Pre-Midterm Content Conferences (1-4) Flashcards

1
Q

How is the Nervous System organized?

A

1) Central Nervous System
-> Brain
-> Spinal Cord

2) Peripheral Nervous System
-> Somatic
-> Autonomic

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2
Q

Neurotransmitters can be

A

Inhibitor or Excitatory

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3
Q

Neurons

A
  • cells of nervous system.
  • able to transmit nerve impulses.
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4
Q

Glia

A
  • cells of nervous system.
  • able to transmit nerve impulses.
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5
Q

synapses

A
  • space between pre- and post-synaptic terminals of two neurons, site of transmission
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6
Q

Neurotransmitters

A
  • a chemical compound released by neurons that act on postsynaptic neurons
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7
Q

Neuron Vocabulary

A

1) Dendrite: primary target for synaptic input
2) Axon: signal transduction from cell body; reads out information
3) Action potential: electrical event that carries signal
4) Pre-synaptic terminal: where molecules are secreted into synaptic cleft
5) Post-synaptic specialization: contains receptors where molecules bind
6) Synaptic cleft: space between pre- and post synaptic terminals

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8
Q

Neurons

A
  • specialized cells because they complete a single function: to transmit information across the nervous system via electrical impulses.
  • sensory: afferent receptor.
  • interneurons: transfer signals between sensory and motor.
  • Motor: efferent effector.
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9
Q

Lobes and functions of the brain

A

1) Frontal: motor and high-level cognitive skills.

2) Parietal: sensory integration; association cortex.

3) Temporal: Auditory.

4) Occipital: Visual.

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10
Q

The brain - Ventricular System

A
  • brain floats in bath of cerebrospinal fluid -> this fluid also fills large open structures, called ventricles, which lie deep in brain.
  • the fluid filled ventricles keep brain buoyant & cushioned.
  • there are 4 ventricles: 2 lateral (1 in each cerebral hemisphere), third ventricle in the diecephalon, and 4th ventricle in the hindbrain.
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11
Q

The brain: Glymphatic System

A
  • cooperation of glial cells and lymph velles (lymphatic system) to transport and accumulate waste out of the brain.
  • clean CSF replaces the ventricular spaces.
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12
Q

Anatomy of the Spinal Cord

A

1) External Anatomy:
-> Anterior median fissure
-> Posterior Median Sulcus

2) Internal Anatomy:
- Grey matter (nerve cells bodies - located in center of Spinal Cord)

  • White matter (surround grey matter, composed of myelinated axons)
  • Central canal: small channel with CSF in center of spinal cord, controls with the ventricular system in the brain.
  • Dorsal (posterior) horns: sensory neurons, in the back of spinal cord.
  • Ventral (anterior horns): motor neurons, in the front of spinal cord.
  • Lateral horns: in thoracic and lumbar segments of spinal cord, contains sympathetic neurons.
  • Dorsal root ganglia: cells bodies of sensory neurons, in dorsal roots of the spinal nerves.
  • Dorsal root: sensory fibres, enters the spinal cord.
  • Ventral root: motor fibers, exits the spinal cord.

3) Meninges:
- Dura mater: tough outermost layer surrounding spinal cord.

  • Arachnoid matter: middle layer, located between dura mater and pia mater.
  • Pia matter: innermost layer that adheres to surface of spinal cord.
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13
Q

What are ways to study neural circuts?

A
  • Electrophysiological Recordings
  • Calcium Imaging
  • Optogenetics
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14
Q

What are ways to study neural circuits?

A
  • Genetic Analysis
  • Structural Imaging
  • Non-invasive functional imaging (EEG, CT, TMS, fMRI)
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15
Q

Somatic Sensory System

A
  • Cutaneous Touch
  • Proprioception
  • Pain, Temperature & Sensual touch
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16
Q

Cutaneous Touch

A
  • Mechanical perturbations lead to depolarization of afferent.
  • Different types of encapsulations detect different features of touch:

1) Small Receptive Field;
- Merkel (shape and texture perception, edges, points, corners, curvature)
- Meissner (motion detection, grip control, skin motion)

2) Long Receptive Field;
- Pacinian (perception of distant events through transmitted vibrations - tool use)
- Ruffini (Tangential force: hand shape, motion direction, skin stretch)

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17
Q

Proprioception

A
  • Sense of Self
  • Sensory afferents coil around intrafusal muscle fibres, which detect the rate of change of muscle length.
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18
Q

Proprioception: Muscle Spindles

A

1) Primary endings - Group Ia
- rapidly adapting
- dynamic limb movement
- mono and polysynaptic excitatory alpha motor neurons

2) Secondary Endings - Group II
- slow adapting
-awareness of static positions
- sustained response to stretch
- polysynaptic excitatory alpha motor connections

3) y-motor neurons
- change intrafusal fibre tension
- increases afferent sensitivity to stretch
- dynamic gamma motor neurons and static gamma motor neurons.

