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BMS 248 - Neural circuits > Fixing faulty neural circuits > Flashcards

Fixing faulty neural circuits Flashcards

1
Q

What is channelrhodopsin selective for?

A

Cations (Na+, Ca2+, H+, K+)

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2
Q

What happens when channelrhodopsin opens?

A

The cell depolarises

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3
Q

How is channelrhodopsin activated?

What wavelength?

A

By blue light

460nm

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4
Q

How can expressing ChR in different brain areas do?

A
  • Modify behaviour

- Help to recover the function of a specific brain area

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5
Q

What travels through halorhodopsin?

A

Chloride ions (Cl)

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6
Q

What is HR activated by?

What wavelength?

A

Yellow light

570nm

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7
Q

What happens when HR is activated?

A

Hyperpolarisation of the cell

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8
Q

What can HR be used in?

A

Correction in the circuitry when the brain is OVER EXCITABLE (eg. treatment for epilepsy)

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9
Q

What can be used to fix faulty neural circuits instead of ChR?

What is the structure of these compounds?

A

Small organic compounds

Structure - double bond and a part that binds to an ion channel

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10
Q

What happens when shine light onto the small organic compounds?

How?

A

Change the configuration of the compound from trans- to cis- configuration

By rotation around the double bond

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11
Q

How are small organic compounds administered when correcting faulty neural circuits?

A

They are injected into the eye or brain

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12
Q

What do the small organic molecules do in trans- configuration?

Cis-configuration?

A

Block the channel in trans- configuration

Don’t block the channel in cis- configuration

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13
Q

How do small organic molecules act on the target channels?

Which is more prolonged?

A

1) From the OUTSIDE of the membrane

2) From the INSIDE of the membrane - more prolonged as they don’t diffuse away

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14
Q

How do the small organic molecules act from the inside of the membrane?

A

They go through channels (TRPV1 or P2XR)

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15
Q

Are the methods of correcting neural circuits with ChR specfic?

HR?

Small organic molecules?

A

Non of them are very specific

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16
Q

Describe the photocontrol of GABA receptors

A
  • Substitution of the part of a compound that binds to the ion channel with a LIGAND for the receptor
  • The configuration of the compound can be changed using a specific wavelength of light
  • In ONE configuration: ligand will bing and activate the channel
  • In the OTHER configuration: ligand doesn’t activate the channel (ligand is AWAY from the binding site of the GABA receptor)
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17
Q

What happens when GABA receptors are activated?

What is this used for?

A

Hyperpolarisation of the membrane

Used to calm down the brain

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18
Q

How can photocontrol be used on other receptors?

What does the outcome depend upon?

A

Outcome depends on the channel and expression of the channel:

  • AchR = hyperpolarisation
  • Na channels = hyperpolarise
  • Glutamate R = hyperpolarise or depolarise depending upon the glutamate channel and the cell
19
Q

What can optical stimulation be used for?

A

To cure blindness

20
Q

What is retinitis pigmentosa?

A

Where the visual field becomes smaller and smaller until the patient cannot see anything

21
Q

What is the main cause of RP?

A

Photoreceptors dying - therefore no transduction

22
Q

What drug can be used to stop photoreceptors from dying?

A

No drugs can be used to stop them dying

23
Q

What can be used to reverse the effects of RP?

A

Artificial retina, containing:

  • Light activated electrodes
  • ChR
  • HR
24
Q

With an artificial retina, when is it best to stimulate the retina itself?

A

Mostly for retinitis pigmentosa

25
Q

With an artificial retina, when is it best to stimulate the visual cortex?

A

When the optic nerve is damaged or not formed

26
Q

Why is it important to activate as early as anatomically possible in the visual pathway?

Examples?

A

The further downstream in the pathway, the more difficult it becomes:

  • Even at the level of the retina - large diversity of neurons that perform complex computations
  • Different ganglion cells have different functions and project to different brain areas
27
Q

When are motion sensitive retinal ganglion cells active?

A

Only when there is motion

28
Q

What are the disadvantages of activating the artificial retina with electrodes?

How can this be overcome?

A

Disadvantages:
- Electrodes don’t survive for very long (tissue around the electrodes die with time)

  • Have to stimulate ganglion cells or cortical cells with electrodes (other cells are more difficult) and these cells are very complex

Overcome by:
- Activating the artificial retina/visual cortex with ChR or HR

29
Q

Why is it easier to activate ganglion cells than bipolar cells/photoreceptors using electrodes?

A

Ganglion cells face the inner eye

Bipolar cells and retinal cells are the other side of the tissue and are harder to get to

30
Q

Why is it useless to stimulate retinal ganglion cells using electrodes?

A

Very complicated:
- Different types of ganglion cells (P-type, M-type) that respond to different stimuli

  • Each ganglion cell also have centre-surround organisation of their receptive fields
  • Also presence of direction selective cells
  • Also have different responses to light in different colours
31
Q

How do they cells in the cortex become even more complicated to stimulate using electrodes?

A

Hypercomplex cells

32
Q

What is the optimal way to stimulate the retina to reconstruct the activity (before suffering with RP)?

A

Using light to stimulate the DEEPER layers of the retina:

  • Bipolar cells
  • Remaining photoreceptors
33
Q

How can HR be used to reverse the effects of reinitis pigmentosa?

A
  • Express halorhodopsin in the remains of the photoreceptors
  • Illuminate with YELLOW light
  • ON cells spike
  • OFF cells stop spiking
34
Q

Why is HR expressed in the remaining photoreceptors and not ChR?

A

Photoreceptors must HYPERPOLARISE in response to light

35
Q

What is seen when the size of the yellow spot on the receptive field is increased? (When there is HR expressed)

A
  • Increase in spike rate
  • Until the yellow spot covers the whole of the receptive field, where the response of the ganglion cells gets smaller and smaller, until no activation
36
Q

When HR is artificially expressed, what does moving yellow spots cause?

A

Activation of halorhodopsin:

- However, some cells respond to movement in one direction (preferred) more and the the other direction (null) less

37
Q

What experiments show that everything past the photoreceptors is still intact?

What does this mean?

A

The same results are seen as would be in a normal retina when:

  • Increase the spot of yellow light
  • Use a moving spot of yellow light

Means if stimulate the remains of the photoreceptors - can restore vision to a very large extent

38
Q

Why is stimulating the remains of the photoreceptors a disadvantage?

How can this be overcome?

A

The remains of the photoreceptors are also likely to degenerate

This can be overcome by:
- Expressing 2 different ion channels very close to the photoreceptors (in the dendrites of bipolar cells?)

OR

  • Injecting small organic molecules into the eye
39
Q

What ion channel is expressed next to ON cells?

A

ChR

40
Q

What ion channel is expressed next to OFF cells?

A

HR

41
Q

How are ChR/HR expressed in the dendrite of different bipolar cells?

A

Using specific promoters:

- Different for ON/OFF cells

42
Q

What are the disadvantages of using small organic molecules?

A

Less specificity

43
Q

What cells is it better the stimulate when trying to recover the function of the retina?

Why?

A

Bipolar cells

  • Less complicated than ganglion cells
  • Remaining photoreceptors are likely to continue to degenerate

BMS 248 - Neural circuits (16 decks)

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