Sensory Systems Flashcards
1
Q
Why is the Optic nerve referred to as an information bottleneck?
A
It has limited capacity, cannot transform everything the eye sees. So the retina has to choose what we see.
2
Q
What side of the brain does the a) right hemifield b) left hemifield activate?
A
a) Right hemifield activates left side of brain
b) Left hemifield activates right side of brain
3
Q
What is the pathway information travels to get from the retina to the visual cortex?
A
- Retina
- Lateral geniculate nucleus
- Through optic radiations
- Primary visual cortex (back of the brain)
3
Q
What is the pathway information travels to get from the retina to the visual cortex?
A
- Retina (Parvocellular Cells)
- Lateral geniculate nucleus
- Through optic radiations
- Primary visual cortex (back of the brain)
4
Q
What 2 areas process visual information, and which does more?
A
1) Retina (before visual cortex)
2) Visual cortex (does more)
5
Q
What are the 2 main visual pathways in the cortex, what information do they process?
A
1) Ventral stream (“what” pathway)
>Process information about object identity
2) Dorsal stream (“where” pathway)
>Process spatial location and speed (spatial and motion)
6
Q
What is the function of the a) pupil b) lens
A
a) Pupil regulate the amount of light that falls on the retina
b) Lens focuses image on the fovea
7
Q
What is the fovea and how is it different to the rest of the retina?
A
> Fovea= retina with highest spatial resolution/ visual acuity due to many cones
The rest of the retina has smaller acuity and contains primarily rods
8
Q
What part of the retina does light travel through to reach the photoreceptors?
A
Muller cells (glial cells)
9
Q
What are the 3 neuronal layers of the retina, listed as 1 being further back in the eye?
A
- Photoreceptors
- Bipolar cells
- Ganglion cells
10
Q
What are the 3 excitatory neurons in the retina and how do they carry out excitatory feedforward mechanisms?
A
> photoreceptors, bipolar cells and ganglion cells
- Photoreceptors release glutamate to bipolar cells express glutamate
- Bipolar cells release glutamate to ganglion cells express glutamate
- Ganglion cells release glutamate onto nerves
11
Q
What are the 2 inhibitory neurons in the retina and how do they carry out inhibitory feedback mechanisms?
A
> horizontal cells and amacrine cells
- Horizontal cells to Photoreceptors express GABA
- Amacrine cells to Bipolar cells and Ganglion cells, express inhibitory neurotransmitters (GABA)
12
Q
How do a) horizontal cells b) amacrine cells carry out inhibitory feedforward?
A
- Horizontal cells release GABA to Bipolar cells
- Amacrine cells release GABA to ganglion cells.
13
Q
What are the 2 synaptic layers of the retina and what synapses does each contain?
A
- Inner plexiform layer
>Contains synapses between bipolar cells, amacrine cells and ganglion cells - Outer plexiform layers
>Contains synapses between photoreceptors, bipolar cells, horizontal cells
14
Q
What are the 4 structures making up photoreceptors (rods and cones) and where does phototransduction occur?
A
> Outer segment (Phototransduction)
Inner segment
Nucleus
Synapse
15
Q
How do photoreceptors respond to light flashes in a) vertebraes b) insects?
A
a) Photoreceptors hyperpolarise
b) Photoreceptors depolarise
16
Q
When do a) rods b) cones activate?
A
a) dim lights
>can respond to single photons
b) bright lights
17
Q
Describe the phototransduction cascade when light hits the retina in 6 steps
A
- Light changes conformation of Rhodopsin receptor,
- Triggering Gq-protein cascade and G-alpha activates phosphodiesterase
- Phosphodiesterase catalysis cyclicGMP into GMP
- Cyclic GMP conc falls so non-selective ion channel closes
- membrane potential decreases (of outer segment of photoreceptor)/ hyperpolarises photoreceptor
- Hyperpolarisation causes the amount of glutamate released at the synapse to the bipolar cell to decrease.
18
Q
What takes place in a photoreceptor when in darkness?
A
> As phosphodiesterase can’t activate without light, In darkness lots of Cyclic GMP present, this activates non-selective cation channels which opens so the membrane depolarises (of outer segment of photoreceptor).
> This leads to a constant release of glutamate from the photoreceptor to the Bipolar cells
19
Q
When is more glutamate released at the synapse between photoreceptors and bipolar cells?
A
> Constant release of glutamate in darkness
Less glutamate is released during activation by light
20
Q
What neurons receive input from photoreceptors in the outer plexiform layer (OPL) of the retina?
A
Bipolar and horizontal cells receive input from photoreceptors in the outer plexiform layer (OPL)
21
Q
What neurons receive input from bipolar cells in the inner plexiform layer (IFL) of the retina?
