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130 Cards in this Set
- Front
- Back
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Young-Helmholtz or Trichromatic color theory (1802) |
-proposed independently by thomas young and hermann von helmoltz -only three idfferent color receptors (cones) are needed to see all shades of color |
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s-cones |
-shortwave or blue -excited by blue light |
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m-cones |
-medium wavelength or green -excited by green light |
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l-cones |
-long wavelength or red -excited by red light |
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trichromats |
-have all 3 cones: s,m,l -normal colour vision |
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dichromats |
-only have two functional cones: S, M or S, L (either m or L is nonfucntional) |
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monochromats |
-only have 1 functional cone -can only see black, white, and grays |
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Dichromats (ex) |
-other mamals and some non human primates are dichromats and only have two types of cones: S and LM (intermediate cones that respond to yellow light |
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colour deficiencies |
-certain colour deficiencies occur most commonly in males because of the genes for cones are on the x chromosome (usually the defective gene is rescued in females by a normal x chromosome) |
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edwald hering (1878) |
opponent process theorist |
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opponent process theory |
-explains negative afterimage and why we can't imagine "reddish green" or "bluish Yellow" colours |
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red-green blue-yellow white-black |
how individual ganglion cells code for colour |
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red light |
-red light activates red cone which activates red-green ganglion cells -result is red |
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green light |
-activates green cone which inhibits red-green ganglion cells -result is green |
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yellow light |
-activates red and green cones eually. the red cone activates both red-green and yellow-blue ganglion cells -the green cone 1. inhibits the red-green ganglion cell (thus canceling activation by red and 2. actives the yellow-blue ganglion cell -result is yellow (red is canceled y activation and inhibition |
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blue light |
-activtes blue cone which inhibits yellow-blue ganglion cells -result is blue |
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retinex theory |
both the cerebral cortex and retina work together to determine brightness and colour perception |
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cornea |
-smooth, transparent covering of front of eyeball -any scratches or damage will create distortions of light passing through to the retina and can cause astigmatism |
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astigmatism |
-blurring of objects in certain orientations |
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aqueaus humor |
-clear liquid between lens and cornea -shape of eyeball is maintained by pressure and aqueous humor drains fluid via ducts. if ducts clog, excess pressure builds up |
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glaucoma |
-damage to optic nerve due to excess pressure leading cause of blindness in the US |
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lens |
-elastic, transparent structure that focuses light onto the the retina |
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presbyopia |
- age-related inability of lens to fatten (less elasticity), which impairs ability to bring close objects into focus |
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cataract |
-lens becomes opaque with age (UV damage). light cannot pass and vision is disrupted. surgical removal of lens and replacement with a monofocal lens (usually a flat lens to allow distant focus only, so glasses would be required for near objects, multifocal lenses are available too).. prevention by sunglasses |
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myopia |
-nearsighted -lens focuses distant objects in front of retina (eyeball too long or lens too strong), but vision for near objects is intact |
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hyperopia |
-farsighted -lens focuses near objects behind retina (eyeball is too short or lens too weak ) but vision for distant objects is intact |
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retina |
multilayered structure containing photoreceptors |
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macular degenerations |
-degeneration of macula lutea (area that contains the fovea and thus cones) -symptoms: loss of ability to see detail or even read -eventually spreads to all photoreceptors and blindness results |
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retinitis pigmentosa |
-genetic disorder (chromosome 8) -affects rhodopsin (rods). -symptoms: night blindness, tunnel vision -eventually, disease spreads to cones, total blindness |
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diabetes |
-can produce blindness due to weakening of blood vessels lining the retina (resulting in bleeding into vitreous humor, as well as oxygen and nutrient deprivation |
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accommodation |
-it takes a stronger lens to focus a near image at the same distance that it takes a weaker lens to focus a distant image -thus, the human lens accommodates (gets fatter or stronger) in order to properly bring a near object into focus on the retina |
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ganglion cell to LGN pathway |
-actuall 2 pathways (parvocellular and magnocellular |
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two kind of ganglion cells project to separate layers of LGN (and thus different targets in V1) |
1. large ganglion cells or magnocellurlar 2. small ganglion cells or parvocellular |
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Large ganglion cells |
-magnocellular -from rods -origin of the "where" or dorsal system -processes form, motion, spatial relations |
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small ganglion cells |
-parvocellular -from cones -origin of the "what" or ventral system -processes colour, form, detail |
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LGN |
-lateral geniculate nucleus (of the thalamus) -6 layers |
