neuron chapter 9

Three ways the eye adapts to bright light

the pupil constricts, photoreceptors adapt as calcium regulates cGMP, and the retina’s circuitry adjusts (the slides list these under dark adaptation and local adaptation, so this three-part list is the best-supported reading, not stated outright)

Pupil change in bright light

the pupil constricts so less light enters, and it dilates in the dark (constriction is not stated on slides)

Photoreceptor response to a sudden increase in light

it hyperpolarizes as the cGMP channels close and glutamate release falls, then slowly depolarizes back as it adapts

Role of intracellular calcium in light adaptation

Ca²⁺ enters through the cGMP-gated channels and inhibits guanylyl cyclase, so it indirectly controls cGMP levels; when light closes the channels, Ca²⁺ falls, the inhibition lifts, and cGMP rebuilds (the rebuild logic is elaboration)

cGMP and channel opening

cGMP holds the cGMP-gated channels open, less cGMP closes them, and cGMP resynthesis during adaptation reopens some (the reopening is not on slides)

Why light adaptation takes time

it depends on calcium-driven changes in cGMP levels and takes about 5 to 10 minutes, while dark adaptation takes minutes to an hour (why the chemistry is slow is not on slides)

Local adaptation vs pupil diameter

pupil size affects all photoreceptors equally, while bleaching and other adaptation mechanisms vary cone by cone

Refraction

the bending of light as it passes from one material into another; the cornea provides fixed refractive power and the lens adds adjustable bending to focus light on the retina

Lens shape for distant objects

flat and thin

Lens shape for near objects

round and bulging

Ciliary muscle and zonule fibers in distant vision

the ciliary muscle relaxes, the zonule fibers pull tight, and the lens is flattened

Ciliary muscle and zonule fibers in near vision

the ciliary muscle contracts, the zonule fibers go slack, and the lens bulges

Myopia

the eyeball is too long (as drawn), so light focuses in front of the retina; corrected with a concave lens

Hyperopia

the eyeball is too short (as drawn), so light would focus behind the retina; corrected with a convex lens (the convex correction is not on slides)

Myopia vs hyperopia

myopia focuses in front of the retina, hyperopia focuses behind it

Why concave corrects myopia and convex corrects hyperopia

a concave lens spreads rays so the focus shifts back onto the retina, and a convex lens converges rays more so the focus shifts forward onto the retina (the convex half is not on slides)

Astigmatism

light forms multiple focal points, so vision is blurred, unlike the single focal point of a normal eye (the cause, uneven curvature of the cornea or lens, is not on slides)

Five principal retinal cell types

photoreceptors, bipolar cells, ganglion cells, horizontal cells, and amacrine cells

Photoreceptors

detect light

Bipolar cells

relay photoreceptor signals

Ganglion cells

send action potentials through the optic nerve

Horizontal cells

provide lateral interactions in the outer retina

Amacrine cells

modify signaling in the inner retinal circuits

Direct (vertical) retinal pathway

photoreceptors → bipolar cells → ganglion cells

How horizontal and amacrine cells modify retinal signals

they make lateral (sideways) connections that change the responses of bipolar and ganglion cells

Rods

contain more disks, make vision possible in low light, sit mainly in the peripheral retina, and are absent from the fovea

Cones

enable daylight and color vision with high acuity, and are concentrated in the central retina within about 10 degrees of the fovea

Why the fovea gives high-resolution vision

it is all cones with no rods, the ganglion cell layer and inner nuclear layer are displaced to the side so light strikes the photoreceptors directly, and few photoreceptors feed each ganglion cell

Fovea in photopic vs scotopic light

in daytime (photopic) light visual acuity is greatest, while in night-time (scotopic) light the fovea is effectively blind and objects lose color

Why the peripheral retina is sensitive to dim light

it is mostly rods, and many photoreceptors feed each ganglion cell

Photoreceptor convergence onto ganglion cells

low convergence in the central retina gives high resolution, and high convergence in the periphery gives better dim-light detection with less detail

Glutamate release when light strikes the retina

photoreceptors release less glutamate (they release it steadily in the dark)

ON-bipolar cell response to reduced glutamate

it depolarizes

OFF-bipolar cell response to reduced glutamate

it hyperpolarizes

Flow chart of visual transduction

light → rhodopsin changes shape → transducin swaps GDP for GTP → PDE activated → cGMP broken down → cGMP-gated Na⁺ channels close → photoreceptor hyperpolarizes → less glutamate released

Phototransduction

the conversion of light energy into changes in membrane potential, which is how light becomes a signal the nervous system can use (the second half is elaboration)

Role of rhodopsin

the photopigment in rod disk membranes, made of opsin plus retinal, which absorbs light and changes shape to start the cascade

What happens to retinal when it absorbs light

it switches from the cis shape to the trans shape at the bond between carbons 11 and 12

Activated rhodopsin and transducin

it makes transducin swap GDP for GTP, and the alpha subunit then activates phosphodiesterase

Phosphodiesterase (PDE)

the enzyme that breaks cGMP down into GMP

Effect of decreased cGMP

the cGMP-gated sodium channels close, the inward Na⁺ dark current stops, and the photoreceptor hyperpolarizes from its dark level of about −30 mV

Why photoreceptors hyperpolarize in light

in the dark cGMP keeps Na⁺ channels open, so the dark current holds the cell at about −30 mV (depolarized), and light destroys cGMP and shuts off that current, because in photoreceptors light decreases the second messenger instead of increasing it

Properties of an image coded by ganglion cells

local changes in illumination (contrast and light-dark edges), color differences, and timing (transient vs sustained), all reflected in center-surround receptive fields

Receptive field

the patch of retina where light changes a cell’s response, with a center and a surround (this definition is not worded on slides)

ON-center ganglion cell

fires more when light falls on the center and less when light falls on the surround

OFF-center ganglion cell

fires more when the center is dark and less when the center is lit, with the opposite response in the surround

Influence of the surround when the center is stimulated

the surround acts opposite to the center, so extending the stimulus into the surround reduces the response

Lateral inhibition

a photoreceptor’s glutamate activates a horizontal cell, which inhibits its neighbor, increasing the difference between lit and unlit neighbors (its role in detecting edges is elaboration)

Small spot vs uniform illumination

a small spot drives the center alone, while uniform light hits center and surround, which oppose each other and give only a weak response

M-type ganglion cell

responds to light with a large burst that decays quickly (transient); the name means magnocellular, large (not on slides)

P-type ganglion cell

responds with a sustained response, and is the type with color-opponent fields; the name means parvocellular, small (the name is not on slides)

Color-opponent receptive fields

the center and surround prefer opposite colors (for example, red ON center and green OFF surround), so the cell signals color differences; red light on the center excites it, red extending into the surround inhibits it, and green on the surround inhibits it even more

Intrinsically photosensitive retinal ganglion cells (ipRGCs)

ganglion cells that transduce light themselves, send axons out of the eye without extra synapses, and have wide dendrites that make them sensitive to light over a large area rather than to fine detail