1. VISION Dr. Janet Fitzakerley jfitzake@d.umn.edu http://www.d.umn.edu/~jfitzake/Lectures/Teaching.html jfitzake@d.umn.edu http://www.d.umn.edu/~jfitzake/Lectures/Teaching.html

2. Critical Facts 1.There are two fundamental protective mechanisms for the eye. Regulation of eyelid position (including BLINKING) involves striated (ACh; nicotinic) and smooth (NE; α1 adrenergic) muscles. TEAR PRODUCTION occurs spontaneously (basal), reflexly or in response to emotional stimuli, and is partially regulated by the parasympathetic nervous system (ACh; muscarinic). EPIPHORA (overflow of tears) can be due to either overproduction or blocked drainage. 2.The cornea and lens focus light on the retina; the cornea has greater refractive power but the focusing power of the lens can be adjusted to allow near vision (accomodation). Refractive errors include cataracts, hyperopia, myopia, presbyopia and astigmatism. 3.Light intensity is regulated by the PUPILLARY LIGHT REFLEX, which causes MIOSIS as a result of parasympathetic stimulation of the sphincter pupillae muscles (muscarinic receptors). MYDRIASIS results from sympathetic stimulation (α1 receptors) that activates the dilator pupillae muscles. 4.Increased intraocular pressure causes loss of vision (potentially permanent). Open angle glaucoma (the most common form) results from overproduction of the aqueous humor. Closed angle glaucoma (typically the most rapidly evolving form) is caused by blockage of fluid outflow. 5.RODS are responsible for SCOTOPIC vision (the monochromatic vision that occurs in low light). The three types of cones (blue, green and red; or Short, Medium and Long wavelength) have better temporal and spatial resolution than rods, making PHOTOPIC VISION better for discrimination of surfaces and movement under bright light conditions. 6.The ability to discriminate fine details of the visual scene is termed VISUAL ACUITY. Three types are recognized: SPATIAL, TEMPORAL and SPECTRAL. Visual acuity is primarily a function of the cone system.

3. Critical Facts (cont’d) 7.PHOTOTRANSDUCTION occurs via a 4 step process that uses a 2nd messenger cascade to amplify the signal. In rods, activation of rhodopsin ultimately results in the closure of cyclic nucleotide gated Na+ channels, and hyperpolarization of the photoreceptor. 8.The VISUAL CYCLE consists of bleaching and recycling of 11-cis-retinol between the photoreceptors and the retinal pigment epithelium (RPE). It is a key component of dark adaptation in rods and is disrupted in vitamin A deficiency, and macular degeneration. 9.Ganglion cells (GCs) are like CNS neurons, in that their contrast-detecting capabilities are enhanced by lateral inhibition provided by amacrine cells. On-center GCs produce more action potentials when stimulated by a bright light in the center of their receptive field, and inhibited by stimuli delivered to the surround. Off-center GCs are stimulated by surround stimuli, and inhibited by center stimuli. 10.Perception of colour is a learned process which involves associating patterns of photoreceptor activity with a particular hue. Even though the distribution of cones within the retina is unique to each individual, the description of hue is standardized by teaching people to associate specific words with their unique pattern of cone response. 11.Within primary visual cortex (V1), inputs from the fovea are overrepresented relative to the periphery. The separate maps that are established for each visual field in primary V1 are merged to form a single perceptual map of visual space. Due to OCULAR DOMINANCE, cortical can extract depth cues based on the disparity in the images, providing the basis for STEREOPSIS (depth perception). 12.STRABISMUS is a muscle imbalance that results in a misalignment of the visual axes of the two eyes. Any type of strabismus that occurs after ~6 months of age causes DIPLOPIA (perception of a single object as double) because the images fall on noncorresponding parts of the retinas. In young children, suppression of the image in the weaker eye can cause a permanent decrease in visual acuity (AMBLYOPIA).

