr→ pr (reverse)

seed germinates + makes pr →breaks through surface of soil + exposed to red light →pr converted to pfr

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24
Q

Flowering in short day plants

Flower in autum

A
  • have short days + long nights = not a lot of light
  • High levels of pfr inhbits flowering in Short day plants
  • during the short day = pr → pfr = inhibits flowering
  • during long nighttime = pfr → pr = flowering can occur
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25
Q

Flowering in long day plants

flower in summer

A
  • Have long days + short nights = lots of light
  • high levels of pfr stimulates flowering
  • day = lots of pr →pfr
  • nights are short = little pfr converted back to pr
  • pfr levels maintained high = flowering occurs
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26
Q

phytochrome and photomorphogenesis

A

photomorphogenesis is the process by which the form + development of a plant is controlled by the level of + type of light

phytochrome Converts between 2 forms:

● Biologically inactive Pr absorbs red light
● Biologically active Pfr absorbs far-red light

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27
Q

What’s an etiolated plant?

A

Plants grown in the dark (all phytochrome is in form Pr) are etiolated :

  • Tall and thin
  • Fragile stems with long internodes
  • Small yellowed leaves
  • Little root growth
  • grow rapidly using food stores in attempt to reach light

-changes that take place when plant becomes etiolated + the reverse of etiolation when germinating seeds break through soil are controlled by phytochrome

etiolated describes form of plants grown in dark

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28
Q

phytochrome in Germination

A
  • phytochrome is synthesised as pr
  • when seedling emerges from seed underground it only contains pr as there’s no light to produce pfr
  • = seedling shows characteristics of etiolation
  • no leaf growth, little root growth, stem lengthens but doesn’t thicken, no chlorophyll (as useless in dark)
  • when shoot break through surface of soil
  • exposed to light = pr →pfr =
  • stem elongation slows down, first leaves open, chlorophyll forms + seedling starts to photosynthesise
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29
Q

phytochrome / Pfr as a transcription factor

A
  • when the stem breaks through the soil, Pfr acts as a transcription factor
  • phytochrome could act as a transcription factor that is involved in switching genes on/off in the nucleus of plant cells
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30
Q

Explain how phytochrome / Pfr can act as a transcription factor

A
  • pr is converted to pfr in presence of light
  • pfr moves into nucleus through pores in nucleur membrane
  • pfr binds to protein phytochrome-interacting factor (PIF3) in nucleus
  • PIF3 is a transcription factor which only binds to pfr
  • PIF3 activates gene transcription when it is bound to pfr
  • the genes activated by PIF3 control different aspects of growth + development in plants
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31
Q

9.4 [structure + function of the mammalian nervous system

Describe the division of the nervous system

A

Nervous system -
1. CNS (central nervous system)
2. PNS (peripheral nervous system)

CNS -
1. Brain
2. Spinal cord

PNS -
1. somatic (Voluntary) system
2. Autonomic system

Autonomic nervous system -
1. Sympathetic system
2. Parasympathetic system

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32
Q

Describe the
CNS + PNS

A

CNS - a specialised concentration of nerve cells that processes incoming information, sends impulses through motor neurons and carries impulses to effectors

  • processing of information

PNS - consists of neurons not in the CNS that spread throughout the body, relays info between CNS + environment

  • has sensory input and motor output
33
Q

Describe the
- Somatic nervous system
- Autonomic nervous system
of the PNS

A

somatic (Voluntary) nervous system

  • under conscious control
  • controls voluntary + conscious activity / actions

Autonomic nervous system

  • Not under conscious control
  • involuntary control of eg heart rate, breathing
34
Q

Describe the
- Sympathetic system
- Parasympathetic system

A

Sympathetic system

  • Usually stimulates effectors = coordinates fight-or-flight response
  • Neurotransmitter is noradrenaline
  • Ganglia are located near CNS

Parasympathetic system

  • Usually inhibits effectors = coordinates rest/digest response + returns body to resting state after F/F
  • Neurotransmitter is acetylcholine.
  • Ganglia located far from CNS

Sympathetic + parasympathetic nervous systems work antagonistically

35
Q

What does it mean that the
Sympathetic + parasympathetic nervous systems work antagonistically?

