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208 Cards in this Set
- Front
- Back
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receptor potential
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a local depolarization or yperpolarization of a receptor membrane (like EPSP) strength determines the amount of excitation or inhibition the receptor sends to th enext neuron on the way to the brain
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tranduce
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when energy is converted into an electrochemical pattern in the brain
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law of specific nerve energies
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Johannes Muller
whatever excites a particular nerve establishes a special kind of energy unique to that nerve, any activity by a particular nerve always conveys the same kind of info to the brain one kind of message-action potentials |
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pupil
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where light enters the eye, opening in the center of the iris
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retina
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rear surface of the eye, lined with visual receptors (rods/cones)
light from th eright side of the world strikes left (vise versa_ light from bottom strikes top (vise versa) innerverted image |
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reception
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light energy attaches to receptors
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transduction
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receptors convert energy of a chemical reaction into an action potential, change from external energy to the energy in th enervous sysetm
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coding
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spatial/temporal patterns of nerve impulses represent the stimulis in some meaningful way (what you think)
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bipolar cells
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receptors in eye send messages to bipolar cells, located closer to the center of the eye
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ganglion cells
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bipolar cells send their message sto ganglion cells, closer to the center of the eye
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macula
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responds to details, contains fovea
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fovea
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central proportion in macula, specialized for acute, detail vision, least impeded vision bc blood vessels, ganglion cells axons are almost absent near the fovea
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cornea
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focus of light on retina
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lens
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finetune focusing process
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blind spot
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pt at which optic nerve leaves eye, no receptors
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why we dont see the cells in our eyes
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1)transparent
2)lack of movement-cells stay in the same position-rods/cones become insensitive-like they dont exist, eyes is always moving, jerky movements allow us to move |
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amacrine cells
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get info from bipolar cells, numerous, diverse, control the ability of ganglion cells to respond sto shapes, movement etc.
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optive nerve
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ganglion cell axons band together to form the optic nerve, an axon bundle that exits through the back of the eye
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midget ganglion cells
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ganglion cells in the fovea are small and respond to a single cone and connect from a single bipolar cell
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birds
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2 fovea, greater density of visual receptors in top of retina
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rods
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most abundunt in the peripherary of the human retina, respond to faint light
outnumber cones more needed for nightime vison-higher in species that come out only at night |
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cones
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most abundunt in and around the fovea, bright light, color vision
more direct route to the brain-each receptor has own line to the brain |
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photopigments
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in codes,rods
chemicals that release energy when struck by light consist of 11-cisretinal, light energy converts it to all-trans retinal, releases energby that activates second chemical messngers in the cell |
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shot wave lengths
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violet, 350nm
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long wave lengths
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blue, green , yellow, red, near 700 nm
wavelengths vary over a continum but we percieve them as several distinct colors |
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no single neuron can simultaneously indicate
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brightness and color
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trichromatic theory of color vision/Young-Helmholtz
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we percieve color through the relative rates of response by three kinda of cones, each maximally sensitive to a different set of wavelengths
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wavelength-sensitivity for cones
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short wavelength (violet), medium-wavelength, long wavelength(red) each cones responds to a broad band of wavelengths but best to wavelengths ina particular range
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WHEN ALL THREE CONES ARE EQUALLY ACTIVE WE SEE
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WHITE OR GREY
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nervous system can determine the color and brightness of the light only by
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comparing the responses from all 3 cones
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long and medium wavelenth cones are far more
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abundunt then shorter ones
cones rae also dsitributed randomly |
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visual field
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the part of the world that you can see
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opponent process theory
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we percieve color in terms of paired oopositis, red and green, yellow and blue, white and black
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color constancy
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limitations of the theories
ability to recognize the color of an object despite changes in lighting requires a comparison of a varity of objects in altered lighting |
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retinex theory
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Edwin Land
