March 20th 2012
March 20th 2012 April-11-12 9:39 AM
Structure of the retina Light enters the eye, and travels to the back of the eye where the rods and cones are located Rods and cones transduce using the same transduction scheme o But they are both sensitive to different wavelengths Most eye diseases result from problems in the photoreceptors o Since they are very metabolically active cells The other classes of eye diseases result from damaged ganglion cells o Usually just from natural cell death Transduction occurs in photoreceptors Melenopsin ganglion cells can transduce a little bit too o React to blue light, and depolarize very slowly o They are responsible for triggering circadian rhythms, they don't produce actual "vision" o Persist longer in damaged retina than other ganglion cells *Light flash causes hyperpolarization, NOT depolarization So dark is the "stimulus" for photoreceptors Rod outer segments In dark: o Have light sensitive molecule Rhodopsin Signal to cyclic nucleotide gated channels (CNG channels) Non-selective cation channels Sodium and calcium go in Potassium goes out Since the channels are non-selective, tend to depolarize the membrane toward 0mV There are also voltage gated potassium channels Bring the rods back to resting potential o Resting potential is -40mV o In light, membrane potential goes to -50 to -60mV Calcium influx is important o It plays a role in adaption o Voltage gated channels present in the "feet" of the receptor for synapses like normal neurons o Inhibits guanylate cyclase Enzyme that finds GTP, and turns it into cGMP So calcium influx prevents formation of molecule that keeps CNG channels open Negative feedback regulation Opsin
Kind of like a neurotransmitter Sits in the photoreceptor membrane
11-cis retinal sits in the middle of it o Changes conformation in response to light (photoisomerization) 1 carbon bond undergoes transformational shift, makes all trans Fits differently into the pocket No longer attaches to g-protein, transducin, properly Allows transducin to bind to GTP, (releasing alpha subunit) The alpha subunit then binds to phosphodiesterase Which breaks cGMP down into several GMP molecules, causing the nonselective cation channels to close 7-transmembrane domain receptor
*retinitis pigmentosa* Photoreceptors die off due to improper reconfiguration of 11-cis retinal Structural difference between rods and cones Rods: o Long rod-like outerstructure o Cytoplasmic disks stacked on top of each other o DO NOT produce action potential o Takes 10 photons to detect light Cones: o Disks not inside the cytoplasmic membrane They are part of it There are fewer of them o Outerstructure is cone-shaped o Take 100 photons to detect light o 100X less seneitive, but much faster signalling (10x faster)
Structure of the retina Light enters the eye, and travels to the back of the eye where the rods and cones are located Rods and cones transduce using the same transduction scheme o But they are both sensitive to different wavelengths Most eye diseases result from problems in the photoreceptors o Since they are very metabolically active cells The other classes of eye diseases result from damaged ganglion cells o Usually just from natural cell death Transduction occurs in photoreceptors Melenopsin ganglion cells can transduce a little bit too o React to blue light, and depolarize very slowly o They are responsible for triggering circadian rhythms, they don't produce actual "vision" o Persist longer in damaged retina than other ganglion cells *Light flash causes hyperpolarization, NOT depolarization So dark is the "stimulus" for photoreceptors Rod outer segments In dark: o Have light sensitive molecule Rhodopsin Signal to cyclic nucleotide gated channels (CNG channels) Non-selective cation channels Sodium and calcium go in Potassium goes out Since the channels are non-selective, tend to depolarize the membrane toward 0mV There are also voltage gated potassium channels Bring the rods back to resting potential o Resting potential is -40mV o In light, membrane potential goes to -50 to -60mV Calcium influx is important o It plays a role in adaption o Voltage gated channels present in the "feet" of the receptor for synapses like normal neurons o Inhibits guanylate cyclase Enzyme that finds GTP, and turns it into cGMP So calcium influx prevents formation of molecule that keeps CNG channels open Negative feedback regulation Opsin
Kind of like a neurotransmitter Sits in the photoreceptor membrane
11-cis retinal sits in the middle of it o Changes conformation in response to light (photoisomerization) 1 carbon bond undergoes transformational shift, makes all trans Fits differently into the pocket No longer attaches to g-protein, transducin, properly Allows transducin to bind to GTP, (releasing alpha subunit) The alpha subunit then binds to phosphodiesterase Which breaks cGMP down into several GMP molecules, causing the nonselective cation channels to close 7-transmembrane domain receptor
*retinitis pigmentosa* Photoreceptors die off due to improper reconfiguration of 11-cis retinal Structural difference between rods and cones Rods: o Long rod-like outerstructure o Cytoplasmic disks stacked on top of each other o DO NOT produce action potential o Takes 10 photons to detect light Cones: o Disks not inside the cytoplasmic membrane They are part of it There are fewer of them o Outerstructure is cone-shaped o Take 100 photons to detect light o 100X less seneitive, but much faster signalling (10x faster)