A
Ganglion cells and amacrine cells receive input from bipolar cell in the inner plexiform layer (IPL)
22
Q
How do a) ON Bipolar cells b) OFF Bipolar cells respond to increasing light intensity and why?
A
a) ON cells depolarise when light intensity increases
>As hyperpolarised photoreceptors release less glutamate, less binds to mGluR channels on Bipolar cells which leads to less non-selective cation channels being closed, so positive ions flow in, causing increased ganglion cell firing.
b) OFF cells hyperpolarise
>As hyperpolarised photoreceptors release less glutamate, less ionotropic glutaminergic receptors are activated so less cations enter so the bipolar cells is hyperpolarised, causing decreased ganglion cell firing.
23
Q
What receptor is present on a) ON bipolar cells b) OFF bipolar cells and the effect of glutamate binding?
A
a) Metabotropic glutamate receptors (mGluR), glutamate binding causes a signalling cascade where non-selective cation channels close (so in darkness are hyperpolarised due to constant glutamate binding, in light are depolarised as less glutamate binds so less channels are closed).
b) Ionotropic glutamate receptors, glutamate binding allows cations to flow through and depolarise OFF bipolar cells in darkness, hyperpolarise ON bipolar cells in light.
24
As well as mGluR, what 2 other proteins are required for ON bipolar cells to function?
> TRPM1 channel: expressed in ON but not OFF cells
>Nyctalopin is a proteoglycan required for light and glutamate responses in ON cells
25
How can we label ON and OFF Bipolar cells?
By expressing GFP (green fluorescence protein) in ON bipolar cells and RFP (red fluorescence protein) in OFF bipolar cells
26
What connections do ON bipolar cells form in the inner (in innermost layer of IPL) plexiform layer?
ON bipolar cells form connections with ON ganglion cells as ON ganglion cell dendrites project into the inner plexiform layer (increase firing rate when light is on, decrease when light is off)
27
What connections do OFF bipolar cells form in the inner (in outer part of IPL) plexiform layer?
Off bipolar cells form connections with OFF ganglion cells as OFF ganglion dendrites project into the outer plexiform layer (decrease firing rate when light is on, increase when light is off)
28
What is a receptive field in the retina?
Receptive field is an area in the retina (or space) which when illuminated activates a visual neuron
29
What does centre-surround organisation of the receptive field mean in the retina?
Illumination of the centre photoreceptors and illumination of surrounding photoreceptors leads to responses in opposite polarities from bipolar and ganglion cells
30
What 2 neurons have centre-surround organisation of the receptive field in the retina?
Bipolar and Ganglion cells.
31
What is normally found at the centre of a bipolar cell's receptive field?
Its cell body (where the synapse is for photoreceptors to bipolar cell)
32
What happens when stimulating (light) photoreceptors at the a) centre b) outer area of the receptive fields of an OFF Bipolar cell?
a) Stimulate centre of OFF cell hyperpolarises (doesn't cause OFF-ganglion cells to fire APs to light)
b) Stimulate outer area of OFF cell receptive field causes depolarisation (light on outer area causes increased OFF-ganglion cell AP firing)
33
Why does activating the photoreceptors at the centre of the receptive field have the polar effect of activating photoreceptors at the outer areas, use light stimulating OFF Bipolar cells in the centre and periphery of the receptive field as an example?
>Photo receptors in centre of receptive field bind directly with bipolar cells (direct synapses), so when an centre photoreceptors are stimulated by light it causes hyperpolarisation of OFF-bipolar cells due to less glutamate being released directly from photoreceptors to OFF-bipolar cells
>Photoreceptors in outer field of receptive field indirectly activate bipolar cells via horizontal cells. Horizontal cells do inhibitory feedback and release GABA to the Bipolar cell causing the opposite response. So if peripheral photoreceptors are hyperpolarised by light, horizontal cells trigger the opposite response in the OFF-bipolar cell so it would be depolarised (increase OFF-ganglion firing rate)
34
What is the effect of light activating a) centre of RF b) surrounding of RF on OFF-ganglion cells
a) In the centre of receptive field:
>Stop spiking when stimulated by light
>When light goes down, start spiking.
b) In surrounding of receptor field:
>Increase spiking when stimulated by light
>Decrease in spiking by dark
35
What is the effect of light activating a) centre of RF b) surrounding of RF on ON-ganglion cells
a) In the centre of receptive field:
>Stimulate centre of receptive field of ON ganglion cell causes increased spiking rate.
>When light is off, spiking rate goes down.
b) In the surrounding of receptor field:
>Decrease spiking rate by light
>Increase spiking rate by dark
36
What inhibitory feedback mechanism allows Bipolar cells to have centre-surround organisation?
centre-surround organisation of the RF of bipolar cells comes from inhibitory feedback from horizontal cells
37
What inhibitory feedback mechanism allows Ganglion cells to have centre-surround organisation?
