5 Retinal Neurochemistry and Light Adaptation Flashcards
what cells use which neurotransmitters in the retina?
- glutamate - PR, BC, GC (vertical pathway)
- glycine - amacrine AII and small field
- GABA - HC, amacrine
is glutamate excitatory or inhibitory?
what are two classes of receptors?
- excitatory
- ionotropic (iGluR)
- metabotropic (mGluR)
what are mGluR coupled to?
how many transmembrane spanning domains?
binding sites?
how many mGluR are there and how are they grouped?
- coupled to G proteins
- 7 transmembrane spanning domains
- extracellular glutamate binding sites, not ligand-binding sites in membrane
- 8 mGluRs, grouped on homology
how many iGluRs are there and how are they grouped? what are the groups?
- 2 types of iGluRs, grouped on selective agonists
- NMDA iGluRs : NMDA
- non-NMDA iGluRs: AMPA, KA, quisqualate
describe NMDA receptors
- open non-selective cation channels more permeable to Ca2+ than to Na+
describe non-NMDA receptors
- open non-selective cation channels more permeable to Na+ and K+ than to Ca2+
- activation allows Na+ to enter cell
where is glutamate found?
- HCs - mGluR, iGluR (AMPA & KA)
- BCs - mGluR, mGluR6, iGluR (AMPA)
- GCs - same as bipolars plus acetylcholine & NMDA iGluRs in brain
describe GABA
- main inhibitory NT in CNS
- ionotropic GABA-A (ligand-gated Cl- channels)
- metabotropic GABA-B mediated by Ca2+ and K+
- GABA-C (ligand-gated Cl- channels) - from vertebrate retina
what types of GABA are found where?
- GABA-A and GABA-C found in PRs, HCs, R/C BCs, amacrines and GCs
- GABA-B found in R/C BCs and GCs
what other NTs are there?
- glycine - inhibitory - amacrines
- dopamine - neurmodulator - “all” retinal neurons
- acetylcholine - excitatory - starbust amacrines
what’s the duplicity theory?
- photopic >0.03 cd/m2
- scotopic <0.03 cd/m2
- mesopic is the range when the two mechanisms work together
describe the 4 sections of the isolated rod system
- dark light (noise) - spontaneous opening of channels and NT release
- square root law - increase in threshold proportional to square root of background illuminance
- Weber’s law - increment threshold to bg intensity constant
- saturation - rod systems unable to detect stimulus (bg luminance too high)
what’s light adaptation?
describe light adaptation characteristics
- ability to distinguish luminous object against bright background
- fast
- cone system doesn’t saturate as much (due to kinetics and calcium of cones)
- neural, not photochemical
- light adaptation is a reduction in sensitivity
what’s dark adaptation?
- ability to adjust luminous object against dark background
- you’ll need less light to see the longer you are in the dark for
what are dark adaptation factors?
- adapting target intensity
- size/position of stimulus
- wavelength of stimulus
- state of rhodopsin regeneration
- age
trends in dark adaptation
- the higher the pre-adapting luminance and the longer you pre-adapt for, the longer it takes to dark adapt
- the longer you’ve bleached, the longer it takes to recover
how does the position of the stimulus matter in dark adaptation?
- no adaptation in fovea, no rods there
- full adaptation beyond fovea
how does the size of the test spot matter?
- if spot is too small, rods and cones not stimulated, so no rod-cone break
how does the stimulus of the wavelength matter?
- rod-cone break not seen with long wavelength lights because rod/cone sensitivities are too similar
- the short the wavelength, the more distinct the rod-cone break
what is the mechanism for dark adaptation?
- dark adaptation = rhodopsin regeneration time
- sensitivity recovery > pigment quantity regeneration, so pigments are responsible for dark adaptation
