Neuroscience - Exam 2

Neuroscience - Exam 2

by Batmanuel

·  Visual System

○  Objectives

§  Point to and name the principle structures of the eye and recount how light is correctly focused onto the retina or refractive errors occur

§  Recognize the retinal layers and name the main classes of neurons in the retina that are in each layer

§  Outline key features in transduction of light energy to transmitter release in photoreceptors and describe differences between rods and cones individually as systems of ‘rod-based’ and ‘cone-based’ information.

§  Describe how ON and OFF pathways contribute to RGC receptive field organization and how this relates to contrast enhancement at edges and contours

§  Define the differences in the anatomical organization of peripheral and central retina and explain how these relate to the receptive field properties of the neurons in these regions and corresponding to the “alerting” and “analysis” functions of the cells

§  Describe the differences between the properties and central projections of the P and M RGCs

§  Name the central processing visual system structures and characterize how M and P pathways utilize separate projection routes and subregions of target structures. Also describe how the visual field is represented (visuotopic map) in visual pathways and main structures.

§  Relate visual field deficits (scotomas) to sites of damage of visual pathways or nuclei

§  Describe the concepts of binocularity and ocular dominance as they apply to neurons in visual cortex. Identify the cortical areas and layers where information from both eyes is kept separate and where it is combined

§  Describe or draw a cortical processing unit composed of ocular dominance columns and orientation columns

§  Give examples of how cortical processing “streams” distil information regarding perceptions of color, shape, and motion of visual images

§  Recognize and describe the basic science issues that pertain to pathophysiological mechanisms of cataract, retinitis pigmentosa, optic neuritis resulting from glaucoma or multiple sclerosis, brain trauma or stroke or surgical lesions to optic radiations (Meyer’s loop example) or higher level cortex.

○  Diseases

§  Retinitis Pigmentosa

·  Inherited eye disease that causes degeneration of photoreceptor cells in the retina causing progressive vision loss

·  Problems seeing in low light, problems adapting to low light levels, restriction of visual field

○  Rods are affected first

§  Optic Neuritis

·  Glaucoma - optic disc destroyed and enlarged

○  Can have normal tension (these patients often have vasospastic diseases like migraine, Raynaud’s disease, hypotension etc.)

○  How to test, since IOP isn’t good test? Moving stimuli are detected less reliably on the peripheral retina in glaucoma patients of all sorts

·  Multiple Sclerosis - myelin breakdown can distort appearance of optic disc and damage optic nerve

§  Damage to Central Pathways (Meyer’s Loop)

○  Parallel Processing (of streams)

§  Detector arrays produce ‘streams’ of information (information from neighboring detectors is usually similar) and higher order analyzers pick out different aspects of information from that stream (color, motion, shape etc.)

·  These higher order analyzers then create their own streams

·  Within each stream information can be processed sequentially too

·  Eventually everything is merged together to make a whole

○  Light and Optics (Image Formation)

§  Light is refracted at the interface of two substances whose optical indicies are unequal

§  Emmetropia - good focusing power

§  Myopia - (near sighted) image focused in front of retina

§  Hyperopia - (far sighted) image focused behind retina

§  Presbyopia - hardening of lens so that it loses its ability to accomadate

§  Visual Angle - used to define size or relative position of an image on the retina

§  Line spread function - light spreads over a much broader visual angle in the eye due to diffusion (a line on a screen actually looks like a blur to the retina)

·  Visual system compensates for this and sharpens the image

§  Depth of Field - when small pupil then sharp focus at all depths,

·  when large pupil then best focus in one plane

·  Large pupil lets in a bunch of light and ↑ light scatter, thus adding to the line spread function and limits depth of field

○  Retina

§  Receptors → outer nuclear layer → outer plexiform layer → inner nuclear layer (horizontal, bipolar and amacrine cells) → inner plexiform layer → ganglion cell layer → RGC axons to optic nerve

·  RGCs are the only ones that have axons

§  Retinal - a Vitamin A aldehyde that is inactive in cis form and active in trans form (housed in rhodopsin protein)

§  Visual Transduction - bright light causes lots of hyperpolarization

·  Light is absorbed by rhodopsin and undergoes rapid transitions into an activated metabolite

·  Activated retinal interacts with a G-protein called transducin

·  Transducin activates an enzyme which depletes cGMP

·  Sodium channels that require cGMP to stay open, close

·  Sodium entry into rod is reduced and rod membrane potential hyperpolarizes

§  Adaptation to light or dark conditions is mainly due to changes in available photopigment

§  Color Vision

·  Principle of Univariance - any single cone photopigment cannot be used to determine what color light is. Signals from multiple pigments must be compared via higher order processing.

