Physiology of Excitable cells - Sensory Integration - Flashcards in University Biology

OVERVIEW OF RETINA: Sclera

white of the eye, protective outer layer comprised of collagen and elastin fibres, eye movements can be seen for communication

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Choroid

vascular layer providing oxygen and nutrients to outer retina - especially fovea

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Retinal pigment epithelium

pigmented layer for light absorption and reducing oxidative stress, tight junctions form blood brain (retina) barrier,supports photoreceptors

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Photoreceptors

CONES: concentrated in fovea high activity day (photopic) vision and colour vision. RODS: dark (scotopic) vision, not present in central retina

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Horizontal cells

interneurons connecting photoreceptors laterally

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Bipolar cells

connect photoreceptors to retinal ganglion cells - facilitate sensory processing through horizontal and amacrine cells

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Amacrine cells

interneurons connecting bipolars laterally

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Retinal ganglion cells

output cells from retina

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Fovea

located in centre of retina, responsible for sharp central vision. only red and green cones found at fovea

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Blind spot

optic nerve - lack of photoreceptors

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Central retina

long narrow cone outer segments - allow high density packing, Henle fibres - run to allow formation of foveal pits, Ganglion cells heaped up around fovea - specialisations to allow high spatial vision

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Visual acuity and why eyes move

measure of foveal vision. Photoreceptors most densely packed on fovea. Eyes move to 1. bring image onto the fovea 2.keep it there

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Types of eye movements

(saccades) - bring image on fovea, (fixations, smooth pursuit, optokinetic nystagmus, vestibulo-ocular reflexes, vergence movements) - keep image on fovea

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Moving images

fast eye movements (saccades) and steady fixations to scan visial scene. head or whole body moves - VOR. single object of interest moving - smooth pursuit. whole visual field moving - OKN

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Saccades

rapid eye movements to bring image onto fovea, short latency, fast, voluntary, conjugate - both eyes moving at same time.

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Fixational eye movements

to keep fovea on fixed target of interest, compromised of mini eye movements, microsaccades-small saccades bringing image back to fovea, drift-slower and more random, tremor - fine oscillations --> prevent retinal adaptation

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Smooth pursuit

tracks single target, requires brain to estimate how fast targets moving, voluntary - need to see moving object, conjugate

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Optokinetic nystagmus (OKN)

tracks movements of visual field, slow phase in direction of target, fast phase to reset eyes, involuntary but driven by moving visual field, conjugate

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Vestibulo-ocular reflex (VOR)

compensates for head movements, keep gaze steady, extremely rapid, involuntary - driven by vestibular system, conjugate

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Vestibular system

semi circular canal: filled with endolymph - flows through canal and ends up in ampular. Hair cells in ampula - stimulated giving info as to which direction plane of movement is in.

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"

head rotation - semi circular canals (3), head translation - (saccule and utricle) The system answers 2 questions: where am i going and which way is up

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Otolith organs

Utricle - sensitive to change in horizontal movement, Saccule - sensitive ti change in ventricular acceleration. vestibular nerve and cochlea - hearing and balance

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Rotational VOR + translational vor

semicircular canals of inner ear measure rotation of head. direction back and forth - thiloths

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Vergence

simultaneous movement of both eyes to maintain single binocular vision. image from each eye must be in centre of retina, allows viewing at diff distances. To view image at rear-eyes move inwards-Convergence. View image at distance-eyes out-Divergence

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Retinal disparity

the way left and right eyes view slightly different images. two images blended to one - important for depth perception. greater disparity between each image - closer image to you

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Pathological Nystagmus

involuntary constant to and from movement of the eyes that is constant. can be infantile (develops first few months of life) or acquired in later life due to neurological disease --> reduced visual acuity

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Classification

Infantile: idiopathic,albinism,retinal diseases,optic nerve disease --> no oscillopsia. Acquired: brain disorder,MS,stroke --> oscillopsia - perception of world in motion. eye movement recordings to help classify

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Quantitative recording of eye movements: 2D-electrooculography (EOG)

difference in electrical charge between cornea and retina, movement of the eye relative to electrode produces electrical signal that corresponds to eye position - easy to set up and use, output can be noisey