RFs of ganglion cells have centre-surround organisation resulting from inhibitory feedback from amacrine cells.
38
What does the centre-surround organisation of ganglion receptive fields cause and how is this a selective evolutionary advantage?
>Illumination of the whole receptive field does not activate ganglion cells, as usually this means no danger.
>So ganglion cells respond to differences in illumination between the centre and surrounding receptive field as this detects a change in environment causing danger.
39
What are the 2 main classes of ganglion cells and what is their organisation of receptive fields?
>Parvocellular and Magnocellular
>Both have centre-surround organisation of receptive fields.
40
What are 5 differences between Parvocellular and Magnocellular ganglion cells?
1. Parvocellular has a small dendritic tree
>Magnocellular has large dendritic tree (usually asymmetrical)
2. Centre and surround of Parvocellular receptive field respond to different colours
>Centre and surround of Magnocellular Rfs respond to difference in brightness
3. Parvocellular has sustained response (exposed to light, continuous spiking)
>Magnocellular has transient response (exposed to light, spike quickly but decrease over time)
4. Parvocellular has slower conduction velocity than Magnocellular
5. Parvocellular less sensitive to light than Magnocellular
6. Parvocellular processes info to recognise objects
>Magnocellular used for motor detection
41
What percentage of ganglion cells in the retina are a) Parvocellular b) Magnocellular
a) 80%
b) 20%
42
What is the difference in function of Parvocellular and Magnocellular ganglion cells?
Parvocellular cells are tuned to process information about shape and colour, while magnocellular cells process information about motion.
43
If a ganglion cell has a small but dense dendritic tree, what type is it most likely to be and why?
More likely Parvocellular cells as are better for processing fine details of objects.
44
If a dendritic tree is asymmetric, what type of ganglion cell is it most likely to be and why?
Magnocellular, as will be good for processing motion in a specific direction.
45
Why is detection in olfactory different from hearing and vision?
As odours don't have clear dimensions, is a multidimensional coding space.
46
How can a) Sound b) Light c) Odour be described as?
a) Intensity and frequency (pitch)
b) Location (where in our field), intensity (brightness), wavelength (colour)
c) Recognition of chemicals.
47
What type of code are odours detected by?
Combinatorial code
48
What is the effect of signal trasnduction on olfaction?
The second messenger amplifies the sensory signals, so a small change in odour can cause a large effect (increases sensitivity).
49
Why does signal trasnduction occur in mammal olfactory but not insects?
Insect olfactory receptors are ion channels while in mammals are GPCRs
50
What does an olfactory receptor respond to?
A specific range of molecules (different olfactory receptor type responds to a different range each).
51
As we mature what changes in the olfactory system?
As we mature, olfactory neurons express a single olfactory receptor each (makes neuron and receptor odour specific).
52
Where do olfactory neurons expressing the same receptor converge to?
Despite random distribution, the axons of all the sensory neurons expressing the same olfactory receptor converge on the same glomerulus in the olfactory bulb (is a glomerulus for each olfactory receptor type).
53
What is the human equivalent of the antennal lobe in Drosophila?
The olfactory bulb
54
What are the Olfactory second order neurons called in a) Drosophila b) Mammals
a) Projection neurons
b) Mitral cells, or Tufted cells
55
How is specificity retained from olfactory sensory neurons all the way to second order olfactory neurons?
>Each projection from sensory neurons with the same receptor converge onto the same glomeruli.
>This specific glomeruli inputs onto second order neurons specific to this glomeruli, keeping the specificity.
56
What are 5 important mechanisms in the early Olfactory processing of odours?
1. Adaptation of synapse between sensory and second order neurons
2. Sensory neuron convergence reducing noise
3. Gain control
4. Decorrelation
5. Lateral inhibition
57
What are the advantages of having a relay synapse between sensory olfactory neurons and second order neurons?
1. Synaptic adaptation
>As vesicles deplete over time, it allows a synapse to adapt and react to changes in odour intensity.
2. Many converging sensory neurons onto second-order neurons
>Helps reduce noise
>Allows a weak odour to trigger a strong response in second order neurons.
58
What are the advantages of having inter-neurons carrying information between glomeruli?
1. Gain control
>When a strong odour activates many glomeruli inhibitory inter-neurons suppress output from sensory neurons so the second order neurons (projection) can detect changes in environment at high odour conc.
2. De-correlation of odour responses
>The response of a neuronal population to different odours is as different as possible.
59
What allows De-correlation of odour responses to occur?