A
  • They act in opposite ways
  • The sympathetic system activates the “fight or flight” response
  • eg increases heart rate
  • while the parasympathetic system activates the “rest + digest” response
  • eg slows heart rate
36
Q

Structure of the spinal cord?

A

Acts as a communication link between the brain + PNS + rest of body.
CNS communicates with PNS through spinal cord

  • Cylindrical bundle of nerve fibres runs from brain stem to lower back
  • Surrounded by spinal vertebrae (protection)
  • Consists of nerve tissue (neurons, glia, blood vessels).
  • 31 pairs of spinal nerves branching out between vertebrae to the body
  • Gray matter: H-shaped region contains neurons
  • White matter: myelinated axons
37
Q

BRAIN STRUCTURES

Functions of

  1. Medulla oblongata
  2. Hypothalamus

NEED TO KNOW LOCATIONS - CHECK DIAGRAM

A

the medulla oblongata
– controls breathing + heart rate
- controls autonomus functions

hypothalamus
– temperature regulation (thermoregulation)
- osmoregulation
- hormone secretion

38
Q

Functions of
1. cerebellum
2. cerebrum

A

cerebellum

– controls balance + coordination of movement
- Controls execution (not initiation) of movement
- Possible role in cognition = attention & language.

cerebrum
– initiates movement
- control for conscious thoughts
- voluntary behaviour - personality

39
Q

Nervous system is made up of nervous cells = neurones

Sensory neuron -
structure + function?

A

Sensory neurons

  • transmit impulses / info from sensory receptors to the CNS
  • long dendrons
  • short axons
40
Q

Relay neuron -
structure + function?

A

Relay neurons

  • transmit electrical impulses from sensory neurons to motor neurons
  • short axons
  • short dendrites
41
Q

Motor neuron -
structure + function?

A

Motor neurons

  • transmit electrical signals from the CNS to effectors like muscles or glands
  • short dendrites
  • long axons
  • myelin sheath (made by Schwann cells)
42
Q

What’s a reflex action?

A
  • rapid responses which take place with no conscious thoughts involved
  • nervous communication via spinal cord
  • controlled by simplest type of nerve pathway in body = reflex arc
  • crucial for survival as they enable quick responses to potentially harmful stimuli
    2 types of reflexes:
    1. spinal reflexes (hand moves from hot object)
    2. Cranial reflexes (blinking, pupil reflexes)
43
Q

describe the response that would happen during a reflex action

A

Stimulus received by sensory receptors→

action potential travels along sensory neurone
into spinal cord →

synapse with relay neurone in grey matter →

synapse with motor neurone in grey matter →

action potential in motor neurone leaves spinal cord →

reaches motor end plate in muscle →

stimulates contraction of muscle = move hand away eg

44
Q

9.5 [nervous transmission]

What do nerve impulses depend on?

what’s potential difference?
(voltage)

A
  • conc of sodium ions (Na+) + potassium ions (K+) outside axon is different than conc inside axon = basis of nerve impulse
  • potential difference measures the difference in charge across a membrane (inside v outside axon)
45
Q

Resting potential?

A
  • = The potential difference across the cell membrane of a neuron at rest which is around -70 millivolts (mV)

Nerve cells are polarised in their resting state
= As a result there is a difference in the voltage across the neuron membrane, with a value of -70mV known as the resting potential

46
Q

What does it mean if nerve cells are polarised?

A

When the inside of the cell is slightly negative in charge relative to the outside (outside is more positive)

inside of cell is more negative compared to outside
= value of charge difference is resting potential

47
Q

How is this resting potential generated and maintained?

A
  • Due to the sodium - potassium pump which moves sodium ions out of the neuron + potassium ions into the neuron
  • Requires energy, so ATP broken into ADP + P (Dephosphyraltion)
  • in order to pump out 3 NA+ and pump in 2 K+ (actively transported)
  • Because for every 3 NA+ pumped out, only 2 K+ pumped in = number of positive ions outside membrane is higher than inside
  • Ion channels allow ions to move down electrochemical gradient through facilitated diffusion
  • Sodium ion channels are mostly closed = low rate of diffusion of NA+ back into axon = membrane relatively impermeable to sodium ions
  • potassium ion channels are mainly opened = high rate of diffusion of K+ back out of axon
  • = makes inside of axon more negative compared to outside (which is positive)
48
Q

Therefore, which 2 factors contribute to resting potential?