-> Tension from muscle stretching opens ion channels. Increases stretching produces increased firing via their mechanically-gated ion channels.

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19
Q

Golgi Tendon Organ

A
  • mechanoreceptor involved in proprioception. Plays a role in less conscious muscle activity - such as reflexes.
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20
Q

Are the somatic motor neurons dorsal or ventral to the somatic sensory interneurons?

A

1) Somatic Motor Neurons:
- located in the ventral (anterior) horn of the gray matter.
- Control skeletal muscles.
- Efferent neurons (carry signals form the CNS to effectors)

2) Somatic sensory interneurons:
- located in the dorsal (posterior) horn of the gray matter.
- process sensory information from the body.
- afferent neurons (carry signals from sensory organs to the central nervous system)

-> positioning due to layout of the spinal cord, with sensory neurons entering the dorsal root and motor neurons exiting via the ventral root.

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21
Q

What are the characteristics of the different order neurons?

A

1) First-order neuron:
- primary sensory neuron
- body: ipsilateral dorsal root ganglion
- face: trimegemial ganglion

2) Second-order neuron:
- brainstem relay station
- body: ipsilateral gracile/cuneate nuclei
- face: trigeminal nucleus

3) Third-order neuron:
- thalamic relay station
- body; contralateral (lateral) nuclei in thalamus
- face: contralateral (medial) nuclei in the thalamus

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22
Q

What are the roles of the different order neurons in “cutaneous touch”?

A

1) First order:
- brings in sensory information from ipsilateral side

2) Second order:
- sends information (axons) to contralateral side (decussation)

3) Third order:
- Sends information to cortex

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23
Q

Pathway in proprioception

A

1) Lower body Proprioception:
- follows dorsal spinocerebellar tract via Clarke’s nucleus.
- First-order neurons synapse in Clarke’s nucleus.
- Second-order neurons ascend to the ipsilateral cerebellum.

2) Upper Body Proprioception:
- Similar to tactile pathway, involving external cuneate nucleus.
- First order neurons synapse in the external cuneate nucleus.
- Second-order neurons convey the information to the ipsilateral cerebellum.

3) General:
- synapse onto the ipsilateral cerebellum - involved in unconscious proprioception.

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24
Q

Somatotopic Representation

A
  • The representation of body parts and
    the various types of sensations are
    highly organized in the thalamus and
    the cortex!
  • The organization of the somatosensory cortex has no relationship to the actual
    proportions of our body.
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25
Q

What is sound?

A
  • displacement of air molecules - pressure waves generated by vibrating air molecules.
  • waveform = its amplitude plotted against time.
  • simplest type of sound is a pure tone (e.g. tuning fork). or a single sine wave (pure tones are NOT common in real life).
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26
Q

What are the properties of sound?

A
  • amplitude = dB
  • frequency = Hz
  • Waveform (amplitude across time)
  • Phase - every cycle of the soundwave. The exact point in time for which the sound is being perceived. Important for localizing where sound comes from.
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27
Q

Complex Sounds

A
  • sounds like speech, music, and environmental stimuli contain energy, distributed across a broad frequency spectrum.
  • examples of different natural sounds.
  • animal vocalizations, speech and music contain highly periodic (tonal and harmonic) elements, whereas environmental sounds such as wind lack periodic structure.
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28
Q

The audible spectrum

A
  • different species emphasize the frequency of their own vocalizations
  • for humans, 20hz to 20kHz
  • as we get older, stop stop being able to hear the higher frequency
  • max 15-17 Hz as an adult
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29
Q

The auditory system

A
  • there is mechnoelectrical transduction of sound (air vibrations) into neural activity.
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30
Q

Auditory Function

A
  • Auditory system transform sound (air vibration patterns) into neural activity (mechanoelectric transduction)

1) External and middle ears collect and amplify sound waves and transmit to the fluid filled cochlea of inner ear.