Lateral inhibition- strongest channels inhibit weaker channels, so population of different odour responses become distinct (means a stronger odour will be smelt over a weaker one)
60
What are the cells found in the Mushroom Body of a Drosophila called?
Kenyon cells
61
After information is processed in the Olfactory bulb, what area of the brain regulates a) Learned b) Innate behaviours in mammals and what is their equivalent in Drosophila?
a) Piriform cortex
>Mushroom body (Drosophila)
b) Amygdala
>Lateral horn (Drosophila)
62
What can be shown by silencing brain regions?
Silencing a brain region shows it is required for a certain behaviour
63
What happens if you silence the cortical amygdala in mice in the presence of a predators scent and why?
They will not run from the odour as they normally would as this processes olfactory information for innate behaviours.
64
If the lateral horn is silenced in a fruit fly, will they avoid laying eggs on toxic food or not and why?
They will lay eggs on the toxic food, as the lateral horn is involved in processing olfactory information for innate behaviours.
65
What is different between the coding of innate and learned olfactory behaviours?
>Innate has dense odour coding (many types of neurons active for an odour) genetically specified to input onto a second order neuron (stereotypical connectivity).
>Learned has sparse odour coding (few neurons active for each odour), without a hard genetically coded pathway of inputs.
66
Would the lateral horn (like Amygdala) or the Mushroom body (like Piriform cortex) respond to more neurons types/ more odours?
Lateral horn/ amygdala would response to more odours as is innate, while the Mushroom body/ Piriform cortex would respond to less of a range of neurons as is learned.
67
What are 2 strategies used for odour localisation?
1. Biased random walk
2. Head casting (active sensing)
68
What is a biased random walk?
Organism moves towards favourable environment or turns around if environment becomes unfavourable.
69
What is head casting (active sensing) and what can it be coordinated with?
Moving your head around lets you sample a larger space and generate fast changes of detected odour concentration, this can be coordinated with the sniff cycle (sniff quicker when a new odour is present).
70
How are both nostrils used in the olfactory system?
We use the difference in odour conc in each nostril to detect the direction of the odour
71
Which taste receptors use a) Ionotropic b) Metabotropic channels?
a) Salt (Na+ channels), Sour (H+ channels)
b) Sweet, bitter and umami use GPCRs
72
What is the pathway of the taste circuit?
1. Cranial nerves from tongue
2. Solitary nucleus in brain stem
3. Ventral posterior medial nucleus (VPM) of the Thalamus
4. Insula or Parietal cortex
73
What process occurs in taste which is similar to olfaction?
Lateral inhibition of 2 conflicting tastes cancels the other taste out
74
If a bitter taste occurs after a sweet taste, what is tasted and why?
Bitter neurons inhibit the sweet by activating GABAA interneurons (lateral inhibition) so bitter is tasted over sweet.
75
What are the areas in the brain that respond to a particular taste called?
Hot spots
76
What are the 3 important features of sound that need encoding and how is this done for each?
1. Frequency (Pitch)
>By the mechanics of cochlea and physiology of hair cells.
2. Intensity (Loudness)
>By firing rate of nerve fibres that contact sensory hair cells
3. Onset
>Rapid onset allows us to localise sounds to build an auditory map.
77
How does sound reach the cochlea?
Sound wave travels down outer ear to tympanic membrane (middle ear), moves down middle ear via ossicles, enters cochlea in inner ear
78
What are the 3 chambers of the Cochlea?
1. Scala media
2. Scala tympani
3. Scala vestibuli
79
What shape is the cochlea and 2 advantages of this shape?
Spiral shape increases range of hearing as much as possible and fits as many sensory hair cells in a small space.
80
Where is the Organ of Corti located?
In the Scala media of the Cochlea, sat on the basilar membrane..
81
What is the concentrations of a) K+ b) Ca2+ c) Na+ in perilymph?
a) Low K+ (5mM)
b) Normal Ca2+ (1.3mM)
c) High Na+ (140mM)
82
What is the concentrations of a) K+ b) Ca2+ c) Na+ in endolymph?
a) High K+ (150mM)
b) Low Ca2+ (20mM0
c) Low Na+ (2mM)
83
Which chambers of the cochlea contain a) Perilymph b) Endolymph?
a) Scala vestibular and tympani contain perilymph
b) Scala media contain endolymph
84
What is the Endochoclear potential and how is it created?
>Cells in stria vascularis actively pump K+ into the Scala Media to build a positive potential compared to the other 2 chambers.
>Endocochlear potential= Endolymph in Scala media is +80mV more positive than Perilymph in Scala vestibular and tympani
85
What is the resting potential of hair cells in the Organ of Corti and how does this work with the Endocochlear potential?
As the Endocochlear potential is +80mV (due to high K+ conc in endolymph) while sensory hair cells resting potential is -60mV, this creates an electrical driving force of 140mV from the Scala Media to the Sensory hair cells.
