- Cornea, Lens, Iris, Vitrous, Retina
- Choroid, sclera
- Conjunctiva, Optic Nerve Head
- 70-80% of refraction
- Clinical involvement: ammetropia, astigmatism
- Accommodation by smooth muscle (ciliary body muscles)
- sphincter action on lens by fibers to change lens radius of curvature.
- Parasympathetically innervated (edinger-westphal nucleus, ciliary ganglion)
- Clinical involvement: cataracts, presbyopia
- Eye color
- Smooth muscle (radial & circumference m.) controlled by sympathetic (superior cervical ganglion) and parasympathetic (eddie-westphal→ ciliary ganglion)
- Clinical involvement: papillary light reflex tests midbrain path through pretectum (brain swelling hurts midbrain because it’s squished against bone)
- Viscous gel; intra-ocular pressure pushes against the sclera to keep eye spherical
- Clinical involvement: “floaters”
- Receptor sheet (photoreceptors)
- Fovea: High acuity central vision; huge concentration of all cone photoreceptors and peeled back retinal layers
- Pigmented epithelium – Black, prevents internal reflections.
- Clinical involvement: retinal detachment, diabetic retinopathy, retinitis pigmentosa
- Has layers: Ganglion cells, anacrine cells, horizontal cells, Photoreceptors( rods, cones)
- Vascular Layer
- Elaborates fluid and nutrients into posterior segment
- Tough outer covering
- White, reflects external light.
- Skin-like membrane from the limbus of cornea to the orbit
- Isolates retro-orbital space
- Clinical involvement: conjunctivitis/pink eye
Optic Nerve Head
- Axons and vasculature exits eye
- No photoreceptors; blind spot is located here
- Clinical involvement – glaucoma
- Receptor potentials happen after light absorption
- Glutamate release decreases in response to light.
- different post-synaptic glutamate receptors that respond with opposite membrane current effect
- Receptor potentials sent to photoreceptor & horizontal cell inputs.
- Stimulated when the center of its receptive field is exposed to
- DEPOLARIZE/increase the firing of the ganglion cell
- Inhibited when the surround is exposed to
- HYPERPOLARIZE/decrease the firing of the cell.
- In darkness: depolarized by glutamate sent
from [depolarized] photoreceptors
- release inhibitory NTs to inhibit photoreceptors
- Use receptor potentials
Amacrine Cells (Bipolar)
- Have BOTH action & receptor potentials
- Will exhibit on, off, or on-off responses (least understood of all the retinal neurons)
- Same antagonistic center-surround receptive fields as described for bipolar cells
- Generate action potentials that propagate (add up) on the optic nerve to the thalamus.
- Do not have action potentials! Only receptor potentials. Have receptor potentials that range between equilibrium potentials
- Outer segment: Light absorption by densely packed photopigments in densely stacked disks; cillium
- Inner segment: Cell nucleus and metabolic machinery
- Rods and Cones
- Synaptic terminal
- Bright light
- Central retina
- Three photopigments (trichromatic)
- Short wavelength = blue cones
- Middle wavelength = green cones
- Long wavelength = red cones
- Clinical involvement: dichromatic red/green color defective or monochromatic (color blind, rare)
- Dim light (night vision)
- Peripheral retina
- Rhodopsin- Broad band (no color vision)
Problems with color vision
- Dichromatic – loss of one cone mechanism
- Protanopia – loss of long-wavelength cone mechanism (no red)
- Deuteranopia – loss of medium-wavelength cone mechanism (no green)
- Tritanopia – loss of short-wavelength mechanism (no blue)
- Genes for both long-wavelength opsins are located on the X chromosome. So, red-green color blindness is sex-linked
- The gene for short-wavelength opsins is located on chromosome 7. So, equal incidence in both males & females (but rare).
- Light photon transforms 11-cis retinal into All-trans retinal
- Frees/activates opsin
- Active opsin activates G-protein transducing
- Transducin activates phosphodiesterase (PDE)
- PDE converts cGMP → GMP, freeing Na+ channel.
- Na+ channel closes, preventing sodium from entering cell.
- Hyperpolarization occurs, preventing neurotransmitter release from bipolar cells
- neurotransmitters being released which prevent sight
- Sodium channels are ALWAYS OPEN (“dark current”) → depolarization
- those neurotransmitters are stopped so that we CAN SEE
- Shorthand of cascade
- Photon → 11-cis-retinal → 11-trans-retinal → active opsin → G-active protein transducing → cGMP phosphodiesterase → GMP → sodium channels close → hyperpolarization of receptor cell!
Optic Nerve Lesion
Sagittal optic chiasm section
Optic Tract Lesion
Contralateral homonymous hemianopsia
Lesion of Meyer’s Loop
upper contralateral quadrantic anopsia (loss of vision in the upper quadrant of the contralateral half of the visual field of both eyes)
Partial lesion of the visual cortex in the upper bank of the calcarine sulcus
deficit in the inferior quadrant of the contralateral visual field.
Partial lesion of the visual cortex in the lower bank of the calcarine sulcus
deficit in the superior quadrant of the contralateral visual field.
Lesion on 5&6
- lesion involving both banks of the calcarine sulcus
- lead to a more extensive deficit, i.e., a contralateral homonymous hemianopsia, however sparing the FOVEAL REPRESENTATION.
Perspective, motion parallax, occlusions, blur, etc.
Relative positions on retina due to image depth with respect to binocular fixation point.
Non spherical aberration
Need reading glasses