2) In the inner ear, hair cells transduce frequency, amplitude, and phase of the signal into electrical signals.

3) Acoustical decomposition results in systemic representation of sound frequency along the length of the cochlea (tonotopy).

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31
Q

External Ear

A
  • Pinna, Concha, Auditory Meatus
  • Boosts and filters sound input
  • Provides clues on the elevation or amplitude of the sound (is the sound coming from up or down)
  • The auditory meatus boosts and concentrates sounds at frequencies around 3khz and focuses this sound energy onto the tympanic membrane.
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32
Q

Middle Ear

A
  • transition of sound from air to water through bones (malleus, incus, stapes)
  • amplification: pressure of the sound get kind of boosted from the tympanic membrane to the ear by 200x
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33
Q

What is the efficiency of sound transmission in the inner ear regulated by?

A
  • tensor tympani
  • stapedius muscles
  • when paralyzed = hyperacusis
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34
Q

The inner ear

A
  • the cochlea transforms sonically generated pressure waves into neural impulses carried by the auditory nerve (sensory transduction) to the cortex
  • also acts as a mechanical frequency analyzer - decomposing acoustical waveforms into their elements - tonotopy
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35
Q

The cochlea

A
  • fluid filled (perilymph/endolymph) tube with specialized hair cells
  • sound waves (in scala media fluid) cause the basilar membrane to vibrate.
  • vibrations cause hair cells to press against tectorial membrane and produce action potentials.
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36
Q

The Cochlea: Basilar Membrane

A
  • differentially sensitive to different frequencies (varying stiffness)
  • base -> high frequencies
  • apex -> low frequencies
    this is called TONOTOPY
  • a complex sound will displace membrane in several regions
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37
Q

Transduction: Hair Cells

A

Hair cells
- sensory neurons
- between the basilar membrane and tectorial membranes

  • inner hair cells: transduction
  • outer hair cells: efferent innervation
    -> cochlear amplifier
    -> otoacoustic emissions
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38
Q

Hair cells and the mechanotransudction of sound waves

A
  • B-tip links that connect adjacent stereocilia are believed to be mechanical linkages that open and close transduction channels
  • inner hair cells are the sensory receptors
  • each hair bundle contains from 30 to a few hundred stereocilia - they are graded in height and arranged in a bilaterally symmetrical fashion.
  • fine filamentouts structures - tip links, connect the tops of adjacent stereocilia and translate hair bundle movement into a receptor potential
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39
Q

Physiology of Inner Ear

A
  • Endocochlear Potential (potential difference between endolymph and perilymph, essential for hair cell function and signal transmission).
  • Endolymph:
    Stereocilia of hair cells
    Rich in K+, poor in Na+
  • Perilymph:
  • Basal surface of hair cells
  • Poor in K+, rich in Na+
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40
Q

What is the process of transduction of hair cells?

A
  • inner hair cells have cilia that have tip links. cilia are displaced.
  • tip links mechanically pull open K+ channels.
  • hair cells depolarize:
    Ca2+ influx
    Neurotransmitter release onto auditory nerve.
  • movement in the opposite direction compresses the tip-links, closes the channels and hyper polarizes the cell.
  • because some channels are open at rest, the receptor potential is biphasic.
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41
Q

Transduction of sound waves

A
  • movement of the stereocilia back & forth modulates ionic flow to produce a graded receptor potential.
  • transmitter release triggers action potential in CN VIII following the up and down vibration of the basilar membrane.
  • Hair cell transduction is fast & sensitive - 10 microseconds - essential for sound localization.
  • Mechanical gating of ion channels is essential for this rapid, high resolution signal.
  • Damage to stereocilia (by high intensity sounds) leads to irreversible hearing loss.
  • damage to tip-links leads to temporary hearing loss as tip links can regenerate within hours.
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42
Q

Auditory Tuning

A
  • auditory nerves fire in the rising phase of low frequency sounds (ie. <3kHz)
    (hair cells potential is biphasic but only release neurotransmitter when depolarized)

-»»> this allows for phase locking

-»> sound localization

43
Q

What does the Cochlear Nerve (CN VIII) synapse on?

A
  • the cochlear nucleus
    -> Anteroventral
    -> Posteroventral
    -> Dorsal
44
Q

What does the Cochlear nucleus synapse?