86
What does the Organ of Corti contain?
Hair cells
87
What is the role of a) Inner hair cells b) Outer hair cells?
a) Inner hair cells are the primary sensory receptors of the cochlear, role is to encode sound info and relay into nerve fibres
b) Outer hair cells, don't have sensory role, important for cochlear amplification.
88
What does it mean that the tonotopic organisation of the cochlear is preserved throughout the auditory pathway?
Neurons in different auditory brain areas up the auditory pathway show the same tonotopic map
89
What is the tonotopic organisation of the cochlea?
>Hair cells at the base respond to high frequency sound
>Hair cells at the apex respond to low frequency sound
90
What is the effect of having the tonotopic organisation of the cochlear?
Sound frequency does not need to be encoded in the firing pattern of the nerves, as it is the location of the specific inner hair cells activated by a certain frequency of sound that encodes sound frequency (Place-frequency code).
91
What is the characteristic frequency in the cochlear?
The location for a specific sound frequency where the basilar membrane has maximal movement.
92
What determines the tonotopic map of the cochlear?
The characteristic frequency is determined by the width and stiffness of the basilar membrane.
93
Where would the characteristic frequency location be on the basilar membrane for a) Low frequency sounds b) High frequency sounds and why?
a) Characteristic Frequency (CF)/ peak movement location closer to the apex
>as the Apex is wide and floppy, so doesn't require a high frequency to move it
b) Characteristic Frequency (CF)/ peak movement location closer to the base
>as the Base is narrow and stiff so requires a high frequency to move it.
94
What do inner hair cells have projected from their apical surface?
Stereocilia hair bundle on top of each inner hair cell.
95
What channels are found on the tips of shorter stereocilia?
Mechanoelectrical Transducer Channels (MET)
96
What joins stereocilia together?
Tip links between Mechanoelectrical Transducer Channels (MET).
97
What nerve fibres are attached to inner hair cells?
Afferent fibres
98
What is the activity of a inner hair cell at rest (no sound present) in 3 steps?
1. Slight tension on tip links cause some MET channels to open allowing K+ to enter inn hair cells (resting inward MET current)
2. The resting inward MET current depolarises the inner hair cell slightly, activating some Ca2+ channels.
3. Ca2+ release triggers neurotransmitter release, causing resting activity in afferent fibres (spontaneous activity)
99
Why does K+ enter the inner hair cells from the endolymph when MET channels are open?
As the Endocochlear potential is +80mV and the resting potential of inner hair cells is -55mV, this creates an electrical driving force of 140mV for K+ to enter the inner hair cells from the Scala Media despite the low concentration difference.
100
Why does K+ leave inner hair cells and into the perilymph?
There is a large concentration gradient for K+ to exit from the IHC (140mM K+) to the perilymph (5mM K+) surrounding the bottom of the cell.
101
Why is it important to have a tight barrier between endolymph and perilymph in the cochlea?
This keeps the two solutions separate, so the hair bundle is surrounded by endolymph (providing electrical gradient for K+ entry into IHC) while the rest of the hair cell body is surrounded by perilymph (providing conc gradient for K+ exit out of IHC).
102
What surrounds the a) apex (stereocilia) b) base of inner hair cells?
a) Endolymph
b) Perilymph
103
What is the activity of a inner hair cell in the excitatory phase of a sound wave in 4 steps?
1. Excitatory phase of sound wave (upwards wave) causes large deflection of hair bundle towards taller stereocilia.
2. Increased tension on tip links, more MET channels open, large inwards MET (transducer) current/ more K+ enters IHC.
3. Depolarises IHC a lot, activating a lot of Ca2+ channels triggering a lot of neurotransmitter release increasing activity of afferent nerve fibres.
4. K+ channels open due to depolarisation, causes K+ to leave IHC to perilymph, repolarising the IHC (K+ efflux from IHC to perilymph).
104
What does inner hair cell depolarisation also activate as well as Ca2+ channels and what is the effect?
>Hair cell Depolarisation also activates K+ channels
>Allows K+ exits down a concentration gradient into perilymph to help repolarise the cell
105
How do inner hair cells respond to hair bundle motion?
With a graded change in membrane potential.
106
What is the activity of a inner hair cell in the inhibitory phase of a sound wave in 4 steps?
1. Inhibitory phase of sound wave (downwards wave) causes large deflection of hair bundles towards shorter stereocilia.
2. Tip links slacken (less tension), closing MET channels, decreasing MET (transducer) current, less K+ enters.
3. Hyperpolarises IHC below resting potential, decreases Ca2+ current, less neurotransmitter released so little afferent neuronal activity.