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6 layers of LGN |
-top 4 layers (L3-6) -bottom 2 layers (L1-2) -thus, each layer of LGN only recieves monocular information (from one eye or the other) |
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-top 4 layers (L3-6) of LGN |
-parvocellular layer -from cones -two layers from left eye, two layers from right eye |
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-bottom 2 layers (L1-2) |
-magnocellular layer -from rods -1 layer from left eye, one layer from right |
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Brodmann |
-used microscopic appearance to classify brain regions (52 regions) -area 17 is primary visual cortex |
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two streams of visual information flow |
-dorsal "where" --magnocellular --from rods -ventral "what" --parvocellular --from cones --well-developed in primates |
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damage to V1 |
-if tiny, scotoma (blind spot) -if in one hemisphere, hemianopia (blind in contralateral visual field) -if complete and bilateral, blindness results (may exhibit blindsight |
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damage to V2 and V3 |
-hard to exclusively damage with damaging V1, usually blindness |
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damage to V4 |
-unable to see, perceive, or even remember seeing colours (achromatopsia) |
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damage to V5
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-unable to preceive movement or moving objects (akinetopsia) |
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Damage to IT (inferior temporal cortex) |
-creates family of disorders called visual agnosia (can't recognize familiar faces) -prosopagnosia -can have visual agnosia without prosopagnosia (thus object recognition areas are not the same as face recognition areas) -pure alexia (cannot put letters together but can recognize individual letters)--results from damage to left IT cortex |
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prosopagnosia |
-cannot recognize familiar faces -results from damage to the right IT alone or from bilateral IT damage -particularly damage to the fusiform gyrus (fusiform face area) |
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damage to posterior parietal cortex |
-creates disturbances in ability to locate and reach for objects -balint's syndrome -visual extinction |
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balint's syndrome |
-difficulty perceiving more than one object at the same time (simultanagnosia) -can't scan environment and fixate on objects -difficulty with visually-guided hand movements (optic ataxia) -results from bilateral damage to posterior parietal cortex |
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visual extinction |
-ignore object in visual field contralateral to damaged area -usually results from unilateral damage to right posterior parietal cortex |
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somatosensory receptors |
-various types of receptors in the skin -various types of receptors in muscles, tendons, and joints |
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kinesthesia |
-ability to sense movement |
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proprioception |
-ability to know where a body part is in 3D space |
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interoception |
-sense that arises from the internal organs (receptors in smooth muscle) |
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kinesthesia and proprioception |
work together to create body image |
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mechanoreceptors |
-somatosensory receptors -annulospiral receptors (muscle spindles and gtos (tendons) -pressure and vibration activate mechanoreceptors in the skin |
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temperature changes activate both mechanoreceptors and chemoreceptors |
-expansion and shrinking of skin with temperature (mechano) -cold sensors and warmth sensors exist (carried by different types of axons) -transduction is via transient receptor potential family of proteins (called trp receptors)- some trp receptors respond to chemicals (menthol, in mints, feels cool) |
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pain information |
-can be carried via both mechanoreceptors and chemoreceptors -excess pressure on skin (mechano) -bradykinin and prostaglandin release from bee sting (chemo) |
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types of receptors in the skin |
-pacinian corpuscles -meissner's corpuscles -basket endings -free nerve endings |
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pacinian corpuscles |
-pressure and vibration -sensory fiber surrounded by concentric layers (located deep, below dermis) |
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meissner's copuscles |
-touch -composed of axonal loops, separated by nonneuronal support cells -important for detecting movement along skin (eg adjusting grip) |
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basket endings |
-movement of hair -wrapped around individual hairs and detect movement |
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free nerve endings |
-pain or temperature -single, bare nerve endings at end of sensory fiber |
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two types of axons carry sensory information to the cns |
-A fibers (large myelinated axons, 3 types) -C fibers( very small diameter axons) |
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A-fibers (3 types) |
-A alpha- large, most heavily myelinated and fastest, axons of muscle spindles -A betta- medium, well myelinated and fast, axons of pacinian and meisner's corpuscles and merkel disks -A delta - small, poorly myelinated and slow, some pain and preassure, cold sensors |
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C-fibers |
-very small -unmyelinated axons and slow conduction axons of free nerve endings most numerous( about 80% of axons terminating in the skin) warmth sensors |
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pressure and touch |
-information travels to the brain quickly (more recent system) -lemniscal path |
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pain and temperature |
-information travels to the brain more slowly (older system) -spinothalamic tract |
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somatosensory paths from the body to the cortex |
-lemniscal path -spinothalamic tract |
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lemniscal path |
-touch -a fibers -ascends dorsal column -crosses over in medulla -processes precise touch and kinesthesia -crosses over in hindbrain |
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spinothalamic tract |
