topic 9 continued (9.2-9.7) Flashcards
9.2 [chemical control in mammals]
What are hormones?
What are target cells?
- 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
Difference between
endocrine glands and exocrine glands
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
endocrine system: Uses hormones for communication
Examples of endrocrine glands + the hormones they produce
- Adrenal gland - Adrenaline
- Pancrease - Insulin / glucagon
- Testes - testosterone
- Ovaries - oestrogen
- Throid gland - thyroxin
- pituitory gland - growth hormone, FSH/LH
Why is there a time lag between hormone production and response by an effector?
It takes time to:
● Produce hormone
● Transport hormone in the blood
● Cause required change to the target protein
- Why does the endocrine system interact closely with the nervous system?
- Release of hormones due to other chemical stimulus?
(negative feedback system)
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
What are the 2 main mode of actions for hormones?
- Attach to receptor sites + trigger the release of a second messenger [adrenaline]
- Enter cells + bind directly to transcription factors [oestrogen]
Hormones’ mode of actions
- Attach to receptor sites + trigger the release of a second messenger
- Adrenaline?
- 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
Hormones’ mode of actions
- Enter cells + bind directly to transcription factors
(oestrogen)
- 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
9.3 [chemical control in plants]
External stimuli which plant respond to as they affect plant development
- 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
Chemical control in plants occurs by which hormones?
-
auxins
(cell elongation, apical dominance, root growth) -
cytokinins
(promote lateral bud growth) -
gibberellins
(stimulate elongation of cells, growth of fruit + breaking dormancy in seeds)
Auxins
- Cell elongation
auxins affect ability of cell wall to stretch
- 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
Auxins
- Root growth
- 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
Auxins
- Apical dominance
(supression of lateral buds)
- 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
Tropisms?
2 types?
- Tropisms are directional growth responses to specific enviornmental cues
- auxins play major role in these
- Phototropism (light)
- Gravitropism (gravity)
Phototropism in plant shoots?
Phototropism in plant roots?
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
Gravitropism in plant shoots?
Gravitropism in plant roots?
Plant shoots:
- Grow against gravity
- Auxins move down plant to promote elongation
- Negative gravitropism
Plant roots:
- Grows in direction of gravity
- Positive gravitropism
Gibberelllins?
how do they stimulate germination?
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
Cytokinins?
- 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
Apical dominance of auxins + cytokinins
- 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
Plant hormones often interact with each other = can be synergistically or antagonistically
- Antagonism?
- when 2 hormones have opposite effects + the balance between them determines response
- Antagonistic actions of Cytokinins + Auxins on apical dominance = they interact antagonistically
- Synergy
- when 2 hormones work together, complimenting eachother
- giving greater response together
- Auxins + gibberellins work together synergistically in the growth of stems
CORE PRACTICAL 14:
Investigate the effect of gibberellin on the production of
amylase in germinating cereals using a starch agar assay
??
How phytochrome controls flowering
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
Flowering in short day plants
Flower in autum
- 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
Flowering in long day plants
flower in summer
- 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
phytochrome and photomorphogenesis
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
What’s an etiolated plant?
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
phytochrome in Germination
- 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
phytochrome / Pfr as a transcription factor
- 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
Explain how phytochrome / Pfr can act as a transcription factor
- 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
9.4 [structure + function of the mammalian nervous system
Describe the division of the nervous system
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
Describe the
CNS + PNS
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
Describe the
- Somatic nervous system
- Autonomic nervous system
of the PNS
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
Describe the
- Sympathetic system
- Parasympathetic system
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
What does it mean that the
Sympathetic + parasympathetic nervous systems work antagonistically?
- 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
Structure of the spinal cord?