4. K+ channels open for longer to fully repolarise (return to resting potential) the cell (K+ reflux from perilymph into IHC) for the next cycle.
107
What is the activity of inner hair cells during sustained sound in 3 steps?
1. Moves hair bundles back and forth at the sound frequency, creates a cycle of membrane potential (depolarisation for excitatory and hyperpolarisation for inhibitory) matching the sound frequency
2. Generates pulses of neurotransmitter release and afferent activity in nerve fibres that matches the frequency.
3. Sensory information relayed to the brain
108
What are 2 advantages to using K+ to depolarise the inner hair cells?
1. Very rapid
2. Energy efficient as K+ enters down electrical gradient (endolymph to IHC) and leaves down a chemical gradient (IHC to perilymph) so doesn't require active pump.
109
What would be the effect of breaking down the separation between perilymph and endolymph?
Become deaf as the electric gradient between endolymph and IHC as well as the conc gradient between IHC and perilymph allowing for K+ movement would be broken so neurotransmitter would not be released to afferent fibres.
110
What is electromotility?
Outer hair cells shorten and lengthen in time with sound frequency.
111
Why do outer hair cells have less afferent neurons connected as inner hair cells?
As OHC don't have a main sensory role, while IHC are the primary sensory receptors for sound frequency.
112
What are the majority of neural contacts with outer hair cells?
Efferent fibres from the brain, these are inhibitory inputs that turn OHCs off.
113
What is the shape of hair bundles (stereocilia) on a) inner hair cells b) outer hair cells?
a) in a line of shortest to tallest.
b) in V-shape
114
What molecule is found in the cell membrane of outer hair cells, what does this allow?
Prestin is the molecule that allows the cell to shorten or elongate in response to changes in membrane potential
115
What is the activity of outer hair cells during a) no sound/ at rest b) excitatory sound waves b) inhibitory sound waves?
a) At rest there is a MET current
>OHC resting potential is around -40mV (more depolarised than IHCs)
b) Depolarise in response to excitatory wave phase
>Causing them to shorten
c) Hyperpolarise in response to inhibitory wave
>Causing them to lengthen
116
How many rows of outer hair cells are there in the cochlea?
3
117
What is the effect of the combined movement of the 3 outer hair cell rows in the cochlea?
>Combined movement of the 3 rows acts as Positive Feedback in the cochlea, amplifying the stimulation of the inner hair cells.
118
How do the outer hair cells provide positive feedback to amplify the stimulation of inner hair cells in the cochlea?
OHC electromotility amplifies the basilar membrane motion over a narrow characteristic frequency region, resulting in sharply tuned and highly sensitive IHCs (as that sound sound frequency in that CF region will cause high basilar membrane movement due to amplification by OHCs).
119
What does damage to the outer hair cells cause and why?
If OHCs are damaged the stimulation of the IHC bundle is weaker, loss of OHCs causes severe hearing loss but not complete deafness as the primary sensory hair cells (IHCs) are sill present.
120
What is sound localisation?
Determining the location of a sound
121
Why do we need sound localisation?
1. Important mechanism for survival
2. Provides a perception for auditory space
122
What are the two methods used to localise sound in the horizontal plane?
1. Detection of Interaural level differences (ILDs)
>The difference in the loudness (level) of the same sound at the two ears (ILD)
2. Detection of Interaural timing differences (ITDs)
>The difference in the arrival time of the same sound at the two ears (ITD)
123
When is the value of a) Interaural level differences (ILDs) b) Interaural timing differences (ITDs) at 0 or at the highest and why?
a) ILD at 0 at the centre line, as is the same loudness in both ears.
>Maximum, when sound is closest to one ear as it will be very loud in that ear.
b) ITD at 0 at the centre line, as the sound will reach both ears at the same time
>Maximum when sound is closest to one ear, as sound will reach the near ear quickly and the far ear with a delay.
124
What frequency of sounds are a) Interneural level differences b) Interneural timing differences used for detection of?
a) Mainly for higher frequency sounds.
b) Mainly for lower frequency sounds.
125
What detects the level and timing differences of sound reaching the ears?
Sound localisation centres in the brain stem.
126
What specialised neuron centres do Sound Localisation Centres (in the brain stem) have and what order is the pathway?
1. Neurons enter ear at the Cochlear Nucleus (CN)
2. Lateral Superior Olive (LSO)
3. Medial Superior Olive (MSO)
4. Medial Nucleus of the Trapezoid Body (MNTB)
127
What are the main centres involved in ILD and ITD detection in the Sound Localisation Centres?
LSO (principle neurons) detects ILDs and MSO (principle neurons) detects ITDs
128
How many Sound Localisation Centres are there and what is the effect of this?
> There is one centre on both sides of the midline (so two of them), each centre is innervated from both ears.
