Sensory Systems

Question 1

Give a brief overview of the visual system

Answer 1

Right hemifield activates the left brain and vice versa
Primary function of the retina is image acquisition; colour and light intensity are encoded in electrical signals once set thresholds have been met. Images are smoothed out due to receptive fields.
Lateral Geniculate Nucleus pre-processes visual information
Visual cortex is responsible for the main processing of visual information and consists of the ventral ‘what’ stream in the inferior temporal lobe and the dorsal ‘where’ stream in the parental parietal lobe

Question 2

List the different types of neurons in the retina and the neurons they synapse to

Answer 2

1. Photoreceptors (rods/cones) synapse with horizontal cells (ff) & bipolar cells (ff)
2. Horizontal cells synapse with photoreceptors (ff) and horizontal cells (fb)
3. Bipolar cells synapse with photoreceptors (ff), horizontal cells (fb), amacrine cells (ff) and ganglion cells (ff)
4. Amacrine cells synapse with bipolar cells (ff) and ganglion cells (fb)
5. Ganglion cells synapse with bipolar cells (ff) and amacrine cells (fb)

Question 3

Which cells synapse in the inner plexiform layer and the outer plexiform layer?

Answer 3

IPL: Bipolar, ganglion, amacrine cells
OPL: Photoreceptors, bipolar, horizontal cells

Question 4

Describe phototransduction

Answer 4

During darkness, photoreceptors constantly release a low level of glutamate.
1. Light enters the eye; photons are absorbed by the chromophore in retinal in rhodopsin isomerizing it.
2. Conformational changes in rhodopsin activates a heterotrimeric g-protein
3. Gαt activates phosphodiesterase which hydrolyses cGMP to GMP
4. cGMP-gated channels close and the cell hyperpolarises
5. Glutamate release to downstream cells decrease, downstream neurons either depolarise or hyperpolarise.

Question 5

Describe how On/Off Bipolar cells function

Answer 5

Off cells simply hyperpolarise in response to light, they are receiving less glutamate.
On cells use mGluR rather than AMPAR as well as a different G protein. There are 2 candidates for why they depolarise.
a) TRPM1 is expressed in ON but not OFF cells
b) Nyctalopin: proteoglycan required for depolarisation in light as well as responding to glutamate in ON cells.

Both TRPM1 and nyctalopin knockouts result in no polarisation.

Question 6

Where do ON/OFF cells project to?

Answer 6

ON cells project deep into the IPL
OFF cells project more shallowly into the bipolar layer
ON/OFF cells project into both layers

Question 7

Describe the principle behind receptive fields in bipolar cells

Answer 7

A receptive field comprises of a centre (spot ~ 43µm diameter) and surround (annulus ~ 437µm diameter) region. Receptive Fields occur due to ON/OFF-centre Bipolar cells having opposite responses to glutamate. ON-centre BC will depolarise in response to reduced glutamate (light) due to their metabotropic glutamate receptors while OFF-centre BC will depolarise in response to increased glutamate (darkness) due to their ionotropic glutamate receptors. Horizontal cells that receive inputs from OFF-centre Bipolar cells release inhibitory neurotransmitters to photoreceptors synapsing to ON-centre Bipolar cells.

Question 8

What are the key differences between parvocellular retinal ganglion cells and magnocellular retinal ganglion cells?

Answer 8

Parvocellular ganglion cells transmit information into the ventral steam key in object recognition. Magnocellular ganglion cells transmit information into the dorsal stream, key in object localisation and as such transduce signals faster and are more sensitive to inputs. Their morphology indicates direction specificity; the dendritic tree points towards the direction they respond to.

Question 9

What is adaptation and sensitisation in neurons?

Answer 9

Adaptation is the decrease in spiking rate in RGC, typically due to prolonged non-harmful stimuli; vesicles containing neurotransmitters are used up.
Sensitisation refers to an increase in spiking rate in RGC due to a stimuli.
Adaptation is often responsible for visual illusions as the brain. When the brain receives little visual stimulation, it is more likely to pick up on ‘background noise’, nerve firing spontaneously, this is normally ignored.

Question 10

Describe olfactory transduction

Answer 10

1. Olfactory receptor binds odorant (>300 different olfactory receptors in humans)
2. Gαolf activated, moves along the membrane and binds to Adenylyl cyclase
3. Adenylyl cyclase catalyses the production of cAMP
4. cAMP binds to and opens cAMP-gated ion channels
5. Sensory neuron depolarises

cAMP as a 2nd messenger is critical to signal amplification

Question 11

Tell me about olfactory specificity

Answer 11

Each olfactory receptor responds to a unique profile of odorants as each neuron expresses a single type of receptor.
As olfactory neurons mature they narrow down to express just a single olfactory receptor, with neurons expressing the same receptor converging on the same glomeruli in order to detect weaker stimuli.

Question 12

Tell me about the basic olfactory circuitry in mammals and drosophilia

Answer 12

In Mammals:
Olfactory sensory neuron TO Glomeruli TO Granule cells & periglomular cells TO Mitral cells and Tufted cells

In Drosophila:
Olfactory receptor neurons TO Glomeruli TO Local neurons to Projection neurons

Receptor specific matching of sensory neurons to 2nd order neurons ensures odour specificity is carried forward.

Question 13

What is synaptic adaptation?

Answer 13

Synaptic adaptation occurs when a stimulus is maintained largely due to readily-available NT vesicles being used up, reducing the spiking rate of the neuron. This is important in distinguishing the start of an odour with a strong response.

Question 14

Describe key advantages of lateral inter-glomeruli crosstalk

Answer 14

Very strong odours activate inhibitory neurons preventing an all-out response ensuring that further increases in intensity are detectable.
Converging sensory neurons onto 2nd order neurons such as glomeruli also allow the reduction in noise; inputs due to the same odour are represented as a single input made up of the average intensity at the glomeruli which is key in allowing the detection of weaker stimuli.
It has a role in decorrelation - making responses of neuronal populations to different odours as different as possible.