A
  1. Sodium potassium pump transfers 3 NA+ out of axon for every 2 K+ in
  2. The outwards movement of potassium ions down electrochemical gradient via facilitated diffusion through ion channels

= these 2 factors mean there’s more positive ions on outside of axon than inside = produces membrane potential

49
Q

What’s action potential?

Name the stages in generating an action potential

A

Action potential:

  • The temporary change in electrical potential across the membrane of an axon in response to the transmission of a nerve impulse

Stages in generating an action potential:

  1. Depolarisation
  2. Repolarization
  3. Hyperpolarization
  4. Return to resting potential
50
Q

What are voltage gated ion channels in action potential?

A
  • voltage-gated ion channels only open when the membrane potential reaches a certain value
  • voltage gated sodium + pottasium ion channels
51
Q

1.

Depolarisation?

A

when impulse travels along axon due to stimulus, making membrane more permeable to sodium ions

  • Neurone stimulated (receives signal from stimulus)
  • = excitation of a neuron cell triggered
  • = causes the voltage-gated sodium channels / gates to open
  • = making it more permeable to sodium ions NA+
  • = NA+ rapidly diffuse down electrochemical gradient into the neuron
  • = making the inside less negative / more positive
  • potential difference across membrane is briefly reversed
  • potential difference is now +40 mV
  • depolarisation lasts around 1 millisecond
52
Q

2.

repolarisation

A
  • pd reaches +40 mV = triggers..
  • Voltage-gated Na+ channels to close
  • +voltage-gated K+ channels to open =
  • Facilitated diffusion of K+ ions out of axon down electrochemical gradient
  • inside of axon becomes more negative relative to outside
  • p.d. across membrane becomes more negative
53
Q

3.

Hyperpolarisation

A
  • Large amount of pottasium ions diffuse out the axon
  • = inside of axon becomes more negative than the resting potential
54
Q

4.

Recovery / return to resting potential

A
  • Voltage-gated K+ channels close
  • sodium-potassium pump re-establishes resting potential by pumping NA+ out and K+ in
  • K+ attracted back into axon by negative charge when the membrane is hyperpolarised
  • = causes PD to rise
  • resting potential equilibrium restored
55
Q

Refractory period?

A
  • The time it takes for ionic movements to repolarise an area of the membrane + restore the resting potential after an action potential
  • depends on sodium/pottasium pump and on membrane permeability to pottasium ions
56
Q

Absolute v relative refractory period

A

Absolute refractory period

  • for the 1st millisecond after action potential, it is impossible for another action potential to be generated
  • as sodium ion channels are completely blocked
  • +resting potential has not been restored

Relative refractory period

  • After this, for several milliseconds, the axon may be restimulated
  • but it will only respons to much bigger threshold than before = the threshold has been raised
  • sodium ion channels are not blocked, butvoltage-depending potassium ion channels are still open
  • its not until they’re closed that normal resting potential can be fully restored
57
Q

Importance of refractory period?

A
  • limits rate at which impulses may flow along a fibre
  • ensures impulse flow is only in 1 direction along nerve
  • (until resting potential is restored, the part of nerve fibre that impulse had just left cannot conduct another impulse = impulse can only continue travelling in same direction)
58
Q

Threshold?

All-or-nothing response?

A
  • Threshold = the point when sufficient sodium ions channels open for the rush of sodium ions into the axon to be greater thanthe outflow of pottasium ions = resulting in an action potential
  • The size of the action potential is always the same = all-or-nothing response
  • Any generator potential which reaches or exceeds the threshold potential will produce an action potential of equal magnitude = all or nothing response

threshold = -55 V

59
Q

Why is speed of transmission greater along myelinated axons than non-myelinated axons?

A

~myelin sheath serves as an insulator of axons + dendrites
~it’s produced by Schwann cells

  • The mechanism by which the speed is increased is known as saltatory conduction
  • In myelinated neurones, ions can only pass in/out of axon at nodes of Ranvier (where there’s no myelin sheath)
  • = action potential can only occur at nodes = action potential ‘jumps’ from one to the next
  • because the myelin sheath is impermeable
  • transmission is sped up as ionic movement associated with action potential occurs less frequently, taking less time
  • impulse doesn’t travel along whole axon + depolarisation of one node causes depolarisation of next node = faster conduction along nerve tissue
60
Q

Synapse?