>This means each centre has a near ear and a far ear that sends input to it (creating ILD and ITD).
129
How are Interaural level differences (ILDs) detected?
>LSO (Lateral superior olive) neurons receives direct excitatory input from the near ear and receives an indirect inhibitory input from the far ear (MNTB/ Medial Nucleus of the Trapezoid Body makes far ear signals inhibitory)
>This same mechanism is mirrored in the sound localisation centre on the other side of the midline. This forms the LSO Excitatory-Inhibitory Pathway.
130
What would be the effect of a) Sound from the left b) Sound moving right on the ILD circuit on the left and right sides?
a) Excitatory input larger than inhibitory (as sound is louder on near ear than far ear) so the overall summation of excitatory and inhibitory is very excitatory for the left side (but very inhibitory on right side)
b) Excitatory input reduces and inhibitory increases on the left side, making overall summation less and less excited (but input increases in excitation on right side).
131
How do both the LSOs work together to form an auditory map of ILDs?
Combination of the two output channels gives us an accurate indication of sound position based off how loud it is in both ears.
132
Why is it important that the two LSO outputs overlap at the centre line?
If we are facing the sound, the loudness (ILDs) will be of equal output from both LSOs, but if that sound moves we will be able to rapidly detect these small changes in position as one ear will provide a greater output (due to increased loudness at that ear) while the other provides a decreased output.
133
How are Interaural Timing Differences (ITDs) detected?
>Two excitatory inputs (one from each ear) converge on principle neurons in the MSO (occurs on both sides of the ear)
>The MSO only becomes maximally active when excitatory inputs from both the near and far ear are present, and due to the nearer ear neuron being shorter, it takes different lengths of time for the near ear and far ear to reach the same MSO allowing for measurement of timing instead of level (MSO Excitatory-Excitatory Pathway).
134
What type of pathway is the a) LSO b) MSO?
a) LSO Excitatory-Inhibitory Pathway
>Near ear inputs excitatory
>Far ear inputs inhibitory
>Measures level of summated output
b) MSO Excitatory-Excitatory pathway
>Both ears inputs excitatory
>Measures timing differences over level.
135
What would be the effect of a) Sound from the left b) Sound moving more right c) Centre line d) Sound at right ear on the ITD circuit on the left side?
a) No summation of two inputs
>Due to the large delay of the excitatory input from the far ear reaching the left MSO, the excitatory input from the near ear has already been and gone so the excitatory input is minimal (no summation)
b) MSO output increases
>The delay of arrival of excitatory input from the far ear is decreasing, so some summation is occurring.
c) MSO output at half of maximum
>Despite there being no ITD between the two ears (sound reaches them at the same time), due to the longer nerve from the far ear, there is still some delay so summation is only half of the maximum.
d) Maximum left MSO output
>The longer nerve distance is compensated by the increased delay (ITD) for sound to reach the left ear. Both excitatory inputs arrive at the MSO at the same time, maximum summation.
136
What are the two factors causing input from the far ear to be slower towards the MSO if the sound is closer to the near ear?
1. The ITD is larger for the far ear, it takes longer for the sound to even enter the ear.
2. Due to the longer nerve to travel down.
137
When is the output of each LSO highest?
Output of each LSO is highest for sounds from the same side of the head (at near ear).
138
When is output of each MSO highest?
The output of an MSO is highest when sound is closer to the far ear.
139
If sound is on the left side of the head, will output be higher at the left or right MSO?
Left MSO very low – right MSO very high
140
If sound is on the left side of the head, will output be higher at the left or right LSO?
Left LSO very high - right LSO very low.
141
When is there most overlap of the inputs from the two MSOs and what does this ensure?
The overlap of two MSOs at the centre ensures accuracy of sound localisation
142
What is a) 1 Similarity b) 2 Differences between the ILD and ITD circuits?
a) Both use a combination of 2 channels to give an accurate indication of the sound's position around the head.
b) Differences
>The side of the head the channels are tuned to are different in both (Left LSO – maximum when sound from the left (as less inhibitory summation from the far ear); Left MSO – maximum when sound from the right (due to delay at near ear compensating for large far ear neuron, causes maximum excitatory summation from the two inputs).
>LSO is Excitatory from near ear, Inhibitory from far ear, MSO is excitatory from both.
143
How does the sound localisation circuit develop?
1. The initial circuits are formed early in development and do not depend on sensory function.
2. Auditory map shows adaptive plasticity, it is refined and aligned to overlay the visual map.
144
What did Eric and Phyllis Knudsen test on barn owls to show how vision is used to calibrate sound localisation?
>Tested how juvenile owls learn to interpret interaural time differences (ITDs) as a location of sound in space, testing if the auditory map would show adaptive plasticity to align with an artificially shifted visual field.