A
  • Superior olivary complex (pons)
  • Monaural pathways
  • Inferior colliculus (midbrain)

-> high degree of bilateral connectivity
-> Bilateral connectivity supports binaural processing and localization of sound based on binaural differences
-> from the cochlea to the brainstem

45
Q

Location of sound: Two systems ITD & IID

A

1) Interaural timing differences:

  • produced by the difference in time it takes for sound to reach ear based on the location of the sound source relative to each ear.
  • humans detect ITDs of 10 microseconds.
  • Artificial manipulation of ITDs creates perception of sound arising from side of the leading ear.
46
Q

Olivary Complex: ITD

A
  • ITD allows for sound localization
    below 3kHz - requires phase locking
  • Coincidence detector in the medial superior olive (MSO)
47
Q

Olivary Complex: IID

A
  • Interneural Intensity Difference allows for sound localization greate than 2kHz - head acts as a “shadow sound”
  • difference in volume processed in lateral superior olive & medial nucleus of trapezoid body
48
Q

Horizontal Plane (Sound)

A

1) Interaural time difference
- low frequency sounds
- MSO

2) Interaural intensity difference
- high frequency sounds
- LSO

49
Q

Vertical plane (elevation - sounds)

A
  • spectral filtering by the external pinna (outer ear)
  • processed in the dorsal cochlear nucleus
50
Q

Monaural Pathways

A
  • information from one ear is represented
  • contralateral nucleus of the lateral lemniscus
  • onset and duration
51
Q

Where does all the sources of sound converge?

A

1) inferior colliculus:
- integration of sound
- timing, intensity, frequency
- topographic auditory space

52
Q

Where does all auditory information pass through?

A

Medial Geniculate Complex (MGC) in the Thalamus.

Detects temporal and spectral information about sound.

53
Q

The Auditory Cortex

A

1) Primary Cortex
- precise tonotopic representation
- inputs from ventral MGC

2) Secondary cortex (belt & parabelt)
- pitch perception & speech comprehension (wernicke’s are)
- input from dorsal MGC

  • reciprocal connections
  • essential for conscious perception of sound including speech recognition
54
Q

Where can vestibular hair cells be found?

A
  • Ampullae (vertical motion)
  • Utricle (horizontal motion)
  • Saccule (rotation)
  • specialized ionic environments created by endolymph and perilymph.
  • the macula is a sensory epithelium in the utricle and saccule
  • hair bundles project into a gelatinous layer
  • above this is the otolithic layer
55
Q

Peripheral Vestibular System

A

Labyrinth (effects of gravity from head movements) - set of interconnected chambers, continious with the cohlea (airborne sound stimuli) , buried deep in the tempoeral bone.

Consist of two otolith organs: utricle and sacule and 3 semicircular cannals.

56
Q

Vestibular Hair Cells

A
  • Much like auditory hair cells
  • Transduce minute displacements into receptor potentials
  • Movement of the stereocilia toward the kinocilium opens mechanically gated transduction channels located at the tips of the stereocilia to depolarize the cell and induce neurotransmitter
    release into the vestibular nerve fibers.
  • Movement of the stereocilia away from kinocilium closes the channels, hyperpolarizing the cell and
    reducing vestibular nerve activity
57
Q

When will hair bundle displacement occur?

A
  • tonically in response to head tilts
  • transiently in response to translational hair movements (when you are moving in a car)
58
Q

Sensory Transduction

A
  • The semi circular canals register
    head movements in three planes.
    The hair cells in the cupula orient in
    the same direction:

Superior canal = x-axis
Posterior canal = y-axis
Horizontal canal = z-axis

  • 3 semi-circular canals sense head rotations arising from self movement or angular accelerations imparted by external force (e.g merry go round, roller coaster)
  • sensory epithelium - crista - is found at each bulbous expansion (ampulla) on each canal.
  • hair bunds extend into a gelatinous mass - cupula.
  • the cupula bridges the entire width of the ampulla and prevents circulation of the endolymph.
  • all hair cells (hair bundles) point in the same direction (no striola or mirror axis).
59
Q

Vestibulo-ocular Reflex

A
  • mechanism for producing eye movements that counter head movements.
  • the VOR permits the gaze to remain fixed on a particular point.
  • e.g.- head turning left, activity in the left horizontal canal excites neurons in the left vestibular nucleus and this results in compensatory eye movements to the right.
60
Q

What is the pathway of vestibular nerve fibres?