to account for color and brightness constancy...the cortex comapres info from various part sof the retina to determine the brightness and color for each area |
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color vision deficiency
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an impairment in perceiving color differences
it is possible t have satisfactory vision when being color impaired, color depends on what our brains do with incoming light, it is not a propert yof light itself |
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retinohypothalmic path
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responds to light/dark, path the retina contains, sends signals to the brain regarding circadian rythms
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horizontal cells
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rods and cones of the retina make synaptic contact with horizntal cells and bipolar cells, horizontal cells make inhibitory contact onto bipolar cells
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optic chiasm
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optic nerves from th etwo eyes meet at the optic chiasm and then travel to opposite side of the brain...the other half of th eoptic nerves stays on the ipsilateral (same side) of the brain
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lateral geniculate nucleus
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must of the ganglion cells axons go here, a nuceus of the thalmus specialized for visual perception (relay station) sends axons to other parts of the thalmus and to the visual areas of th eoccipital lobe
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superior colliculus
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smaller number of axons go here
unconscious aspects of vision-may be responsible for blind sight |
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lateral inhibition
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retinas way of sharpening contrasts to emphasize the borders between one object and another
the reduction of activity in one neuron by the activity in neighboring neurons |
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rods/cones
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have inhibitory synapses onto bipolar cells so light decreases their inhibitory effects-so they do excite bipolar cells
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level of activity by inhibitry horiz cells.....see pg 169 bc this is poco complicated
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greatest excitatory activity-middle, least activity is outside
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receptive field
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area of visual field striking receptoreach cell in the visual system has a receptive field, which is part of the visual field that either excites or inhibits it
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the receptive field of a ganglion cell
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combined receptive fields of previous receptors (bipolar cels connectedto receptors)
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categories of ganglion cells
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parvocellular, magnocellular, koniocellular
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parvocellular
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small cell bodies, small receptiv fields, mostly in or near the fovea
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color constancy
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limitations of the theories
ability to recognize the color of an object despite changes in lighting requires a comparison of a varity of objects in altered lighting |
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retinex theory
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Edwin Land
to account for color and brightness constancy...the cortex comapres info from various part sof the retina to determine the brightness and color for each area |
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color vision deficiency
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an impairment in perceiving color differences
it is possible t have satisfactory vision when being color impaired, color depends on what our brains do with incoming light, it is not a propert yof light itself |
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retinohypothalmic path
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responds to light/dark, path the retina contains, sends signals to the brain regarding circadian rythms
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horizontal cells
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rods and cones of the retina make synaptic contact with horizntal cells and bipolar cells, horizontal cells make inhibitory contact onto bipolar cells
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optic chiasm
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optic nerves from th etwo eyes meet at the optic chiasm and then travel to opposite side of the brain...the other half of th eoptic nerves stays on the ipsilateral (same side) of the brain
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lateral geniculate nucleus
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must of the ganglion cells axons go here, a nuceus of the thalmus specialized for visual perception (relay station) sends axons to other parts of the thalmus and to the visual areas of th eoccipital lobe
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superior colliculus
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smaller number of axons go here
unconscious aspects of vision-may be responsible for blind sight |
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lateral inhibition
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retinas way of sharpening contrasts to emphasize the borders between one object and another
the reduction of activity in one neuron by the activity in neighboring neurons |
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rods/cones
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have inhibitory synapses onto bipolar cells so light decreases their inhibitory effects-so they do excite bipolar cells
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level of activity by inhibitry horiz cells.....see pg 169 bc this is poco complicated
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greatest excitatory activity-middle, least activity is outside
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receptive field
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area of visual field striking receptoreach cell in the visual system has a receptive field, which is part of the visual field that either excites or inhibits it
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the receptive field of a ganglion cell
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combined receptive fields of previous receptors (bipolar cels connectedto receptors)
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categories of ganglion cells
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parvocellular, magnocellular, koniocellular
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parvocellular
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small cell bodies, small receptiv fields, mostly in or near the fovea
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magnocellular
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larger, dist evenly throughout the retina
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koniocellular
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small cell bodies
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primary visual cortex (v1)
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in occipital lobe, info from lateral geniculate nucleus, area of cortex responsible for first stag eof visual processing, consciou vision, imagination of visual activity