Synaptic cleft?
Synaptic knobs?

A

Synapse

  • The junction between 2 neurons that nerve impulses cross via neurotransmitters

Synaptic cleft

  • the gap between the pre + post synaptic membranes in synapse

Synaptic knobs

  • bulges at end of presynaptic neurone where neurotransmitters are made (contains vesicles filled with neurotransmitters)
61
Q

How synapses work?

A
  • Action potential arrives at presynaptic knob
  • = presynaptic membrane depolarises
  • causing the calcium channels to open
  • = calcium ions diffuse into neurone
  • causes synaptic vesicles filled with a neurotransmitter (eg acetylcholine) to fuse with the presynapc membrane
  • = causing release of neurotransmitters (exocytosis)
  • they diffuse across the synaptic cleft
  • neurotransmitter binds to the receptors on postsynaptic membrane
  • this can have 2 effects (excitation / inhibition)
62
Q

Postsynaptic potentials

Excitatory post-synaptic potentials
(EPSP)

A
  • neurotransmitters bind to specific protein receptors on sodium channels of post-synaptic membrane = Stimulates opening of cation channels
  • This opens sodium ion channels in the membrane
  • Lots of NA+ enter nerve fibre
  • reduced PD raises membrane to threshold potential
  • causing an action potential
  • =travels along post-synaptic neurone
63
Q

Postsynaptic potentials

Inhibitory post-synaptic potentials
(IPSPS)

A
  • When neurotransmitters bind to specific protein receptors on post-synaptic membrane = neurotransmitter has opposite effect = Stimulates opening of anion channels
  • different negative (anion) ion channels open in membrane (anion)
  • allowing inwards movement of negative ions (eg chloride ions Cl-)
  • makes inside more negative than normal resting potential
  • less likely that action potential will occur
  • (p.d. becomes more negative - hyperpolarisation)
64
Q

2 main types of neurotransmitters in PNS

Neurotransmitter
1. Acetylcholine (ACh)

A
  • synthesised in synaptic knob using ATP produced from many mitochondria present
  • found in all nerves in voluntary + parasympathetic autonomic system
  • nerves using ACh = knows as cholinergic nerves
  • once ACh has done its job = its broken down / hydrolised by enzyme acetylcholinesterase into acetate + choline (which diffuse back to presynaptic membrane)
  • ACh usually results in excitation at post-synaptic membrane

INSERT INTO EPSP / IPSP EVENTS BUT SUB ACh FOR ‘neurotransmitter’

65
Q

2 main types of neurotransmitters in PNS

Neurotransmitter
2. Noradrenaline

A
  • found in nerves of the sympathetic autonomic nervous sytem
  • nerves using this = adrenergic nerves
  • binding of it to receptors in post-synaptic membrane depends on conc of it in synaptic cleft
  • as release of it from presynaptic knob stops = levels in synaptic cleft fall
  • = noradrenaline released from post-synaptic receptors back to synaptic cleft
  • +most is reabsorbed y presynaptic knob = repackaged + reused when another action potential comes

INSERT INTO EPSP/IPSP EVENTS BUT SUB noradrenaline FOR ‘neurotransmitter

66
Q

9.6 [ Effects of drugs on the nervous system]

Drugs + the nervous system

A
  • some drugs can affect the function of synapses + cause changes to synaptic transmission

These drugs include

  • nicotine
  • lidocaine
  • cobra venom
67
Q

Main ways in which drugs affect synapses

  • effects increasing the response include:
A
  1. Increases the amount of neuritransmitter synthesised
  2. Increases the release of neurotransmitter from the vesicles at the presynaptic membrane
  3. Binds to post-synaptic receptors + activates them or increases the effect of the normal neurotransmitter
  4. Prevents the degradation of neurotransmitter by enzyms OR prevents reuptake into presynaptic knob
68
Q

Main ways in which drugs affect synapses

  • effects decreasing the response include:
A
  1. blocks the synthesis of neurotransmitter
  2. causes neurotransmitter to leak from vesicles + be destroyed by enzymes
  3. prevents the release of neurotransmitter from vesicles
  4. blocks the receptors + prevents neurotransmitter binding
69
Q

How does nicotine work?