A
  • vestibular nerve fibres from the left semicircular canal project to the medial and lateral vestibular nuclei
  • excitatory fibers from the medial vestibular nuclei cross to the contralateral abducens nucleus
  • the outputs of the abducens nucleus are:
  • a motor pathway that causes the lateral rectus muscle of the right eye to contract.
  • an excitatory projection that crosses the midline (via the medial longitudinal fasciculus) to the left oculomotor nucleus, where it activates neurons that cause the medial rectus muscle of the left eye to contract.
61
Q

Phototransduction

A
  • 4 OPSIN PROTEINS
  • there is sensitivity to light from binding to retinal, the molecule absorbing photon energy
  • when two types of photoreceptors: rods (x1) and cones (x3). Each has its own opsin protein fro sensory transduction.

Dark:
- rhodopsin: rods

Light:
- Red cone opsin
- Green cone opsin
- blue cone opsin

62
Q

What is the process of phototransduction when it is dark outside?

A

1) Opsin phosphorylation (by rhodopsin kinase)

2) Arrestin stops transducin

3) No hydrolyzed cGMP

4) More cGMP = depolarization

63
Q

What is the process of phototransduction when it is light outside?

A

1) Retinal binding

2) Retinoid Cycle
-> Photoisomerization
-> all-trans retinal to all-trans retinol
-> Interphotoreceptor retinoid binding protein
-> 11-cis retinol to 11-cis retinal (ready for retinal binding)

3) Transducin -> phophodiesterase -> hydrolyzed cGMP

4) Less cGMP = hyperpolarization

64
Q

Tritanopia

A
  • light: colour blindness
  • no functional blue cone opsins - visual acuity is not noticeably reduced since blue cones are not very sensitive to light.
65
Q

Protanopia

A
  • light: colour blindness
  • no functional red cone opsins
66
Q

Deuteranopia

A
  • light: colour blindness
  • no functional green cone opsins
67
Q

Archromatopsia

A
  • light: colour blindness
  • no functional cones
68
Q

Light pathway: Eye to Cortex

A

1) light enters the eye through the cornea, which bends the light.
2) Epithelial cells (outermost layer of the eye)
3) Cones and Rods (photoreceptors) located in the retina.
4) Retinal Ganglion Cells & Bipolar Cells.
- Bipolar: connects photoreceptors to retinal ganglion cells.
- then axons form the optic nerve and sends information to the brain!

69
Q

Eye movements

A

1) Saccadic
- Rapid, jerky shifts

2) Pursuit
- Follows moving objects

70
Q

Receptive field in the centre of retina (fovea)

A

Fovea (also called the macula lutea)
- only contains cone cells
- one to connection of photoceptors to bipolar to ganglion cells
- high resolution
- colour vision

71
Q

Receptive field in periphery of retina

A
  • peripheral vision
  • convergence to multiple cells
  • low resolution
  • faint light and shapes
72
Q

What regulates photoreceptor membrane potentials?

A
  • cyclic-GMP gates channels
73
Q

Photoreceptors

A
  • no action potentials
  • graded glutamate release at between -40mV and -70mV
  • leaky sodium ion channels are open in dark and already depolarized
  • release more glutamate in the dark than in the light
74
Q

Horizontal cells

A
  • regulate adjacent photoreceptor and bipolar cells
  • mediate the surround response.
  • while the horizontal cells receive glutamate from cone cells, they may also reciprocally inhibit centre cone cells to influence net depolarization.
75
Q

Bipolar cells

A
  • there are ON bipolar cells and OFF bipolar cells
  • no action potential
  • graded glutamate release depending on membrane potential
  • ON in the sun, OFF in the dark.
76
Q

What are the characteristics of ON bipolar cells in the dark vs the light?

A

1) Dark:
- Sodium channels open -> depolarized.
- Photoreceptors release more glutamate.
- ON bipolar cells have inhibitory metabotropic glutamate.
- ON bipolar cells inhibited by glutamate.

2) Light:
- sodium channels close -> hyperpolarized.
- photoreceptors release less glutamate.
- ON bipolar cells are less inhibted.

77
Q

What are the characteristics of OFF bipolar cells in the dark vs the light?

A

1) Dark:
- Sodium channels open -> depolarized.
- Photoreceptors release more glutamate.
- OFF bipolar cells have inhibitory metabotropic glutamate.
- OFF bipolar cells excited by glutamate.