Question 15

Describe key aspects of the gustatory system

Answer 15

1. Metabotropic and ionotropic receptors bind tastants and are key in amplifying signals
2. Cranial nerves carry signals from the tongue to the solitary brainstem nuclei:

Cranial nerves VII, IX, X TO Solitary nuclei of the brainstem TO either a) Ventral posterior medial nucleus of thalamus TO Insula & parietal cortex b) Hypothalamus C) Amygdala

3. Lateral inhibition ensures that sweet signals are suppressed if there’s a poisonous signal too.

Question 16

What is encoded within sound?

Answer 16

Pitch via sound frequency (20-20,000 Hz)
Loudness via sound intensity, 10^12 range, largest of any biological system
Onset - when a sound started, key in sound localisation
Duration - how long a sound lasts for, due to nerves being sensitive for long periods of time without fatiguing

Question 17

Describe perilymph, and where it’s found

Answer 17

Perilymph is contained in the Scala Vestibuli and the Scala Tympani.
It contains low [K+] 5mM, normal [Ca2+] 1.3mM and high [Na+] 140mM.
It is approximately 0mV

Question 18

Describe endolymph and where it’s found

Answer 18

Endolymph is contained in the Scala Media.
It contains high [K+] 150mM, low [Ca2+] 20µM and low [Na+] 2mM.
It is approximately +80mV

Question 19

Tell me about the organ of corti

Answer 19

The Organ of Corti is approximately -60mV with an electrical driving force into it of 140mV. It is a structure which contains the inner and outer hair cells.

Question 20

Describe the place-frequency code in the cochlea

Answer 20

Low frequency sounds are detected at the apex of the cochlea, and high frequency sounds at the base. The position of an Inner Hair Cell along the cochlear depends on the sound frequency it encodes. By knowing the position of an active IHC alongside the cochlea, the brain can interpret which frequency the sound is.

Question 21

Describe characteristic frequencies and how they are established

Answer 21

Cochlea tonotopicity is established by the basilar membrane travelling wave. Specific frequencies cause maximal movement of the basilar membrane at a specific location - the characteristic frequency.

Lower frequency sounds travel further along the basilar membrane, with a CF nearer the apex of the cochlea.
Higher frequency sounds don’t travel as far along the basilar membrane, with a CF nearer the base of the cochlea.

CF location is decided by the stiffness and width of the cochlear membrane. CF is responsible for the place-frequency code.

Question 22

Describe IHCs

Answer 22

Inner Hair Cells contain a bunch of stereocilia which contain mechanoelectrical transducer (MET) channels which are connected via tip-links. The stereocilia and MET channels are exposed to endolymph while the rest of the IHC is exposed to perilymph.
IHCs have many afferent fibres leaving them.

Question 23

Tell me about IHCs at rest

Answer 23

At rest, IHC’s are at -55mV.
Slight tension on tiplinks induces a resting inward MET current. K+ enters the IHC via a large electrical driving force rather than concentration gradient (150mM to 140mM). K+ then exits the cell via a large concentration gradient into perilymph (140mM to 5mM).
There are limited spontaneous APs

Question 24

Tell me about IHCs during excitatory conditions

Answer 24

There is large excitatory deflection towards the larger stereocilia increasing tension on the tiplinks opening MET channels. Large inward MET current depolarises the IHC. There are lots of APs.
Depolarisation of the IHC stimulates more k+ channels to open acting to repolarise the cell via K+ diffusion into the perilymph.

Question 25

Tell me about IHCs during inhibitory conditions

Answer 25

There is large inhibitory deflection towards the shorter stereocilia. Tiplinks slacken closing MET channels. The cell repolarises due to a lack of MET current and K+ diffusion out of the cell via still-open K+ channels between IHC and perilymph.

Question 26

Tell me about the impact of sustained stimulus on IHC

Answer 26

As sound waves cycle, so does membrane potential, matching the excitatory and inhibitory movements of the basilar membrane. This results in the release of neurotransmitter in intervals giving the cell time to ‘reset’. Key to this process is the use of K+ to de and repolarise the IHC, a very efficient method due to the strict regulation of endo and perilymph.

Question 27

Describe OHCs

Answer 27

OHCs contain V-shaped rows of stereocilia, like IHCs they have MET channels at the tips, connected to tiplinks.
They function to amplify the movement of the basilar membrane, increasing IHC sensitivity and activity in response to sound.
This occurs due to the shortening and lengthening of the cells, a process known as electromotility in which the molecule prestin is essential.
There are 1-2 afferent fibres per OHC.

Question 28

Tell me about OHCs at rest

Answer 28

There is a resting inward MET current, OHC maintains a membrane potential of -40mV.

Question 29

Tell me about OHCs under excitatory conditions

Answer 29

Excitatory deflection towards the taller stereocilia increases tension of tiplinks on MET channels opening them. Large inward MET current depolarises the cell to -20mV stimulating the shortening of prestin molecules and the cell, amplifying the basilar membrane movement.

Question 30

Tell me about OHCs under inhibitory conditions

Answer 30

Inhibitory deflection towards shorter stereocilia decreases tension of tiplinks on MET channels closing them. No MET current leads to cell hyperpolarisation to -50mV stimulating prestin to lengthen the cell.

Question 31

What are the impacts of OHC amplification of basilar membrane movement?

Answer 31

Increased basilar membrane movement at a narrow range around the CF of the sound in question leads to increased sensitivity and response of IHCs allowing the detection of weaker stimuli.
Damaged OHC lead to severe hearing loss but not deafness.