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2D-limbus tracker

measures reflected infrared light shone onto limbus - high temporal resolution,non invasive - set up needs to be precise

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2D-video oculography

infrared tracking of pupil for eye movement and screen markers for head - high temporal and spatial resolutions - can record gaze - doesnt record during blinks

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3D scleral search coil

magnetic contact lens inserted into eye - offers high spatial and temporal recordings of 3D eye movements - invasive and uncomfortable technique

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3D video oculography

IR cameras, partially reflective mirrors, face mask - tracks pupils for vertical movements and iris to follow torsional. lower temporal and spatial resolution, non invasive and comfortable - suitable for clinical setting

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Nystagmus characteristics

usually conjugate, horizontal, vertical, torsional, pendular or jerk(fast/slow) phase, frequency and amplitudes may vary, some - null point, dependent upon: time occlusion covergence eccentricity

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Infantile Nystagmus

idiopathic - often hereditary, no other problems with visual system, vision usually good, head nodding. Horizontal, conjugate, null point, foveation strategy

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Albinism

absent/decreased melanin in conjuction with visual system abnormalities - poor vision/partially sighted. Oculocutanous albinism - hair and skin as well as visual affected, Ocular albinism - only visual affected

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Visual system abnormalities

hypopigmentation, iris translumation, retinal abnormalities - poor vision sensitivity to light variable nystagmus, chiasmal abnormalities - only half info crosses to brain, nystagmus - similar to idiopathic infantile

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Acquired nystagmus

MS-demyelinating disease, myelin sheaths in brain/spinal cord damaged, can be relapsing or progressive, suffer oscillopsia, nystagmus. Wernicke encephalopathy-lesions in CNS due to lack of vitamin B, alcohol/drug abuse, reverse symptoms-thiamine supp

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Why no oscillopsia in infantile nystagmus

plasticity of brain until about 7 years of age. 1.sampling theory -info from most stable retinal images used and rest of nystagmus cycle ignored. 2.Remapping theory- efference copy signal of nystagmus waveform used to cancel effects of motion

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Retinal structure

--> Light (ganglion cell layer) output to brain (inner plexiform layer, inner nuclear layer, outer plexiform layer) signal processing (outer nuclear layer) light detection - photoreceptors

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Interneurons

Bipolar cells - vertical information flow, Horizontal and Amacrine cells - lateral information flow

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Visual integration in the retina

vertical flow of information-bipolar cellss transfer signals from photoreceptors to retinal ganglion cell outputs - allows 2 regions for signal processing

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horizontal cells

inhinitory cells functioning at the photoreceptor/bipolar cell interface, helps form receptive fields of RGCs for detecting contrast

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amcrine cells

inhibitory cells functioning at the bipolar/retinal ganglion cell interface, helps form receptive fields of RGCs for detecting motion

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Retinal ganglion cells

Parvocelullar cells - small receptive fields, detect fine features, colour sensitive. Magnocellular cells - large receptive fields, not colour sensitive, high motion sensitivity

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Detection of contrast - ON center cells

if shine light - centre of receptive field - responds, if shine light around centre - stops firing, if shine light whole area - activity doesnt change. mGluRs (metabotropic)

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OFF center cells

shine light centre - stops firing, shine light around centre - fires intensly, shine light whole area - no change. AMPR receptors (ionotropic)

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contrast enhancement

RGC receptive fields - example of lateral inhibition. If introduce inhibitory interneurons can change output because theres more inhibition in certain areas. can change response and accentuate signal.

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Herman Grid

lateral inhibition in Retina (+cortex), more inhibition at intersections, less inhibition for lines

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Scintillating Grid

lateral inhibition greater in peripheral retina because larger receptive fields

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Detection of Motion - Starburst Amacrine cells

central cell body and star shaped dendritic arbour - produces inhibition along dendrites in direction of motion. relative location of retinal ganglion cells to starbust amacrine cells determine directional selectivity.