2) Light:
- sodium channels close -> hyperpolarized.
- photoreceptors release less glutamate.
- OFF bipolar cells hyperpolarize.

78
Q

Amacrine cells

A

Regulate excitability of adjacent bipolar and ganglion cells.

79
Q

Ganglion cells

A
  • have action potentials and are excited by glutamate.
  • have centre-surround receptive fields for light and colour.
  • receptive field: area of the visual space (relative to a fixation point) where light is capable of changing the activity of a neuron.
80
Q

Retinal Pathways: Amacrine cells

A

-> Day vision:
Cone bipolar cells synapse directly with ganglion cells.

-> Night Vision:
- rod cells synapse with A2 amacrine cells which then transfer potentials to ON bipolar cells and finally ganglion cells.

  • sensitivity to the direction of light is driven by asymmetrical inhibition:

1) Starbust amacrine cells (SAC) inhibit one side of a ganglion dendritic field.

2) If light comes from preferred direction, ganglion cells excited by bipolar cells before it is inhibited by SAC.

3) If light comes from opposite (null) direction, SAC’s activated first -> inhibition blocks bipolar excitation.

81
Q

What is the pathway of conscious vision vs subconscious vision?

A

1) Conscious vision:
Lateral Geniculate Nucleus to V1

2) Subconscious Vision:
Reflexes, circadian rhythms, subconscious perception.

82
Q

Subconscious Vision: Pupil Reflex

A
  • Crucial in regulating the size of the pupil in response to changes in light intensity.
  • helps control the amount of light entering the eye and maintaining visual clarity.

When its light:
1) RCs to pretectum
2) Edinger-Westphal nucleus
3) Oculomotor nerve -> Cilary Ganglion
4) Contrictor muscles of iris

83
Q

Subconscious Vision: Optokinetic Reflex

A
  • Gaze stabilizing reflex with fast saccades and sow smooth pursuit component.
  • Direction sensitive RGCs
  • Nucleus of the optical tract
  • Oculomotor nerve -> cilary ganglion.
  • Constrictor muscles of iris.
  • stabilizes vision while there is continuous motion (e.g. viewing large moving scenes).
  • even such a relatively simple reflex results in wide-scale activity throughout the brain.
84
Q

Primary Visual Pathway

A
  • Retinal ganglion cells project to the lateral geniculate nucleus of the thalamus.
  • LGN serves as a relay station, relaying input from the optic tract and transmitting info to the primary visual cortex.
85
Q

What is the difference between the temporal and nasal half of the retina?

A
  • temporal retina corresponds to the outer portion of the retina.
  • nasal: inner portion.
  • light -> retina -> electrical signals -> optic nerve to brain (cross over happens at optic chiasm)
  • fibers carrying visual information from the temporal halves remain on the same side while fibres carrying information from the nasal halves of the retinas cross over to the opposite side.
86
Q

Binocular Vision

A
  • Each eye has its own distinct visual field providing different perspectives of the external environment.
  • Brain creates a unified and 3D perception of the world.
  • Central visual field relies on input from both eyes.
  • Peripheral vision depends on input from one eye or the other (monocular vision).
  • Optical flipping of images are projected to the retina.
87
Q

Projections from LGN to V1

A
  • There are different paths from LGN to V1 depending on represention from superior vs inferior visual fields (differential pathways from lgn to V1)
  • Superior visual field -> inferior portion of V1.
  • Inferior visual field -> superior portion of V1.
88
Q

Lateral Geniculate Nucleus (Visual Pathway from Retinal Ganglion Cells (RGCs) to Visual Cortex (V1))

A

1) Parasol Ganglion Cells:
Type of RGCs.
Project to the magnocellular layers of the Lateral Geniculate Nucleus (LGN).
From LGN, they synapse onto Layer 4Ca of the Primary Visual Cortex (V1).

2) Midget Ganglion Cells:
Type of RGCs.
Project to the parvocellular layers of the LGN.
From LGN, they synapse onto Layer 4Cb of the Primary Visual Cortex (V1).

3) Non-Midget and Non-Parasol Ganglion Cells:
Type of RGCs.
Project to the koniocellular layers of the LGN.
From LGN, they synapse onto Layer 2/3 of the Primary Visual Cortex (V1).