>They artificially shifted the owl's visual field by 20 degrees using prisms for 7 weeks (head would be orientated 20 degrees to the right of an object they looked at) to test if the shifted visual field would also shift the head orientation for the auditory map.
145
What were the results of Eric and Phyllis Knudsen's experiment on barn owls a) before the prisms (that shifted visual field 20 degrees) b) after 1 day with prism c) after 42 days with prism d) after prism was removed?
a) Before prisms
>The head orientates to look directly at the visual and auditory stimuli
b) After 1 day of prism wearing
>Head orientation quicky adapts to shifted vision
>Head still turns to face the auditory stimulus
c) After 42 day of constant prism wearing -
>There is the same response to visual stimulus
>The auditory response has now shifted to align with the modified visual field
d) After prism removal (day 49)
>The visual response quickly re-aligns
>The auditory response remains shifted
146
What were the 3 conclusions of Eric and Phyllis Knudsen's experiment on barn owls?
1. The auditory space map is modified based on changes to the visual map (as the artificially altered visual map changed the auditory map despite no artificial modification to it).
2. The visual map is dominant for space perception and is used to realign the auditory map If there are differences between the two
3. The visual map rapidly adapts to changes in the visual field while the auditory map takes longer to adjust (as when the prism was taken off, the visual map immediately went back to normal, but the auditory map didn't).
147
Why is the visual map more dominant than the auditory map?
Because map of space is directly represented by the receptors in the retina, while auditory system has to be learnt from auditory inputs. So visual inputs are more reliable.
148
How does vision change the auditory map?
Vision is used as a template to teach the interpretation of auditory cues for sound localisation. Initial auditory circuits are established by genetic programmes, they are refined by sensory experiences and adaptive plasticity.
149
Describe the biased tumble walk by bacteria and C.elegans?
If things get better they run forwards more and tumble less, if conditions get worse they tumble more.
150
What does Retinotopic mean?
Retinotopic refers to the spatial organization or mapping of visual stimuli onto the retina and its representation in the visual processing areas of the brain.
151
How do a) ON Bipolar cells b) OFF Bipolar cells respond to decreasing light intensity and why?
a) ON cells hyperpolarise when light intensity decreases
>As depolarised photoreceptors release constant stream of glutamate, more binds to mGluR channels on Bipolar cells which leads to more non-selective cation channels being closed, so less positive ions flow in (hyperpolarisation), causing decreased ganglion cell firing.
b) OFF cells depolarise when light intensity decreases
>As depolarised photoreceptors release constant stream of glutamate, more ionotropic glutaminergic receptors are activated so more cations enter so the bipolar cells is depolarised, causing increased ganglion firing.
152
What is the effect of a) Light on centre RF b) Light on surrounding RF of ON and OFF ganglion cells?
1. ON Ganglion cells
a) Hyperpolarisation of photoreceptors in centre causes direct release of less glutamate to ON-bipolar cells, leads to depolarisation and increased ON-ganglion firing rate.
b) Hyperpolarisation of photoreceptors in peripheral causes less glutamate to bind to horizontal cells, so horizontal cells release less GABA which means more glutamate can bind to ON-bipolar cells causing hyperpolarisation of ON-Bipolar cells and decreased ON-ganglion firing.
2. OFF Ganglion cells
a) Hyperpolarisation of photoreceptors in centre causes direct release of less glutamate to OFF-bipolar cells, leads to hyperpolarisation and decreased OFF-ganglion firing rate.
b)Hyperpolarisation of photoreceptors in peripheral causes less glutamate to bind to horizontal cells, so horizontal cells release less GABA which means more glutamate can bind to OFF-bipolar cells causing depolarisation of OFF-Bipolar cells and increased OFF-ganglion firing.
153
What is the effect of a) Darkness on centre RF b) Darkness on surrounding RF of ON and OFF ganglion cells?
1. OFF Ganglion cell
a) Depolarisation of photoreceptors in centre causes direct constant release of glutamate to OFF-bipolar cells, leads to depolarisation and increased OFF-ganglion firing rate.
b) Depolarisation of photoreceptors in peripheral causes horizontal cells to release a lot of GABA causing less glutamate to bind to OFF-Bipolar cells casing them to hyperpolarise and decrease OFF-ganglion firing.
2. ON Ganglion cell
a) Depolarisation of photoreceptors in centre causes direct constant release of glutamate to ON-bipolar cells, leads to hyperpolarisation and decreased ON-ganglion firing rate.
b) Depolarisation of photoreceptors in peripheral causes horizontal cells to release a lot of GABA causing less glutamate to bind to ON-Bipolar cells casing them to depolarise and increase ON-ganglion firing.