respond strongly to bar or edge shapped patterns |
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blind sight
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ppl with damage to v1, an ability to resppond in some ways to visual info that they report not seeing may be a result of superior colliculs or tiny islands of helathy tissue remain within an otherwise damaged visual cortex
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secondary visual cortex v2
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info sent from v1..processes info further-recirpical connection v1 to v2, v2 to v1
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ventral stream
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visual pathway in the temporal cortex, "what" pathway, specialized for identifying and recognizing objects
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3 pathways of ventral stream
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1)mostly magnocellular-movement/perception
2)mixedmagno/para-color and brightness 3)parvo-shape analysis (damage=difficulty analyzin faces & shapes) |
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dorsal stream
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visual pathway in parietal cortex
"where or how" integration of movement with vision, helps motor system find objects and determine how to move towards them |
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david hubel/torsten wiesel
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distinguished 3 categories of cells in the visual cortex-simple, complex, end stopped
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columns of neurons in the visual cortex
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cells with the same properties are grouped together in th evisual cortex in columns perpendicular to the surface, process similar info
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feature detectors
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neurons whose responses indicate the presenc eof a particular feature
movement-->motion blindness-->unable to perieve motion |
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waterfall illusion/spinning activity on a blank screen as in class
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prolonged exposure to a given visual feature decreases sensitivity to that feature
a cortical cell that responds best to one stimulis also responds to many others. any object stiulates a large population of cells, and any cell in the visual system responds somwaht to many stimuli |
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inferior temporal cortex
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cells in this area have huge receptive fields, foveal field of vision, their response provide no info about stimulis location, respond selectively to complex shapes, respond to mirror image and reversal of contrast- detect an object no matter how it is displayed
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shape constancy
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ability to recognize an objects shape even as it changes location or direction
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visual agnosia-video with guy
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inability to recognize objects, despite other wise satisfactory vision, damage in temporal cortex
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john in video
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cannot recognize what he is looking at
-hard for him to read a whole word -visual association cortex-perceptions of shapes/patterns-puts together image-blindness dueto damage in visual cortex -can copy objects, identify details-lost ability to see colors -graps things little by little-does not get whoel picture-perceives 1 part at a time....lost some segmnet o fhis consciousness |
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prosopagnosia
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inability to recognize faces, after damage to the fusiform gyrus of th einferior temporal cortex
but pertains to visual expertise of any kind-cars, flowers also respondsto the idea of a face |
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v4
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color constancy, visual attention
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stereoscopic depth perception
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many of the cells of the magnocellular pathway specialized for this-ability to detect depth by the differences in what the two eyes see
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2 temporal areas activated by any type of visual motion
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MT(middle temporal cortex/V5
MST receive info from branches of magnocellular path, respond to stimulis moving a certain direction, also of still photos implying movement respond when an object moves relative to its background |
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MST neurons
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enable you to distinguish bw the result of eye movements and the result of object movements
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saccades
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quick eye movements, why you do not see your own eyes move-br5ain decreases activity in the visual cortex during saccades-neural activity and blood flow decrease previous to saccades
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motion blind
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able to see objects but unable to determine whether they are moving and in what direction
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cat video-cats raised in darkness/horizontal stripes
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3 week-3 month sensitive period
-cats will not follow moving objects, lack visual placing, does not show startle reactions -preffered orientation to horizontal lines-ENVIRONMENTAL MODIFICATION TO FRONTAL CORTEX -peak sensitivity=28 days after birth |
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preffered orientation/normal task
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-preference of vision may be aquired rather then innate
-environmental interactions indicate preference |
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built in "face recognition model"
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infants show strong preference for a right side up face, even if it was a disorted one
even in the first two days of birth infants look more at faces then other stimulis` |
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not until about what age can infants shift visual attention from one object to another
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6 months
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binocular input
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neurons in th evisual cortex receive stimulation from both eyes
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the visual system can mature to a certain point without experience but it needs
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visual experience to maintain and fine tune its connections
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sensitive/critical period
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when experiences have a particularly strong and long lasting influence, last longer during complete visual deprivation, begins when GABA becomes widely available in the cortex
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retinal disparity
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the discrepancy bw what the left and right eye sees, makes possible stereoscopic depth perception (method of perceiving distance)
fine tuning must depend on experience |
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srabismus
