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65 Cards in this Set
- Front
- Back
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optic nerve |
axons of the optic ganglion cells |
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optic chiasm |
location when ganglion cell axons cross |
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lateral geniculate nucleus |
recieves inputs from the optic nerve |
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thalamus |
subcortical sensory structure |
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primary visual cortex |
contains simple and complex cells (V1) |
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striate cortex |
another name for V1 |
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retinotopic map |
organization by location in the visual field |
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iris |
controls diameter of the pupil |
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pupil |
lets light into the eye |
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rods |
photoreceptors sensitive to light, high convergence |
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cones |
photoreceptors sensitive to colour, low convergence |
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fovea |
specialized area of the eye for high-acuity vision, high density of cones |
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photoreceptors |
sensory cells that translate light stimulus itno changes in membrane potential |
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retina |
located in back of eye, contains photoreceptors, bipolar cells, retinal ganglion cells, horizontal and amacrine cells |
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blind spot |
area of eye with no photoreceptors |
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process of retinal signalling |
light activates photoreceptors → signal goes to bipolar cells → RGCs → horizontal + amacrine cells modify the signals |
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rhodopsin - where found, made of, how does it work |
found in rods - opsin: GPCR - retinal: molecule that absorbs light, derived from vitamin A → light changes the orientation of retinal, which activates opsin → GPCR initiates a signaling cascade → closure of Na+ channels |
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phototransduction |
- light: hyperpolarizes, less glutamate release - dark: depolarizes, more glutamate release |
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lateral inhibition |
- causes photoreceptors in the surround to have the opposite response as the photoreceptors in the center - horizontal cells enhance the difference in activity level between the center and surrounding cones - creates optical illusions |
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retinal ganglion cells |
respond to contrast |
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simple cells in V1 |
- have ON/OFF region - stimulated by bars of light in ON region - small receptive fields, and sensitive to line orientation |
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complex cells in V1 |
- receptive fields larger and more complex than simple cells - also orientation selective, respond to movement of lines over larger area |
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V1 → ? |
V1 → Ventral or Dorsal pathway - ventral pathway goes through inferotemporal cortex - dorsal pathway goes through posterior parietal cortex |
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akinetopsia |
- inability to see movements in a smooth fashion - caused by damage to MT area (V5), part of dorsal pathway |
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prosopagnosia |
impairment in face recognition - caused by damage to fusiform face area (ventral surface of temporal lobe) |
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timbre |
quality of the sound |
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sound waves enter the ear canal and... |
cause the ympaic membrane to vibrate at the same frequency |
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the tympanic membrane pushes on the: |
ossicles that press on the oval window of the cochlea |
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cochlea |
filled with fluid, vibrating oval window generates a pressure wave through fluid → wave goes to apex of cochlea then travels back to where it dissipates in the round window 2 membrane: tectorial, basilar |
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auditory transduction |
takes place in the hair cells on the basilar membrane when basilar membrane moves up and down, hair cells on top will move → push over stereocilia → channels open, positive ions enter cell, depolarization (graded potential) → graded potential causes vgCach to open → hair cells releases more glutamate onto auditory nerve → AP → brain |
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what has allowed the creation of cochlear implants |
tonotopic organization of teh basilar membrane |
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superior olivary nuclei |
receive inputs from both ears and help determine the localization of sound - via orderly maps of ITDs |
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ITD |
interneural time difference, caused by sound coming from the side also causes a difference in sound intensity in ear |
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where is sound intensity processed |
brainstem |
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sound signals from thalamus → |
primary auditory cortex (A1), in temporal lobe, tucked into lateral fissu |
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A1 |
organized tonotopically in columns, neurons in one column of A1 cortex all respond best to one particular frequency of sound A2 surrounds A1 |
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after A1 → A2 |
signals go anterior to frontal lobe or posteriorly to parietal lobe |
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association cortex |
areas of cortex where signals from different sensory systems interact |
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mechanoreceptors |
sense light touch and pressure, have ion channels that are mechanically-gated, open when membrane deformed |
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thermoreceptors |
