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What is happening in the eye? 1. Draw the sensory receptors in the eye 2. Draw...

What is happening in the eye?

1. Draw the sensory receptors in the eye

2. Draw what an action potential looks like in a neuron (intercellular communication) Note: go through all the steps to show how membrane potential changes from the beginning to the end of an action potential

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Answer #1

Look at this picture from standard textbook.

Now, The rod and the cone cells are the sensory receptors in the eye.

Rods are responsible for black and white vision and are more active at night during low levels of light. Your cones are for color vision and are used during the day when light is ample.

Let's look closely at these receptors.

Cone cells are somewhat shorter than rods, but wider and tapered, and are much less numerous than rods in most parts of the retina, but greatly outnumber rods in the fovea. Structurally, cone cells have a cone-like shape at one end where a pigment filters incoming light, giving them their different response curves. They are typically 40–50 µm long, and their diameter varies from 0.5 to 4.0 µm, being smallest and most tightly packed at the center of the eye at the fovea. The S cone spacing is slightly larger than the others.

Like rods, each cone cell has a synaptic terminal, an inner segment, and an outer segment as well as an interior nucleus and various mitochondria. The synaptic terminal forms a synapse with a neuron such as a bipolar cell. The inner and outer segments are connected by a cilium. The inner segment contains organelles and the cell's nucleus, while the outer segment, which is pointed toward the back of the eye, contains the light-absorbing materials.

Unlike rods, the outer segments of cones have invaginations of their cell membranes that create stacks of membranous disks. Photopigments exist as transmembrane proteins within these disks, which provide more surface area for light to affect the pigments. In cones, these disks are attached to the outer membrane, whereas they are pinched off and exist separately in rods. Neither rods nor cones divide, but their membranous disks wear out and are worn off at the end of the outer segment, to be consumed and recycled. by phagocytic cells.

Rods are a little longer and leaner than cones but have the same basic structure. Opsin-containing disks lie at the end of the cell adjacent to the retinal pigment epithelium, which in turn is attached to the inside of the eye. The stacked-disc structure of the detector portion of the cell allows for very high efficiency. Rods are much more common than cones, with about 120 million rod cells compared to 6 to 7 million cone cells.

Like cones, rod cells have a synaptic terminal, an inner segment, and an outer segment. The synaptic terminal forms a synapse with another neuron, usually a bipolar cell or a horizontal cell. The inner and outer segments are connected by a cilium, which lines the distal segment.The inner segment contains organelles and the cell's nucleus, while the rod outer segment (abbreviated to ROS), which is pointed toward the back of the eye, contains the light-absorbing materials.

A human rod cell is about 2 microns in diameter and 100 microns long. Rods are not all morphologically the same; in mice, rods close to the outer plexiform synaptic layer display a reduced length due to a shortened synaptic terminal.

How action potential looks like?

Without Light. With Light.

It clearly depicts the entire proces till the generation of action potential.

In the absence of light, the photoreceptors are depolarized to a membrane resting potential of -40mV. Light will hyperpolarize the plasma membrane of the photoreceptor to -70mV. This stimulus-induced hyperpolarization is a distinctive characteristic of the photoreceptor response, as many other neuronal types depolarize when stimulated.

A key second messenger molecule responsible for maintaining a depolarized rest state in photoreceptors is the nucleotide cyclic guanosine 3’-5’ monophospate (cGMP). High cGMP levels keep cGMP-gated ion channels in the open state and allow them to pass an inward Na+ current.

Phototransduction involves three main biochemical events:

Light entering the eye activates the opsin molecules in the photoreceptors

Upon photon absorption, 11-cis-retinal undergoes an isomerization to the all-trans form, causing a conformational change in the rhodopsin. The activated rhodopsin is called metarhodopsin II.

The precursor for 11-cis-retinal is all-trans-retinol (vitamin A). A diet rich in vitamin A is crucial for vision, since vitamin A cannot be synthesized by humans.

Activated rhodopsin causes a reduction in the cGMP intracellular concentration.

The cytoplasmic cGMP levels are controlled by cGMP phosphodiesterase, an enzyme that breaks down cGMP. In the dark, the activity of this enzyme is relatively weak. When the photoreceptor is exposed to light, metarhodopsin II stimulates the activity of cGMP phosphodiesterase via transducin, a G protein. GDP-bound inactive transducin will exchange GDP for GTP following interaction with activated rhodopsin. GTP-bound active transducin will increase the activity of cGMP phosphodiesterase. The result is decreased levels of cGMP in the cytoplasm.

The photoreceptor is hyperpolarized following exposure to light

Decreased levels of cGMP cause the closing of cGMP-gated ion channels which will lead to membrane hyperpolarization.

Termination of the phototransduction cascade

The light response is terminated by several mechanisms.

(1) Inactivation of rhodopsin occurs through phosphorylation by the opsin kinase, followed by the binding of arrestin to phosphorylated rhodopsin.

(2) Inactivation of transducin occurs through the hydrolysis of bound GTP to GDP (Tα-GTP to Tα-GDP) via an intrinsic GTPase activity that is accelerated by the GTPase activating protein RGS9 (regulator of G-protein signaling).

(3) Inactivation of phosphodiesterase (PDE) is coupled to the inactivation of transducin. Inactivated transducin (Tα-GDP) dissociates from PDE, resulting in a cessation of PDE-mediated cGMP hydrolysis.

(4) Activation of guanylate cyclase by guanylate cyclase activating protein (GCAP) restores cGMP levels and thus promotes the re-opening of cGMP-gated channels.

Amplification in the phototransduction cascade

The activation of a single rhodopsin by a single photon is sufficient to cause a significant change in the membrane conductance. This is possible due to amplification steps present in the transduction cascade.

A single photoactivated rhodopsin catalyses the activation of 500 transducin molecules. Each transducing can stimulate one cGMP phosphodiesterase molecule and each cGMP phosphodiesterase molecule can break down 10^3 molecules of cGMP per second. Therefore, a single activated rhodopsin can cause the hydrolysis of more than 10^5 molecules of cGMP per second.

From here on,

Extracranial

The optic nerve is formed by the convergence of axons from the retinal ganglion cells. These cells in turn receive impulses from the photoreceptors of the eye (the rods and cones).

After its formation, the nerve leaves the bony orbit via the optic canal, a passageway through the sphenoid bone. It enters the cranial cavity, running along the surface of the middle cranial fossa (in close proximity to the pituitary gland).

Intracranial (The Visual Pathway)

Within the middle cranial fossa, the optic nerves from each eye unite to form the optic chiasm. At the chiasm, fibres from the nasal (medial) half of each retina cross over to the contralateral optic tract, while fibres from the temporal (lateral) halves remain ipsilateral:

  • Left optic tract – contains fibres from the left temporal (lateral) retina, and the right nasal (medial) retina.
  • Right optic tract – contains fibres from the right temporal retina, and the left nasal retina.

Each optic tract travels to its corresponding cerebral hemisphere to reach the lateral geniculate nucleus (LGN), a relay system located in the thalamus; the fibres synapse here.

Axons from the LGN then carry visual information via a pathway known as the optic radiation. The pathway itself can be divided into:

  • Upper optic radiation – carries fibres from the superior retinal quadrants (corresponding to the inferior visual field quadrants). It travels through the parietal lobe to reach the visual cortex.
  • Lower optic radiation – carries fibres from the inferior retinal quadrants (corresponding to the superior visual field quadrants). It travels through the temporal lobe, via a pathway known as Meyers’ loop, to reach the visual cortex.

Once at the visual cortex, the brain processes the sensory data and responds appropriately.

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