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a condition in which the eyes do not point in the same direction, do not develop stereoscopic depth perception
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skeltal muscles
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control movement of th ebody in relation to the environment
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neuromuscular junction
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where a motor neuron axon meets a muscle fiber, pt of transduction, acetylcholine is released from all axon terminals @ the neuromuscular junction
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what excites the muscle to contract
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acetylcholine
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antagonistic muscles
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required for moving a leg or arm in two directions, require opposing sets of muscles (antagonistic)
one flexes, one relaxes, vise versa |
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flexor muscle
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,uscle that flexes or raises limb
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extensor muscle
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muscle that extends or straightens it
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axon fibers of muscles
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can innervate many fibers- making their movements less precise then eye movements
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myasthenia gravis
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any deficit of acteylcholine impairs movement
autoimmune disease, immune system attacks actyl receptors at neuromusculr junctio, causing progressive weakness and fatigue of muscles |
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fast twitch fibers
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produce fast contractions but fatigue slowly
anaerobic begin with aerobic muslce activity with use of glucose as glucose suppl y dwindles , gene is activate dto inhibit further glucose use and the exercise becomes anerobc |
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slow twitch fibers
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less vigorous contractions without fatiguing
nonstrenuous activities lik etalking they are aerobic-use air |
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proprioceptor
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receptor that detects th eposition or movement of a part of the body, muslc eproprioceptors detect the stretch and tension of a muslce and send messages to the spinal cord
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stretch reflex
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when a muslce is streteched th espinal cord sends a reflective signal to contract it, reflex is caused by a stretch it is NOT produced
stretch causes contraction |
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muscle spindle
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type of proprioceptor, a receptor parellel to the muscle that responds to a stretch
causes contraction from stretch (negative feedback system) |
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golgi tendon
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inhibits muscle contraction when too intense, procioreceptor that responds to incraeses in muscle contraction, acts as a brake
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babinski reflex
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spanning of toes
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allied reflexes
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children have more then adults
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ballistic movement
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movement executed as a whole, once initiated it cannot be altered or corrected while it is in progress (stretch reflex, dilation of eyes) many movements are partially ballistic, finger to nose test
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central pattern generators
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neural mechanisms in th espinal cord that generate rythmic patterns of motor output (rapid sequences-speaking, writing,playing musical inst)
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motor program
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fixed sequenceof movements
can be learne dor built in by nervous system, can be produced by 1)central pattern generator-built in system in brain stem-dog wagging its tail 2)learning-olympic divers 3)other neural mechanisms |
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Gustav Fritsch Eduard Hitzig
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discovery of the primary motor cortex stimulation ilicits movement, the motor cortex has no direct connections to the muscles, its axons extend to the brainstem and spinal cord which generate activity patterns for control of muslces-orders outcome and leaves it to spinal cord and other areas to make the outcome
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prefrontal cortex
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sensory signals that lead to movement planning and judging
responds to lighht, noises, and other sensory signals that lead to movement |
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premotor cortex
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preparations for movement
receives info about target in space in which body is making movement towards |
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supplementary motor cortex
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prepares for rapid series of movements, planning. pushing, pulling and turning a stick in a certain direction
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somatosesnroy cortex
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alerts primary motor cortex
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posterior parietal cortex
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track of position of body relative to world, allows us to convert preception int action
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mirror meuons
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enable the observer to understand and identify with the movements another individual is making. motor cortex becomes active when we imagine movements and when we see other ppl move
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dorsolateral tract
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axons from primary motor cortex, extend from brainto target neurons in spainal cord
precise discrete movement of dorsal limbs |
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pyramids
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bulges in the medulla where the in medulla where dorsolateral tract crosses from one side of the brain to the other
control of movemnts in peripherak ,m hands ingers and toes |
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ventromedial tract
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axons also originate from many parts f the cortex, vestibular nucleus(a brain area that recieves input from th evestibular system)
axons go to both sides of th epsinal cod not just the contralateral side controls neck, shoulders, trunk muscles potential adjustment-standing, turning, bending walking movements require bilateral control |
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readiness poential
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motor cortex produces a particular type of activity called a readiness potential before any voluntary movement or conscious decision, begins at least 500ms before movement
"what we identify as a conscious decision is more of a perception of an ongoing process then the cause of it on average the brain red potential began almost 300ms before the repeated decision which occured 200ms before the movement |