A
  • mimicks effects of acetylcholine
  • component of cigarette smoke which affects synapses in brain + in the PNS
  • these synapses have nicotinic acetylcholine (ACh) receptors = which are normally stimulated by neurotransmitter ACh but also respond when nicotine binds
  • this can increase heart rate + blood pressure due to nerves being stimulated
  • triggers release of dopamine in brain = feeling of hapiness
  • at low dose nicotine has stimulating effects
  • at high dose nicotine blocks acetylcholine receptors + can kill

Action on postsynaptic neuron: excitatory

70
Q

How does lidocaine work?

A
  • Used as local anaesthetic
  • block voltage gated Na+ channels in postsynaptic membrane
  • Na+ ions cannot enter neurone when neurotransmitter binds
  • action potential cannot form in the postsynaptic neurone
  • = prevents impulses from being conducted along nerve fibres responsible for causing pain sensations

Action on postsynaptic neuron: Inhibitory

71
Q

How does cobra venom work?

A
  • binds + blocks acetylcholine receptors in postsynaptic membrane
  • prevents transmission of impulses across synapse
  • When nerves that stimulate breathing are affectes = muscles not stimulated to contract = eventually become paralysed
  • when toxins reach muscles involved in breathing = causes death

Action on postsynaptic neuron: Inhibitory

72
Q

9.7 [detection of light]

Structure of human retina?

A
  • ganglion cell (from optic nerve fibre)
  • bipolar neurones
  • photoreceptors
  • = light-sensitive cells - rods + cones (which provide info needed for brain to produce images)
  • Rods + cones respond to different intensities of light = giving effective vision in different conditions

DIRECTION OF LIGHT PASSING THROUGH RETINA:
ganglion neurone –> bipolar neurones –> cones + rods

73
Q

Interpretation in the Brain

A
  • Electrical signals are sent from
    photoreceptors → bipolar cells → ganglion cells → along the optic nerve → to the visual cortex of the brain
  • The brain interprets these signals, allowing us to perceive attributes of light such as colour + intensity
74
Q

2 types of photoreceptors (light sensitive cells)

Rods v Cones

A

Cones

- provide colour vision
- responsible for vision in bright light
- 3 types: red, green + blue cones = each sensitive to a different wavelength of light

Rods

- provide greyscale vision 
- responsible for vision during night / low intensity light
- very sensitive to light
- contain a light-sensitive pigment called rhodopsin
75
Q

Where are rod and cone cells located in the retina?

A

Rod:

  • evenly distributed around periphery but NOT in central fovea

Cone:

  • mainly central fovea

No photoreceptors at blind spot where ganglion axon fibres form optic nerve

76
Q

What do the rhodopsin in rod cells do?

A
  • absorbs light energy
  • and as a result splits into retinal + opsin
77
Q

How do rod cells generate an action potential in the light

A
  • when rhodopsin (in rod cells) absorb light = it splits into retinal + opsin = this is called bleaching
  • opsin causes Na+ channels to close
  • Na+ ions stop moving into the cell
  • sodium/potassium pump continues = Na+ still move out
  • inside the cell becomes more more negative as there’s less positive ions inside
  • = hyperpolarisation occurs
  • = stops inhibitory neurotransmitter release (glutamate)
  • allows depolarisation / action potential in bipolar / ganglion cell

[ as it allows the bipolar neurone to stimulate the sensory nerve fibre to depolarise + cause action potential = AP transmitted to the brain via the opc nerve + subsequently processed by the brain]

78
Q

rod cells response in dark?
Why no action potential generated?

A
  • Na+ ions diffuse into rod through open channels
  • Na+ ions actively pumped out of rod cell
  • inside of the cell only slightly more negave compared to the outside = causing membrane to be slightly depolarised
  • = stimulates secretion of a neurotransmitter glutamate, which inhibits depolarisation of bipolar neurone
  • = no information is transmitted to the brain

bio (alevel) (10 decks)

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