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Infantile nystagmus

Directional selectivity to horizontal motion lost in infantile nystagmus - possibly due to wrong horizontal ganglion cells relative to amacrine cells

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Optic chiasm

X shaped structure in brain formed by crossing of optic nerves in brain. 55% of retinal ganglion cells fibres cross contralaterally, right brain sees left visual field + vice versa. each cortical hemisphere recieves input from right and left eyes

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Need for optic chiasm 1.Improve signal to noise

dissimilar information between two eyes - random noise, similar information between two eyes - signal

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2.So we see hands on same side of brain that controls it

90% decussation of corticospinal tracts that control hand muscles - improves speed of control

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3.Amount of crossing at chiasm is proportional to amount of binocular field across species

lateral eyes - no binocular field but wider coverage, forward facing eyes - larger binocular field - better binocular vision --> to provide retinal disparity through seperation of two eyes for 3D vision

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Retinal disparity

Horoptor - surface where no disparity between 2 eyes (images correspond), everything nearer = crossed disparity, everything further away = uncrossed disparity

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Primary visual cortex VI

main cortical recieving station of visual information - Retinotopic - retina mapped spatially onto primary visual cortex, cortical magnification of fovea region

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Ocular dominance columns

alternating stripes across the visual cortex from left and right eyes - equivalent representations of visual field from each eye brought together in area VI - affected by amblyopia (lazy eye) due to strabismus (eye turn)

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Type os straTypes of Strabismus

normal-two eyes looking same direction, esotropia-one eye turned inwards, exotropia-one eye turned outwards, hypertropia-one eye turned upwards, hypotropia-one eye turned downwards. Input from one eye supressed to prevent double vision

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Amblyopia (lazy eye)

can be reversed by patching better eye during visual development, - example of neural plasticity in response to visual experience

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Extrastriate cortex

ventral pathway=WHAT pathway (object recognition), dorsal pathway=WHERE pathway (vision processing for action)

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Damage to inferior temporal cortex - ventral

Damage leads to 2 types of visual agnosia. Aperceptive - cant copy or match objects/integrate. Associative - cant interpret understand or assign meaning to objects + problems with recognition

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Intraparietal cortex - dorsal

Important for reaching and grasping with hands, directing eye movements - eye movement signals are subtracted from neural signal - spatial constancy

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Damage to intraparietal cortex - dorsal

Damage to right parietal lobe leads to - hemi neglect of left visual field, only occurs with damage to right lobe. Right parietal cortex sees whole of visual field whereas left parietal cortex only sees right visual field

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Bottom up processes

sensory (exogenous) info - stimulus influences our perception - data driven

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Top down processes

internal (endogenous) information - background knowledge to influence our perception - theory driven

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Binding Problem

binding=integration of highly diverse neural information to form a cohesive experience. challenges - how does brain integrate diff visual properties, bottom up and top down processes and how does it bind features that are processed seperately

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Binding problem 1

Segregration problem - how are complex patterns of sensory input allocates to discrete objects

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Binding problem 2

Combination problem - how are various features combined into single perceptual experience

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theory 1

Timing of inputs-synchronised activity of different populations of neurons indicate that two features are bound - oscillstory potentials important, coincidence detection - allows inputs to arrive at diff times.

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theory 2

Location of inputs - binding linked to common location in visual field

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Balance - vision

(dorsal pathway) - where objects are relative to us, stable view of world, vision to guide eye movements, vision for action

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Balance - vestibular system

rotations and translations of the head sensed using sense organs in inner ear

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Balance - somatosensory system

proprioceptors and cutaneous inputs, muscle spindles - muscle stretch, golgi tendon organs - muscle tension, joint receptors - joint angle, pressure sensors on bottom of feet

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Balance - efference copy

brain-internal copy of outflowing, motor signal: fast movements dont need to wait for sensory feedback, movements where unlikely that external forces likely to affect movements but dont allow for unexpected changes, less accurate for slower movements

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measuring inputs by looking at postural control

computerised dynamic posturography-measures body sway using force platform, sensory organisation test - remove vision by closing eyes, remove somatosensory by causing platform to sway with body

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measuring visual evoked potentials - measuring electrical activity in visual cortex

need to place electrodes precisely, need to provide powerful visual stimuli,- need to average responses to see signal amongst noise. Electrode positioning - hair clean and gel free, electrodes applied to head by parting hair and using small dot adhes

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