-pain -c fibers -crosses over in spinal cord -processes pain and temperature |
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"What" system |
-what is the perceived sensation -inferior parietal cortex -damage to inferior parietal cortex produces tactile agnosia, an inability to recognize objects through touch |
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"Where" system |
-where on my body is the sensation coming from -posterior parietal cortex (note, this is also part of visual "where" system too) -damage to posterior parietal cortex produces inability to process the location of a stimulus and its spatial relationship to other tactile stimuli |
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plasticity of the somatosensory system |
-the cortex is continuously being re-organized by experience -the 1 somatosensory cortex is also reorganized following amputation of a body part--in such cases inputs to neighboring cortices invade the hand area, thus the brain can hallucinate the presence of a phantom limb every time an area which invaded the phantom limb's cortex is activated (eg touching face would now activate neurons in amputated hand |
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gate control theory (melzack and wall, 1965) |
1. c-fibers carry information to substantia gelatinosa (dorsal horn of spinal cord) 2. substantia gelatinosa relays informatino to the brain stem 3. brain stem relays informatino to the cerebral cortex (concious experience) 4. certain brain structures and a fibers can stop pain messages by sending inhibitory signals to the substantia gelatinosa (thus closing the gate on pain). a. PAG b. PVG c. A-fibers |
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neurotransmitter that transmits pain messages |
-substance P |
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Substance P |
-neurotransmitter used by pain receptors -released by c fibers that synapse onto substantia gelatinosa neurons -signals the presence of tissue of damage and pain |
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class of neurotransmitters that inhibit pain messages |
endorphins |
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endorphins |
-endogenous opiates (also called enkephalins) -neurons in PAG and PVG send axon terminals to substantia gelatinosa -- there they form axoaxonic synapses onto the c fiber terminals -- they release endorphins onto c fiber terminals -- block ascending pain by presynaptic inhibition -also released by pituitary gland in response to stressful or painful situations -effects of endorphins can be blocked by opiate antagonists such as naloxone |
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PAG |
-periaqueductal gray -located in midbrain |
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PVG |
-periventricular gray -hypothalamic area, near third ventricle |
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3 dimensions of pain perception |
1. sensory discriminative 2. motivational affective 3. cognitive evaluative |
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sensory discriminative |
- detect pain and identify its source -processed initially in secondary somatosensory cortex |
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motivational affective |
-emotional and motivations aspects- can be indured -processed in anterior cingulate cortex if anterior cingulate is damaged, pain is felt, but not viewed as unpleasant |
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cognitive evaluative |
-severity and how to deal with the pain -processed in prefrontal cortex |
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allodynia |
-may be experienced following tissue and nerve damage (abnormal enhanced pain response) |
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frontal lobe |
-in humans, the largest lobe -1/3 of the brain -divided into 3 functional zones or areas |
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3 zones of the frontal lobe |
1. prefrontal cortex 2. premotor cortex 3. primary motor cortex |
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prefrontal cortex |
-most anterior region -cognition, planning -important for working memory |
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premotor cortex |
-anterior to motor cortec -movement |
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primary motor cortex |
-precentral gyrus -movement |
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working memory |
-Baddely and Hitch 1974 -coordinated, temporary storage of information in various sites in the cerebral cortex -allows you to perform calculations in your head, to read, solve problems -intelligence may be linked to working memory capacity |
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object identification |
-can hold an object or series of objects in mind -thus can put a series of objects in order (also face recognition) -IT cortex (visual object recognition) and PFC (storage centers) |
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Spatial Location |
-holding in memory the spatial location of several objects at the same time (eg playing chess) -right hemispheric regions are involved: posterior parietal, hippocampus, pfc |
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verbal information |
-holding words in mind (eg reading or listening to someone speaking) -Broca's and Wernicke's areas (speech centers in the left hemisphere) -anterior cingulate cortex (in medial PFC) -left premotor cortex (rehearsing verbal material sub vocally) |
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anterior cingulate cortex (in medial PFC) |
-activated when working memory is used -coordinates working memory? |
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Short term and long term memory |
-william james, 1890 .. theorist |
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short term memory (working memory) |
-a limited memory system (can hold about 7 pieces of information) -holds information effortlessly for about 30 seconds before decaying -can hold information longer with rehearsal -postulated by donald hebb (1949) to result from reverberating circuits in the frontal lobes |
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consolidation (and reconsolidation) |
-postulated by Hebb to describe the shift of a memory from a relatively labile short term to a relatively stable long term from -can be made labile again by retrieval of the memory-- reconsolidation |
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Long term memory |
-a memory system capable of storing large amounds of information for long periods of time (years to decades) -hebb proposed that long term memory results from structural changes to memory circuits -there are two main long term memory systems (declarative and nondeclarative) |