sense temperature, ion channels that are temp sensitive |
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nociceptors |
respond to noxious stimular that we perceive as pain e.g. extreme temp. extreme pressure, chemicals released by damaged tissue |
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propioceptors |
located in skeletal muscles, tendons, joints, send information about body's position to the brain → proper voluntary movement |
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dorsal root (+ganglion) |
dorsal root: where sensory nerves enter the spinal cord dorsal root ganglion: where cell bodies of sensory neurons lie, just outside of spinal cord |
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dermatome |
area of body innverated by a particular dorsal root |
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somatotopic map |
somatosensory cortex organized by body position, areas devoted to certain parts of body not proportional to area of skin |
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large area in somatosensory cortex |
= more sensory neurons with smaller receptive fields in periphery high density of sensory neurons in area where we have fine discrimination of touch |
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phantom limb pain |
partially result of plasticity of somatosensory cortex, neighboring areas take over the region of S1 that was previously innvervated by the amputated limb |
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ACC |
anterior cingulate cortex, seems to be involved with the emotional response to pain, also active during socially stressful/painful situations → if ACC removed, patient feels pain, but does not bother them |
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skeletal muscles |
AKA extrafusal muscle, attaches to bones via tendons and produce the force necessary to move the different parts of the body |
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(alpha) motor neurons |
control muscle contraction at synapses called the NMJ (neuromuscular junction) |
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NMJ |
neuromuscular junction, always cholinergic and always excitatory, muscles have nicotinic acetylcholine receptors |
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when motor neurons releases NT onto muscle |
cause AP in muscle → muscle contraction |
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two types of propioceptors |
golgi tendon organ muscle spindle |
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golgi tendon organ |
embedded in tendons, sense muscle tension - the more tension in the muscle, the more tendon will be pulled, the more AP in GTO - also participates in reflex: protects muscle + tendons from damage → automatic, fast and unconscious, only involves spinal cord and brain |
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muscle spindle |
embedded in muscle tissue, senses muscle length -muscle spindle has own muscle fibers on either ends, intrafusal muscle, controlled by gamma motor neurons |
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why do muscle spindles have their own muscles |
during muscle contraction, extrafusal muscle → shorter, spine gets shorter an no longer be stretched, can't fire AP silent muscle spindle useless, no longer sending info about body position to brain during muscle contraction, gamma MN cause IF muscle to contract, tightens up muscle spindle, so can always send AP to brain |
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TMS |
transcranial magnetic stimulation: can be used to study the organization of the motor cortex - TMS coil placed on head, creates a magnetic field, induces an electric field in the underlying cortex → stimulating the neurons in the area |
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secondary motor areas |
1. premotor cortex 2. supplementary motor area involved in planning complex movements, receive inputs from sensory association areas (mvmt in response to sensory stimulus) + prefrontal cortex (mvmt consciously planned) |
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fMRI |
functional magnetic resonance imaging - use large magnetic field to scan brains, measures differences in blood flow to brain (active neurons: oxygen + glucose) |
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cerebellum |
connection between parts of NS, receives input from sensory systems (propioception), communicates with cortex, thalamus, brainstem → important for regulating mvmt accuracy, error correction, compares intended movement to actual movements and makes adjustments |
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basal ganglia |
groups of neurons connected to each other under the cortex, include striatum + substantia nigra → form circuit with thalamus and cortex to influence motor signals |
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huntington disease |
hyperkinetic disorder caused by degeneration of the striatum caused by mutation of huntingtin gene inherited dominantly → age of onset 35-45 years old → mutant protein clumps up inside neurons, might damage cells → neurons in striatum usually the first to die off in HD, but neurodegeneration will spread through the cortex eventually, loss of neurons in the striatum specifically affects the indirect pathway → no cure, but embryo selection can help stop the disease from being passed to offspring |
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parkinson disease |
hypokinetic disorder caused by the degeneration of the substantia nigra slower movement, difficulty initiating movement, shuffling walk, rigidity and trembling of extremities → not caused by problem with single gene, environment also plays a role → dopaminergic in substantia nigra progressively die off → too much activation of direct pathway, more inhibitory signals are going to the thalamus and cortex, making it harder to start movements → no cure, but helpfultreatments |
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treatments for parkinson disease |
deep brain stimulation - electrodes implanted in basal ganglia, helps relieve motor symptoms, used once L-dopa stops working |
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Braille |
fingers have small receptive fields, firing → dots → respond as skin is stretched by the dot, large receptive fields prevent a representation of form, good for detecting vibration and texture |