·  Color Blindness - L (long, red) and M (medium, green) cone pigments are adjacent to each other on the X chromosome so males are more likely to have red-green deficiency

○  blue deficiencies are rare and not sex linked

·  Color vision is best centrally at fovea where there are no rods and many cones

§  Cones vs Rods

Rods / Cones
Relative properties of individual photoreceptors
High sensitivity to light, specialized for night vision / Lower absolute sensitivity, specialized for daytime vision
More disks and photopigment molcules, thus captures higher % of photons / Less photopigment
High amplification, single photon detection / Less amplification
Lower temporal resolution; slow response; long integration time / Faster initial activation and shorter response duration provides better temporal resolution
More sensitive to scattered light, thus poorer image formation ability / Most sensitive to direct axial light (wave guide properties), thus higher spatial resolution for sharper images
Characteristics of rod and cone ‘systems’ (2nd, 3rd etc order neurons connected to R or C)
Low acuity / High acuity
Peripheral retina dominant / Fovea and central retina dominant
Highly convergent pathways / Non-convergent pathways
Achromatic (only one type of pigment) / Chromatic information pathways (3 types of cone pigments with different spectral absorbances = basis for color vision)

§  Retinal Neuron Circuits & Receptive Fields

·  All photoreceptors respond to increased light intensity with hyperpolarization

○  This signal is interpreted in opposite directions by either on-bipolar (metabotropic) or off-bipolar (ionotropic) cells

§  These cells send their signals to RGCs in a spatial pattern of concentric regions where the

○  Center - depolarizes at either light onset or light offset (depending on if signal comes from on or off bipolar cells)

○  Surround - antagonizes (does not inhibit) or cancels the center response

§  On Pathways - activated by light, inhibited by dark

§  Off Pathways - activated by dark, inhibited by light

§  Ex - Off center ganglion cell receives dark spot and surround receives light → large stimulation

○  Same cell receives dark spot in center and surround does too → surround antagonizes excitatory signal from center and stimulation is less

·  Herman Grid Illusion (dark boxes, white lines)

○  See picture

○  this means that less activity in second case in middle so middle will look darker

○  Specialized Processing

§  M and P systems

·  Both types of cells get bigger the farther away you get from the fovea

·  P cells - smaller RGCs (smaller than M cells at any distance from fovea)

○  Small receptive fields which allow for high resolution at fovea and central areas

○  Color-selective, high visual acuity, less significant for movement and flicker detection

○  Thinner axons and project to different areas in brain

·  M cells - larger RGCs (more sensitive to small differences in contrast?)

○  Larger receptive fields which are poor for high resolution but good for movement detection and fast flickering sensitivity (more in periphery)

○  High speed, thick axons into the brain

§  Grating Responses in terms of Center-Surround receptive field structure

·  The grating bar (alternating dark/light) that lines up with the size of the center-surround receptive field best will stimulate the cell the most

○  M cells have broader fields than P cells and so they respond better to larger grating bars

○  Central Visual Pathways

§  M & other → superior colliculus (midbrain) →

·  motor pathways (pons & spinal cord) - for eye movements, head movements

·  pulvinar (thalamus) - for visual attention

§  M & P

·  Pathway

○  Retina (M & P) → lateral geniculate nucleus (thalamus) → primary visual cortex (V1) (coding of form, color, motion, position, depth) independence of M & P maintained

§  Optic chiasm - axons from the nasal portion of each retina cross over to other side, while axons from the temporal side stay ipsalateral.