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anosognosia
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ignoranc eof the presence of a disease, insist that they can make movements when they cannot
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cerebellum
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-motor control
-learned motor behavior -70 billioin neurons -important for movement with aiming and timing -alcohol damage-deficits in rapid ballisic movements with aiming and timing |
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basal ganglia
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group of l;arge subcortical structures in the forebrain
damage= impairment of movement, srround thalamus, surrounded by cerebral cortex contains caudate nucleus, putamen (receptive areas) and the globus pallidus (output area) track=cerebral cortex, caudate nucleus, putamen, globus pallidus(release of GABA, constant inhibition of thalamus)thalamus, midbrain-motor and prefrontal areas of cerebral cortex |
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motor learning
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no specific area for learning new skills, neurons adjust their responses as persona learns new skill, but basal ganglia critical for habit learning, bycycle, shifting in car
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parkinsons disease
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rigid slow tremors, slow movements, difficulty initiating physical an dmental thinking , slow on cognitive tasks, depressed
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bio of parkinsons
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death of neurons in the substantia nigra and amygdala, increased inhibition of thalamus, loss of dopamine if number of neurons declines below 20-30% of normal amount parkinsons develops
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genetic basis
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early onset parkinsons disease is gentically related , monozygotic twin before age 50 means other mono twiare very likley to get it, if you get parkinsons later in life reradless of whether you are mono or diz, little or no heritibility for late-onset
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MPTP
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chemical th ebody converts to MPP+, which accamulates in and then destroys neurons that release dopamine , postsynaptic cells compensate by incraesing their number of dopamine receptors
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causes
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many different ones, toxins possibily, cig, coffee-less chance
damage to the mitochondria |
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L DOPA
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crosses th ebarrier, daily pill neurons convert it to dopamine, not a cure, many side effects, ineffective for osme patients, too much dopamine can kill cdopamine contaning cells
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other therapies
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neurotrophins, mao inhibitors, antioxidant drugs, drugs that decrease apoptosis, nicotine, electrical stimulation
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Huntington's disease
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arm jerks, facial twitches, tremors that spread to other parts of the body into withering, psychological disorders, bw ages of 30-50, fatal
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cause
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autosomal dominant gene
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presymptomatic test
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gene for it is on chromosone number 4, identifies who will dvelop the disease later in life, protein it codesin huntington
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Curt Richter
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animals generate approx 24 hrs cycles of wakefullness and sleep
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endogenous circannual rhythm
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rhythm, an internal calender that prepares it for seasonal changes
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endogenous circadian rythms
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rhythms that last about a day, urge to sleep depends on what tim eof the day it is, not just how recently you have slept, will reset a rhythm slightly longer then 24 hrs when it has nothing else to rest it
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body temp
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reaches it low for the day about 2 hrs after sleep onset, peak about 6 hrs before sleep onset
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biological clock
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circadian rythm is steady despite other frms of interference, despite lack of food or water, deprivation, x rays, alcohol, anesthesia
internal mechanism 24.2 hrs per day clock resets every morning difficult or impossible for humans to adjust to a sleep wake cycle much different from 24 hr/day |
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eeg (electrocencephalograph
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provides an objective way for brain researchers to compare brain activity at different times of the night
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polysomnograph
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combination of eeg and eye movement records, identifies stages of sleep
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alpha waves
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characteristic of relaxtion (not all wakefullness) at a frequency of 8 to 12 seconds per second
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stage 2 characteristicsd
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sleep spindles, K complexes
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sleep spindles
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12-14hz waves during a burst that lasts at least half a second, result from oscillating interactions between cellsin the thalamus and cortex
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K complex
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sharp high amplitude waves
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as you get deeper into sleep
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heart rate, breathing, brain activity decrease and slow large amplitude waves become more common
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STAGE 3/4
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SLOW SLEEP WAVES, slow high amplitude
stage 4-lots of delta and thelts, sensory input to cerebral cortex is greatly reduced |
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michel jouvet
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paradoxical sleep, after testing sleep in cats, deep sleep in some ways and light sleep in others
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Nathaniel Kleitman Eugene Aserinsky
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discovery of REM sleep
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REM (rapid eye movements)
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periods of rapid eye movements, synomonous with paradoxical sleep,
-fast low amplitude irregular brain waves, lots of EOG activity that indictaes incraesed neuronal activity -but posural muscles of body or more relaxed in REM then in any other stag eof sleep -erection in males and vaginal moistening in femals |
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dreams in different stages