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
BRAIN STRUCTURES
Functions of
- Medulla oblongata
- Hypothalamus
NEED TO KNOW LOCATIONS - CHECK DIAGRAM
the medulla oblongata
– controls breathing + heart rate
- controls autonomus functions
hypothalamus
– temperature regulation (thermoregulation)
- osmoregulation
- hormone secretion
Functions of
1. cerebellum
2. cerebrum
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
Nervous system is made up of nervous cells = neurones
Sensory neuron -
structure + function?
Sensory neurons
- transmit impulses / info from sensory receptors to the CNS
- long dendrons
- short axons
Relay neuron -
structure + function?
Relay neurons
- transmit electrical impulses from sensory neurons to motor neurons
- short axons
- short dendrites
Motor neuron -
structure + function?
Motor neurons
- transmit electrical signals from the CNS to effectors like muscles or glands
- short dendrites
- long axons
- myelin sheath (made by Schwann cells)
What’s a reflex action?
- 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)
describe the response that would happen during a reflex action
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
9.5 [nervous transmission]
What do nerve impulses depend on?
what’s potential difference?
(voltage)
- 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)
Resting potential?
- = 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
What does it mean if nerve cells are polarised?
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
How is this resting potential generated and maintained?
- 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)
Therefore, which 2 factors contribute to resting potential?
- Sodium potassium pump transfers 3 NA+ out of axon for every 2 K+ in
- 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
What’s action potential?
Name the stages in generating an action potential
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:
- Depolarisation
- Repolarization
- Hyperpolarization
- Return to resting potential
What are voltage gated ion channels in action potential?
- voltage-gated ion channels only open when the membrane potential reaches a certain value
- voltage gated sodium + pottasium ion channels
1.
Depolarisation?
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
2.
repolarisation
- 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
3.
Hyperpolarisation
- Large amount of pottasium ions diffuse out the axon
- = inside of axon becomes more negative than the resting potential
4.
Recovery / return to resting potential
- 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
Refractory period?
- 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
Absolute v relative refractory period
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
Importance of refractory period?
- 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)
Threshold?
All-or-nothing response?
- 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
Why is speed of transmission greater along myelinated axons than non-myelinated axons?
~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
Synapse?
Synaptic cleft?
Synaptic knobs?
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)
How synapses work?
- 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)
Postsynaptic potentials
Excitatory post-synaptic potentials
(EPSP)
- 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
Postsynaptic potentials
Inhibitory post-synaptic potentials
(IPSPS)
- 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)
2 main types of neurotransmitters in PNS
Neurotransmitter
1. Acetylcholine (ACh)
- 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’
2 main types of neurotransmitters in PNS
Neurotransmitter
2. Noradrenaline
- 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
9.6 [ Effects of drugs on the nervous system]
Drugs + the nervous system
- some drugs can affect the function of synapses + cause changes to synaptic transmission
These drugs include
- nicotine
- lidocaine
- cobra venom
Main ways in which drugs affect synapses
- effects increasing the response include:
- Increases the amount of neuritransmitter synthesised
- Increases the release of neurotransmitter from the vesicles at the presynaptic membrane
- Binds to post-synaptic receptors + activates them or increases the effect of the normal neurotransmitter
- Prevents the degradation of neurotransmitter by enzyms OR prevents reuptake into presynaptic knob
Main ways in which drugs affect synapses
- effects decreasing the response include:
- blocks the synthesis of neurotransmitter
- causes neurotransmitter to leak from vesicles + be destroyed by enzymes
- prevents the release of neurotransmitter from vesicles
- blocks the receptors + prevents neurotransmitter binding
How does nicotine work?
- 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
How does lidocaine work?
- 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
How does cobra venom work?
- 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
9.7 [detection of light]
Structure of human retina?
- 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
Interpretation in the Brain
- 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
2 types of photoreceptors (light sensitive cells)
Rods v Cones
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
Where are rod and cone cells located in the retina?
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
What do the rhodopsin in rod cells do?
- absorbs light energy
- and as a result splits into retinal + opsin
How do rod cells generate an action potential in the light
- 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]
rod cells response in dark?
Why no action potential generated?
- 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