○  This creates the left and right hemifields

§  These axons end up in LGN and stay in centers divided into 6 layers by whether they are ipsa or contralateral within larger groups of whether they are M (layers 1 and 2) or P (layers 3-6)

§  From LGN to V1, some axons go laterally into temporal lobe and are called Meyer’s Loop

§  At V1 the visual field is represented topographically (upside down and reversed like retina)

○  Left fovea on outermost part of right occipital lobe (left peripheral on medialmost)

○  Upper fovea is below calcarine fissure (lower fovea is above calcarine fissure)

·  Lesions and Scotomas

○  Scotoma - blind area in visual field (homonopsia? Heteronopsia?)

○  See Picture

§  Geniculostriate Projection (LGN to V1)

·  These projections end in layer 4C in alternating columns from the right and left eye

·  From layer 4C, cells send axons to supragranular layers and this is the first time that information from the right and left eye is mixed → allowing for the first bit of binocular vision

§  Abnormal Visual Development

·  Esotropia - one eye crossed inward (exotropia is one eye crossed outward)

·  Monocular Deprivation - causes ocular dominace columns to develop

○  Treatment can be to patch the non-deprived eye

○  See Picture

§  Monocular Cues for Depth

·  Two eyes are not completely necessary for depth perception

·  This section needs help

·  Orientation Selectivity - some neurons in V1 are highly selective to the orientation of a moving bar of light (ie they only activate the most when the bar is at a certain angle)

○  Interestingly - if optic tract axons are forced to innervate the auditory thalamic nucleus instead of the LGN, the ATN will send visual stimulation to auditory cortex and it will process it

·  Cortical Processing Module - side-by-side ocular dominance columns comprised of numerous orientation columns

§  Higher Order Visual Areas (Visual Processing Streams)

·  From LGN → V1 layer 4C → V2 → V3 → V4 V5

·  Dorsal stream pathways - go from V1 to parietal cortex via MT

○  These are for image movement and spatial relationships

·  Ventral stream pathways - go from V1 to temporal cortex via V4

○  These are for color and perception with lots of specificity

§  Face Recognition

·  In monkeys the inferotemporal cortex is especially responsive to facial profile

·  Seems to be same spot in humans?

·  Prosopagnosia - inability to recognize faces (measure reaction time)

§  Agnosias (don’t know what we need to know)

·  See picture

·  Autonomic Nervous System

○  Objectives

§  Understand the basic functions of the autonomic nervous system underlying “fight and flight” and “rest and digest” behaviors

§  Be able to identify the three main divisions of the ANS as well as their major functions, preganglionic inputs, postganglionic outputs, and targets

§  Be able to describe the sensory componens of the ANS

§  Be familiar with the chemistry of synaptic transmission in the ANS and its physiological implications

§  Understand the concept of referred pain

§  Be able to identify and explain the autonomic circuits that control heart rate, urination, and male sexual function

○  General Information

§  Autonomic nervous system is mainly a visceral motor system

§  Main task is homeostasis

§  Controlled by the hypothalamus via the dorsal longitudinal fasciculus

§  Sympathetic Division - “Fight and Flight”

·  Pathway = stress → hypothalamus releases corticotropin-releasing hormone → pituitary releases adrenocorticotropin into blood → adrenal glands release epinephrine, norepinephrine and cortisol

○  Epinephrine - ↑ blood pressure, ↑ HR, diverts blood to muscles

○  Cortisol - releases glucose from body reserves

·  General Effect - ↓ gut motility, dilation of the bronchioles, ↑ BP, ↑ sweating, pupillary dilation, piloerection, ↓ watery gland secretion (dry mouth)

·  Normally feedback mechanisms turn it off when threat has passed

§  Parasympathetic Division - “Rest and Digest”

·  General Effect - maintaining basal heart rate, respiration, and metabolism under normal conditions

○  General Layout of ANS

§  Efferent Component

Somatic Efferent System / Autonomic Efferent System
Voluntary / Involuntary
Innervates skeletal muscles / Innervates smooth, cardiac and glandular cells
Motor neuron cell bodies housed within CNS in cranial nerve nuclei and spinal cord ventral horn / Neuron cell bodies housed outside the CNS in peripheral autonomic ganglia
Monosynaptic pathway to effector / Disynaptic pathway to effector, one synapse for preganglionic neuron, one for postganglionic
All outputs are excitatory / Outputs are either excitatory or inhibitory depending on which subsystem

§  Afferent Component