L12 - correction of faulty neural circuits Flashcards
what is channelrhodopsin
non-selective channel, stimulated with light, causing channel to open
what light is channel rhodopsin stimulated by
blue light 460nm
what happens if switch of the light
closes faster when stimulated with 360nm
what happens when switch on the light - channelrhodopsin
neuron is depolarised and sufficient to trigger a strike
the spike occurs everytime the neuron is stimulated
halorhodopsin
stimulated by yellow light 570nm. causes hyperpolarisation of the membrane
what is the problem with using rhodopsin channels in humans
don’t have the technologies to do so - express them in viruses which may not be safe
what can be used instead of channelrhodopsin
2 small molecules - optical isomers of each other
important parts of the small molecules
maleimide - binds to a specific channel
azobenzene - functions to change depending on stimulation of light
quaternary ammonium - serves as a block of the channel
at what light does the trans isomer turn into the cis isomer
380nm
at what light does the cis isomer turn back into the trans isomer
500nm
what does the trans isomer do?
block the channel - when turned into cis isomer, the block is removed
how does the small molecule work ?
enters the TRPV1 channel and acts on the channels from the inside of the cell
why is it important that it works inside the cell
stays inside the cell longer
what is the GABA receptor important for
regulating the overall excitability of the NS
what causes epileptic seizures
overexitability of neurons in the brain
what wavelength can activate the GABA receptors
380nm light
what occurs when the GABA receptors are activated
hyper polarise the cells and remove hyperexcitabiltiy of the neurons
what is retinitis pigmentosa
a disease in which the field of view becomes smaller and smaller until the patient becomes blind
what causes retinitis pigmentosa
retinal degeneration which starts with the dying of the photoreceptors - rods and cones
as it progresses other cells in the retina become degernated (bipolar and ganglion cells)
what is the treatment for retinitis pigmentosa
artificial retina or gene therapy
can use electrodes or tools to stimulate the visual system
problems with using electrodes to stimulate neurons
chronic implantation of electrodes in the brain/retina will cause degeneration of the tissue around the electrodes as electrodes may hear up and kill surrounding neurons
what are the 2 areas needed to stimulate to cure blindness
retina - for retinitis pigmentosa
visual cortex - when optic nerve didn’t develop/destroyed
how are the retina and visual cortex stimulated
either by electric stimulation of channelrhodopsin and halorhodopsin
problems with artificial stimulation of retina
stimulates ganglion cells but not photoreceptors or bipolar cells
what are the 2 main classes of ganglion cells
parvocellular and magnocellualr
size of parvocellular dendritic tree
small
size of magnocellular dendritic tree
large
what type of receptive fields to ganglion cells have
centre surround organisation
what is a centre surround organisation
if stimulate ganglion cell in centre of the receptive field will have increase / decrease in spiking rate. if stimulate outside of receptive field will get opposite result in spiking rate
what happens when switch of the light stimulating a ganglion cell
decrease in spiking rate
what occurs when stimulate halorhodopsin in photoreceptors
get hyperpolarisation - leads to decrease in release of glutamate from the synapses
what does intact centre surround organisation of RGCs in retinitis pigmentosa show
shows that can restore the basic properties of the cells
what is intact during retinitis pigmentosa
diversity
center surround organisation
direction selectivity
what are the 2 ways to control seizures
- use halorhodopsin expressed in excitatory cells - hyperpolarise the excitatory cell
use channelrhodpsin - depolarise inhibitory cells - so when stimulate the cell with blue light they release more GABA
what tools are used to inject a virus to treat seizures
ontogenetic tools
questions needed to ask to treat
where to express optogenetic tools
where is the seizure of the origin
excitatory or inhibitory neurons