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declaritive memory AKA explicit memory |
-involves conscious retention of facts and events -requires the hippocampus for initial storage --patients with hippocampal damage exhibit amnesia -over time, the hippocampus is no longer required for declaritive memory retrieval, thus hippocampus serves a temporary, time limited role |
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retrograde amnesia (backward) |
-cannot remember events just prior to injury |
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anterograde amnesia (forward) |
-cannot create new declarative memories -eg. patient cannot form new memories |
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episodic memory |
-memory for evens or episodes in one's own life -organized in time and identified by a particular context -includes not just verbal memory, but also the perceptions |
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semantic memory |
-general knowledge or learned facts -does not include information about the context in which facts were learned |
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-emotionally charged events |
-memory is greater
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hormone release, eg epinephrine |
-when aroused, your body releases hormones -epinephrine activates the amygdala which enhances consolidation of memory -- drugs that block effects of epinephrine interfere with enhanced memory formation |
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nondeclarative memory AKA implicit or procedural memory |
-involves nonconscious memory for learned behaviours -does not require hippocampus, involves cerebellum and corticostriatal system -priming effect |
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priming effect |
-improved ability to recognize particular stimuli after experience with them -priming involves posterior parietal and occipital cortex for the visual information and Broca's area for conceptual information |
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Alzheimer's diseas |
-neurodegenerative disease characterized by severe memory loss -diagnosed by presence of plaques and tangles -initially, the disease destroys synapses, then eventually kills neurons -ACh levels are severely depleted -amnesia -current therapies involve acetylcholinesterase inhibitors (don't work well) |
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plaques and tangles |
-beta amyloid protein deposts and tau protein filaments -form in temporal lobes and spread throughout forebrain |
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disorders associated with prefrontal cortex damage |
1. dysexecutive syndrome 2. disinhibition 3. emotional impairments 4. difficulty planning |
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dysexecutive syndrome |
-inability to coordinate complex behaviours with respect to goals and task specific constraints |
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disinhibition |
-lack of behavioural control -impulsive, quick to anger, prone to rude childish behavior.. utilization behaviour -can also be tested using the stroop test or wisconsin card sorting test |
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emotional impairments |
-indifferent and apathetic to their own situation and to the needs of others -irritable and prone to angry outbursts |
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difficulty planning |
-unable to organize behavioural to plan several steps in advance -assessed by using tower of hanoi test or multiple errands task |
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classical or pavlovian conditioning |
-model system for studying associative learning (implicit and explicit) -allows for excellent experiemental control over stimuli -studied in many species -engages both cortical and subcortical brain regions |
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delay conditioning |
-CS and US are temporarily contiguous -requires fewer training trials -depends on brainstem and cerebellar ciruitry -implicit learning |
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trace conditioning |
-CS and US are discontiguous (separated by stimulus free trace interval) -requires many more training trials -still depend on brainstem and cerebellum to elicit a CR -now depends on higher brain structures to learn (hippocampus) -explicit learning |
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synapses in learning and memory |
-plastic -can be added or removed - strengthened or weakened |
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synaptic plasticity |
-long term potentiation or LTP (strengthening), form of cellular memory -long term depression or LTD (weakening) |
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Long term potentiation.. strong stimulus |
-high frequency stimulation -stimulation must be sufficient to produce enough postsynaptic depolarization to open NMDA receptors |
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two different pathways are stimulated |
(one weak, one strong) -weak alone does nothing -strong alone strengthens strong pathway only -weak and strong strengthens both pathways -weak path--> CS, strong path--> US (classical conditioning) |
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Action potential |
-back propagation through dendrites primes NMDA receptors so that now any weak synapses that are also active at the same time will become strengthened |
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induction of LTP |
-requires strong postsynaptic depolarization -the postynaptic Ca2+ influc during depolization is a critical trigger for this |
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long term potentation (LTP) |
-synaptic stimulation activates only AMPA receptors (and thus a small synaptic response or EPSP occurs) -strong depolarization leads to activation of NMDA receptors which let Ca2+ inot the cell -Ca2+ influx activates 2nd messengers, which leads to insertion of more AMPA receptors (thus a larger synaptic response or larger EPSP) |
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expression of LTP and LTD |
-silent synapses result from an absense of postynaptic AMPA receptors -synapses that were previously silent can become active following LTP (due to LTP causing insertion of AMPA receptors) |
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insertion of AMPA receptors |
-LTP, strengthening of synapse strength |
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removal of AMPA receptors |
-LTD, weakening of synapse strength |
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V1 (primary visual cortex) |
-located in the occipital lobe -corresponds to brodmann area 17 |