4. Essential Material from Other Lectures 1.Structure of the eyeball, including the innervation of the levator palpebrae superioris and superior tarsal muscle, the lacrimal gland, the cornea and the lens (Dr. Severson, Applied Anatomy) 2.CSF formation (Dr. Drewes, Nervous System) 3.Pupillary reflex/innervation of the dilator and constrictor muscles of the pupil (Dr. Forbes, Nervous System) 4.Anatomical structures associated with aqueous humor formation and flow, including the ciliary body and the canal of Schlemm (Dr. Severson, Applied Anatomy). 5.Histology of the retina (Dr. Downing, Nervous System). 6.Receptor potentials and lateral inhibition (Dr. Fitzakerley, Nervous System) 7.Visual Fields (Dr. Forbes, Nervous System)

5. Learning Objectives 1.Be able to describe the neurotransmitters involved in eyelid movements, and characterize the purpose and types of blinking. Explain tear production and how it is regulated. 2.Explain the processes of refraction and accomodation as they apply to transmission of light to the retina. Define the following refractive errors: cataracts, hyperopia, myopia, presbyopia and astigmatism. 3.Describe the processes of mydriasis and miosis, including the neurotransmitters involved. 4.Explain how the aqueous humor is formed and drains, and outline control mechanisms for each part of the process. Detail the differences between closed angle and open angle glaucoma. 5.Compare and contrast the physiology of rods and cones. Relate the physiological differences between rods to the different forms of visual acuity. Differentiate between retinopathy and retinitis pigmentosa. 6.List the steps in phototransduction, including the properties of the receptor potential. 7.Describe the visual cycle, and understand the perturbations that occur to this process during vitamin A deficiency and macular degeneration. 8.Outline how lateral inhibition contributes to the receptive field properties of ganglion cells. Describe the function of bipolar, horizontal and amacrine cells. 9.Explain how the primary visual cortex processes color and motion, and generates depth perception. Describe how amblyopia develops from stabismus and diplopia.

6. OPTICS

7. Protective Mechanisms There are two fundamental protective mechanisms for the eye. Regulation of eyelid position (including BLINKING) involves striated (ACh; nicotinic) and smooth (NE; α 1 adrenergic) muscles. TEAR PRODUCTION occurs spontaneously (basal), reflexly or in response to emotional stimuli, and is partially regulated by the parasympathetic nervous system (ACh; muscarinic). EPIPHORA (overflow of tears) can be due to either overproduction or blocked drainage.

8. Blinking eyelid movements are mediated by the orbicularis oculi (OO) and levator palpebrae superioris (LPS) muscles, as well as by the superior tarsal muscle (ST) oOO and LPS are striated muscles (ACh acts on nicotinic receptors to cause contraction) othe superior tarsal muscle is a smooth muscle (sympathetic innervation via α 1 receptors) three types of motions: 1.maintaining ocular opening tonic activation of LPS and ST; inactivation OO 2.gentle opening/closing, adjustment to changes in globe position activation/inactivation of LPS; inactivation OO 3.blinking, firm closure of eyesOO activation; inhibition of LPS

9. Blinking blinking serves a number of functions, including: ocorneal lubrication oeye protection ovisual information processing blinking can be spontaneous or reflex ospontaneous blinking: is precisely conjugated, periodic, symmetrical, brief and occurs in the absence of external stimuli or internal effort show a wide variation in rate (typically 10-20 blinks/minute in adults; lower in children) originates in premotor brainstem structures that are highly influenced by dopaminergic activity –decreased in Parkinson's disease, and increased in schizophrenia and Huntington's disease, for example othe blink reflex: can be initiated by either touch to the cornea (afferents in the trigeminal nerve) or by bright light/rapidly approaching objects (afferents in the optic nerve) is faster than spontaneous blinking

10. Tear Production the tear film that covers the suface of the eye has 3 layers: olipid secred by oil glands in the eyelids oaqueous-based solution from lacrimal gland (contains lysozyme and other enzymes that provide protection against infection) omucous from the conjunctiva the composition of the tear layer varies depending upon the stimulus and with age oemotional tears contain more hormones, such as prolactin, ACTH and enkephalin obasal tear production decreases with age

11. Tear Production tear flow occurs via evaporation and drainage through the nasolacrimal ducts into the nasal cavity oparasympathetic stimulation produces epiphora (overflow of tears) by: 1.increasing tear production by the lacrimal gland 2.decreasing outflow by facilitating closure of the lacrimal duct passage oepiphora can be induced by: stimulation of the cornea (cranial nerve V) which produces reflex tears strong emotional responses (mediated by the limbic system, especially the hypothalamus) which produce psychic tears (crying or weeping) strong parasympathetic stimulation is accompanied by other symptoms, like reddening of the face and convulsive breathing

12. Focusing The cornea and lens focus light on the retina; the cornea has greater refractive power but the focusing power of the lens can be adjusted to allow near vision (accomodation). Refractive errors include cataracts, hyperopia, myopia, presbyopia and astigmatism.