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dream like episodes can occur in 1-4 but they are not clear, coherent or organized, ppl awakened during rem sleep reported dreams 80-90% of the time, rem dreams are more likley then nrem dreams to cntain striking visual imagery
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non rem sleep
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stages other then rem
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cycle
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1, 2, 3, 4, 1 h of sleep4 3 2 REM 2 3 4 2 REM 2 3 4 2 each cycle about 90 minutes early in the morning stages 3 4 dominate, duration of 4 grows shorter and more REM tendency to incraese REM depends on time
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stage 1 -"onset stage"
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sometime swith Hypnagogic imagery and occassionally by more dreamlike episodes
60-90 minutes 432 REM REm sleep periods increase throughout the night other cycles decraese as the night goes on, see pg 277 |
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more on dreams
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after dream content of dream often fails to consolidate, not that the memory is lost, average of 4-6 dreams per night
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when you awake really randomly and go to sleep again you
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start at beginning of cycle instead of going to the stage that you wer eawakened in
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dorsal raphe
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secretes serotonin
0active during wakefulness and NREM-inactive during REM |
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basal forebrain
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releases acetylcholine which is excitatory and increases arousal, significant for dreaming and readily involved in sleep
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gaba
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essentiakl for sleep bc of inhibition, explains decrease in body temp, metabolic rate, activity of neurons
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getting to sleep......
!) decreased arousal |
adenosine-during metabolic activity adenosine monophosphate breaks down into adenosine, when th ebreak is awake an active adenosine accumulates, adenosine inhibits the basal forbarin cells responsibe for arousal-shuts off arousal (ach) neurons in basal forebrain
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2)
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decrease stimulation
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3)
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inhibit arousal systems excited by acteylcholine
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4) prostaglandins
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chemicals that promote sleep, built up during the day until they provoke sleep, in response to infection the immune system produces more to cause sleepiness that accompnies illness-like taking an antihistamine-stimulates other systems to promote sleep
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5)
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decrrease activity in other arousal areas
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caffeine
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increases aousal by blocking adenosine receptors, constricts blood vessels in the brain , decreasing blood supply
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hypothalmus, histamine, orexin
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arousal, wakefulness
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PGO waves
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REM sleep, each pgo wave is synchronized with an eye movemnt in REM sleep, high amplitude electrical potentials (pons-geniculate occipital)
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during REM sleep...
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activity increased in the pons an dlimbic system(emotional responses) activity decreased in the primary visual cortex, motor cortex
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waves o f pons activity first detected
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in pons then lateral geniculate nucleus of thalamus, occipital cortex, during prolonged REM sleep deprivation, PGO waves begin to emerge during stages 2-4, when they do not normally occur, cells in pons also send message sto spinal cord inhibiting motor neurons that control bodys large muscles
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function of pons
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cells in pons also send message sto spinal cord inhibiting motor neurons that control bodys large muscles
prevent activity during REM sleep, motor blockade characteristic ofREM sleep |
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stimulation of act pathways
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move a sleeper in REM
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stimulation of serotonin pathways
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shorten REM sleep
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insomnia
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inadequate sleep, whether someone is rested enough, causes include temp, stress, pain, diet. medications
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onset insomnia
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trouble falling asleep
phase de;ayed rhythms |
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maintenance insomnia
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staying asleep
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termination insomnia
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waking up too early
phase advanced rhythms |
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#1 cause of insomnia
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when the bed become sthe CS for everything but sleep
-poor conditioning due to inappropiate behavior, biological rhythm abnormalies -us eof sleeping pills, taking pills becomes reverse of UR |
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sleep apnea
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inability to breathe while sleeping, irregular breathing , obesity, loss of neurons leads to defencies in learning, reasoning, attention
possibe cause for SIDS, as well as strokes/death later in life |
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narcolepsy
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1)frequent periods of sleepiness during the day
2) cataplex-attack of muscle weaknessn while the person remains awake 3)sleep paralysis-inability to move while falling asleep or waking up 4)hypnagogic hallucinations-dreamilke experiences that the person has trouble distinguishing from reality-intrustion of REM like state into wakefulness |
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caus eof narc
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orexin-ppl with narc lack th ehypothalamic cells that produce and release orexin
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Periodic limb movement disorder
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linked to insomnia, NREM-not sleep walking, a repeated involuntary movement of the legs and soetimes arms, legs kick once every 20-30 seconds for a period of minutes or hours during NREM sleep, may awaken person
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REM behavior disorder
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move around during rem periods, acting out their dreams most of them injure themselves or ppl and damage property, 90%=men. older ppl esp men with parkinsons disease, damage to the cells in th epons that send messages to inhibit neurons that control muscle movements, motor blockade not being complete enough.