89
Q

Hubel Experiments

A
  • Discovery of orientation-selective
    neurons in the visual cortex.
  • Certain neurons in V1 respond
    selectively to specific orientations
    of visual stimuli such as vertical,
    horizontal or diagonal edges.
  • Experiments revealed hierarchical
    organization of visual processing
    in the brain.
90
Q

What areas are beyond V1?

A
  • MT (v5)-> selectivity for
    motion, direction and speed
    of objects
  • v4 -> colour selective cells.
91
Q

Face Cells

A
  • Mostly found in higher visual areas of the brain.
  • Selectivity for facial features over other stimuli.
92
Q

Vision Loss and Restoration

A
  • Eye based vision loss.
  • Leading cause of visual impairment in the world -> uncorrected refraction errors (people not having access to glasses)
  • common issues:
    cataracts, glaucoma, macular degeneration, retinitis pigmentosa, diabetic retinopathy.
93
Q

Cataracts

A
  • Clouding of the lens
  • Half blindness and 1/3 visual impairment world wide
  • Can be born with it but most likely due to aging
  • Risk factors:
  • Smoking, diabetes, prolonged exposure to sunlight
  • First cataracts ‘surgery’ done 3000 years ago.
  • can be replaced with a new lens.
94
Q

Glaucoma

A
  • Cause is not 100% known but has
    to do with an issue in the recycling
    of the aqueous and vitreous humor.
    (too much fluid leads up to
    pressure to the nerve head and
    ganglion cell death).
  • second leading cause of blindness after cataracts.
  • risk factors: increased intraocular pressure and family history of the condition.
  • may result from increased intraocular pressure, lead to damage of the optic nerve.
95
Q

Macular Degeneration

A
  • affects photoreceptors in the macula
    and fovea (macula lutea), affecting high resolution
    central vision.
  • Wet AMD~ 10% of AMD- arises
    from ‘leaky’ blood vessels behind
    the retina that disturn the connection
    between retina and retinal pigment
    epithelium.
  • Dry AMD- 90% of AMD.
  • More slowly progressing, but no
    good treatments.
  • often age related.
96
Q

Retinitis Pigmentosa

A
  • Heterogenous group of hereditary diseases.
  • results in photoreceptor degeneration in the peripheral retina.
  • results in night-blindness and tunnel vision.
  • mutation in rods.
97
Q

Diabetic Retinopathy

A
  • Leading cause of blindness in the US.
  • Affects 80% of people have had diabetes for at least 20 years.
  • Damage can be caused by macular edema -> blood vessels leak their contents into the eye/retina.
98
Q

Brain based visual impairments

A
  • blindsight
  • hemispatial neglect
  • cerebral akinetopsia
  • prosopagnosia
99
Q

Blindsight

A
  • Damage to primary visual cortex (v1)
  • Loss of conscious blindness
  • However other subconscious form of vision passing via de superior
    colliculus or LGN to secondary visual areas can persist
  • Residual visual function
100
Q

Hemispatial Neglect

A
  • Usually arising from strokes and brain injury occurring unilaterally in the right cerebral hemisphere in the
    parietal lobe (so the left visual field is
    neglected).
  • Though all the visual scene is ‘seen’
    by the eyes, people with certain brain
    injuries not only are unable to see half
    the visual field, but they can also be
    totally unaware of what they are
    missing.
101
Q

Cerebral Akinetopsia

A
  • Motion blindness
  • Can arise from damage to the visual motion sensitive middle temporal area (MT)
  • moving images appear as slowly refreshing static images.
102
Q

Prosopagnosia

A
  • Prosopagnosia is thought to arise
    after damage to, or improper
    development of, face selective visual
    regions in the inferotemporal cortex
    (high visual areas in the ventral
    stream)
  • characterized by difficulty
    recognizing familiar faces, including
    those of family members, friends,
    and acquaintances. Individuals with
    prosopagnosia may have intact
    vision and cognitive functioning but
    experience specific challenges in
    identifying and remembering faces.
103
Q

Vision Restoration for gene-based problems

A

1) Cell therapy:
- a stem cell approach to grow different retinal cell types for implant.

2) Gene therapy:
- Delivering healthy gene copies through adeno-associated viruses.

3) Retinal Prosthetic Implants:
- Implantation of an electronic chip electrically stimulates RGCs.

4) Optogenetic Therapy:
- Delivery of optogenetic channels to neurons that are normally light-insensitive.

104
Q
A