13. Refraction

14. Accomodation

15. Refractive Errors

16. Regulation of Light Intensity Light intensity is regulated by the PUPILLARY LIGHT REFLEX, which causes MIOSIS as a result of parasympathetic stimulation of the sphincter pupillae muscles (muscarinic receptors). MYDRIASIS results from sympathetic stimulation (α 1 receptors) that activates the dilator pupillae muscles.

17. Formation of the Aqueous Humor Increased intraocular pressure causes loss of vision (potentially permanent). Open angle glaucoma (the most common form) results from overproduction of the aqueous humor. Closed angle glaucoma (typically the most rapidly evolving form) is caused by blockage of fluid outflow.

19. Glaucoma

20. PHYSIOLOGY OF THE RETINA

22. Visible Light

23. Photoreceptors Rods are responsible for SCOTOPIC vision (the monochromatic vision that occurs in low light). The three types of cones (blue, green and red; or Short, Medium and Long wavelength) have better temporal and spatial resolution than rods, making PHOTOPIC VISION better for discrimination of surfaces and movement under bright light conditions.

25. RODSCONES Amount of photopigment MoreLess Pigment type1 = rhodopsin 3 overlapping  patterns of activity for colour (see page 15) Sensitivity High (1 photon if dark adapted)  Saturated in daylight  Smaller dynamic range Low (multiple photons to activate)  Saturate in very intense light  Large DR Temporal resolution Low  Slow response  Responses are integrated High  Fast response  Less integration Spatial resolution Poor  Respond to scattered light  Not in fovea  large amount of convergence onto bipolar cells Very good  Respond to narrow spots of light  In fovea  little amount of convergence onto bipolar cells

26. Visual Acuity The ability to discriminate fine details of the visual scene is termed VISUAL ACUITY. Three types are recognized: SPATIAL, TEMPORAL and SPECTRAL. Visual acuity is primarily a function of the cone system.

28. Phototransduction PHOTOTRANSDUCTION occurs via a 4 step process that uses a 2 nd messenger cascade to amplify the signal. In rods, activation of rhodopsin ultimately results in the closure of cyclic nucleotide gated Na + channels, and hyperpolarization of the photoreceptor.

30. Receptor Potential

31. Retinosis Pigmentosa

32. Retinopathy

33. Visual Cycle The VISUAL CYCLE consists of bleaching and recycling of 11-cis- retinol between the photoreceptors and the retinal pigment epithelium (RPE). It is a key component of dark adaptation in rods and is disrupted in vitamin A deficiency, and macular degeneration.

35. Vitamin A Deficiency

36. Macular Degeneration

37. Ganglion Cell Physiology Ganglion cells (GCs) are like CNS neurons, in that their contrast- detecting capabilities are enhanced by lateral inhibition provided by amacrine cells. On-center GCs produce more action potentials when stimulated by a bright light in the center of their receptive field, and inhibited by stimuli delivered to the surround. Off-center GCs are stimulated by surround stimuli, and inhibited by center stimuli.

39. VISUAL CORTEX PHYSIOLOGY

41. Colour Perception

42. Perception of colour is a learned process which involves associating patterns of photoreceptor activity with a particular hue. Even though the distribution of cones within the retina is unique to each individual, the description of hue is standardized by teaching people to associate specific words with their unique pattern of cone response.

43. Edge Perception

44. Topographic Maps Within primary visual cortex (V1), inputs from the fovea are overrepresented relative to the periphery. The separate maps that are established for each visual field in primary V1 are merged to form a single perceptual map of visual space. Due to OCULAR DOMINANCE, cortical can extract depth cues based on the disparity in the images, providing the basis for STEREOPSIS (depth perception).

46. Depth Perception

47. Development STRABISMUS is a muscle imbalance that results in a misalignment of the visual axes of the two eyes. Any type of stabismus that occurs after ~6 months of age causes DIPLOPIA (perception of a single object as double) because the images fall on noncorresponding parts of the retinas. In young children, suppression of the image in the weaker eye can cause a permanent decrease in visual acuity (AMBLYOPIA).