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night terrors
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experiences of intense anxiety from which a person awakens screaming in terror
occur during NREM sleeo, and hypogenic imagery |
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sleep talking
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NREM-flat & dissassociated meaning
REM- affect, relate dto dream content |
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why sleep-REpair and restoration theory
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rest our muscles, decrease metabolism, rebuild proteins, reorganize synapses and strengthen memories, brain needs to repair after exertions of the day
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Evolutionary Theory
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conserve energy, temp decreases by 1-2C
both theories are correct not muually exclusive |
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animal speciea vary in their sleep habits depending on how many hours a day they devote
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to finding food and how safe they are from predators at night, animals in danger of being attacked while they sleep spend less time asleep
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restorative functions of sleep
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enhances memory, brain activity in areas while sleeping that is active when particpants had been learning the skill
without sleep unpleasant mood, decreased alertness, impaired performance |
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Freud
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manifest content is irrelevant, latent content is everything, interpetation in terms of underlying sexual symbolism, road to consciousness, but no evidence to support this.
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need forREM sleep
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when ppl are deprived of REM sleep they increase their attempts to get more in later sleep, memory storage discard useless connections
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Activation-synthesis hypothesis
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dreams begin with periodic bursts of spontaneous activity in the pons-the pgo waves-these activate many but not all parts of the cortex, the cortex combines this input with what input may have already was occuring and does its best to synthesize a story that makes sense of all of this info-basically brain makes up a story to support all of this activity going on in brain.
as well as that...the primary rol eof REM s just to shake th eeyeballs back and forth enough to get sufficent oxygn to the corneas of the eyes when eyes are motionless the fluid that usually contains oxygen becomes stagnant and does not get to the corneas |
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clinico-anatomical hypothesis
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regards dreams as just thining except that the thinking takes place under unusual circusmatnces, brain is geting little info from the sense organs so it is free to generate images without constrains or interference, less emphasis on pons PGO waves orREM
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zeitgeber
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"time giver", stimulis that resets biological clock=light
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jet lag
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harder to adjust going east then west-going east-go to sleep and awaken earlier then usual (phase advance of rhythms rather then phase delay
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night shiifts
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working in very bright lights and sleeping in dark rooms helps circadian rhythms
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superchiamtic nuclei
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located in hypothalmus, above optic chiasm, neurons generate rhythms in gentically controlled unlearned, cntine to produce rhythms even when removed from brain patterns
maincontrol for circadian rhythms for sleep and temperature |
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Retinohypothalmic path
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retina->scn
receptive sysetm sensitive to only light and dark, specialized group of ganglion cells directly sensitive to light, fibers of optic nerve, contain melanopin , pathway starts at retina dn ends at optic chiasm |
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melatonin
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released by pineal gland, increases sleepiness
2-3 hrs before bedtime, stimulates receptos in scn helps reset biological clock |
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melatonin pills
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help jet lag (.5mg or less) small amount, taken in the afternoon, after traveling east, phase advances the clock, help individual get to sleep earlier
morning after traveling west, phase advances |
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beta waves
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low amplitude high frequ-active/alert wakefullness
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alpha waves
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quiet relaxed wakefullness
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theta higher amp, lower frequ, during deep sleep
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kjhkjh
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delta
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very high amp, low freq
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