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Khan Academy Notes

by: Tejaswi Sudhakar

Khan Academy Notes MCAT

Tejaswi Sudhakar

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This 112 page Study Guide was uploaded by Tejaswi Sudhakar on Thursday April 21, 2016. The Study Guide belongs to MCAT at NYU School of Medicine taught by MCAT in Spring 2016. Since its upload, it has received 67 views. For similar materials see MCAT in Professional Education Services at NYU School of Medicine.

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Date Created: 04/21/16
Processing the Environment Sensory Perception Visual Cues  Depth, Form, Motion, Constancy  Binocular Cues - retinal disparity (eyes are 2.5 inches apart). Convergence – things far away, eyes are relaxed. Things close to us, eyes contract.  Monocular Cues – relative size, interposition (overlap), relative height (things higher are farther away), shading and contour, motion parallax (things farther away move slower) o Constancy – our perception of object doesn’t change even if it looks different on retina. Ex. size constancy, shape constancy, color constancy. Sensory Adaptation  Hearing - inner ear muscle: higher noise = contract.  Touch - temperature receptors desensitized  Smell – desensitized to molecules  Proprioception – mice raised upside down would accommodate over time, and flip it over.  Sight – down (ex. Light adaptation, pupils constrict, rods and cones become desensitized to light) and upregulation (dark adaptation, pupils dilate) Weber’s Law  2 vs. 2.05 lb weight feel the same.  2 vs. 2.2 lb weight difference would be noticeable.  The threshold at which you’re able to notice a change in any sensation is the just noticeable difference (JND)  So now take 5 lb weight, in this case if you replace by 5.2 weight, might not be noticeable. But if you take a 5.5 lb it is noticeable.  I = intensity of stimulus (2 or 5 lb), delta I = JND (0.2 or 0.5).  Weber’s Law is delta I to intensity is constant, ex. .2/2 = .5/5 = .1. o Delta I/I = k (Weber’s Law)  If we take Weber’s Law and rearrange it, we can see that it predicts a linear relationship between incremental threshold and background intensity. o Delta I = Ik. o If you plot I against delta I it’s constant Absolute threshold of sensation  The minimum intensity of stimulus needed to detect a particular stimulus 50% of the time  At low levels of stimulus, some subjects can detect and some can’t. Also differences in an individual.  Not the same as the difference threshold (JND) – that’s the smallest difference that can be detected 50% of the time.  Absolute threshold can be influenced by a # of factors, ex. Psychological states. o Expectations o Experience (how familiar you are with it) o Motivation o Alertness  Subliminal stimuli – stimuli below the absolute threshold. The Vestibular System  Balance and spatial orientation  Focus on inner ear - in particular the semicircular canals (posterior, lateral, and anterior)  Canal is filled with endolymph, and causes it to shift – allows us to detect what direction our head is moving in, and the strength of rotation.  Otolithic organs (utricle and saccule) help us to detect linear acceleration and head positioning. In these are Ca crystals attached to hair cells in viscous gel. If we go from lying down to standing up, they move, and pull on hair cells which triggers AP.  Also contribute to dizziness and vertigo o Endolymph doesn’t stop spinning the same time as we do, so it continues moving and indicates to brain we’re still moving even when we’ve stopped – results in feeling of dizziness. Signal Detection Theory  Looks at how we make decision under conditions of uncertainty – discerning between important stimuli and unimportant “noise”  At what point can we detect a signal o Origins in radar – is signal a small fish vs. large whale. o Its role in psychology – which words on second list were present on first list. o Real world example – traffic lights. Signal is present or absent (red).  Strength of a signal is variable d’, and c is strategy o d’: hit > miss (strong signal), miss <hit (weak signal) o c: 2 strategies – conservative (always say no unless 100% sure signal is present. Bad thing is might get some misses). Or liberal (always say yes, even if get false alarms).  For any signal, have noise distribution. And get a second graph – the signal distribution. o The difference between means of the two is d’. So if signal shifted to right, d’ would be big and easy to detect. If left, d’ very small and more difficult to detect. o X-axis have intensity. o The strategy C can be expressed via choice of threshold – what threshold individual deems as necessary for them to say Y vs. N. Ex. B, D, C, beta, just dif variables. o If we were to use B, let’s say choose this threshold – 2. So anything greater than 2 will say Y to, anything less say N. So probability of hit is shaded yellow, and false alarm is pink. o D = d’-B, so let’s say d’ in this example is 1, so 2-1=1. So if we use D strategy, anything above 1 = Y. o C strategy is an ideal observer. Minimizes miss and false alarm. C = B – d’/2. So in our example, it’s 2- ½ = 1.5. So anthing above a 1.5  When C = 0, participant is ideal observer. If <1, liberal. If >1, conservative. o Beta, set value of threshold = to the ratio of height of signal distribution to height of noise distribution. lnbeta = d’ x C = 1 x 1.5 = 1.5 Bottom-Up vs. Top-Down Processing  Bottom up: stimulus influences our perception.  Top-down: background knowledge influences perception. Ex. Where’s waldo Gestalt Principles  Similarity – items similar to one another grouped together  Pragnanz – reality is often organized reduced to simplest form possible (Ex. Olympic rings)  Proximity – objects that are close are grouped together  Continuity – lines are seen as following the smoothest path  Closure – objects grouped together are seen as a whole Sight (Vision) Structure of the Eye  Conjunctiva is first layer light hits  Cornea – transparent thick sheet of tissue, anterior 1/6 .th  Anterior chamber – space filled with aqueous humour, which provides pressure to maintain shape of eyeball.  Pupil is hole made by iris, which determines eye color  Lens bends the light so it goes to back of eyeball.  Suspensory ligaments, attached to a ciliary muscle. These two things together form the ciliary body, what secrets the aqueous humor.  Posterior chamber Is area behind the ciliary muscle, also filled with aqueous humor.  Vitreous chamber – filled with vitreous humour, jelly-like substance to provide pressure to eyeball.  Retina is filled with photoreceptors. o Macula – special part of retina rich in cones. o Fovea – completely covered in cones, no rods.  Choroid – pigmented black in humans, a network of blood vessels. Bc black all light is reflected. th  Sclera – whites of the eye, thick fibrous tissue that covers posterior 5/6 of eyeball. Attachment point for muscles. Visual Sensory Information  Sensation requires light -> neural impulse, by a photoreceptor  What is light? o Electromagnetic wave part of a large spectrum o EM spectrum contains everything from gamma rays to AM/FM waves. Light is in the middle o Violet (400nm) – Red (700nm) o The Sun is one of most common sources of light  Light enters pupil and goes to retina, which contains rods and cones o There are 120 million rods, for night vision  Light comes in, goes through pupil, and hits rod. Normally rod is turned on, but when light hits turns off.  When rod is off, it turns on a bipolar cell, which turns on a retinal ganglion cell, which goes into the optic nerve and enters the brain. o There are 6-7 million cones  3 types: red, green, blue  Almost all cones are centered in fovea o Phototransduction cascade: what happens when light hits rod/cone Phototransduction Cascade  Retina is made off a bunch of dif cells – rods and cones.  As soon as light is presented to him, he takes light and converts it to neural impulse. Normally turned on, but when light hits it’s turned off.  PTC is set of steps that turn it off. o Inside rod are a lot of disks stacked on top of one another. o A lot of proteins in the disks. One is rhodopsin, a multimeric protein with 7 discs, which contains a small molecule called retinal (11-cis retinal). When light hits, it can hit the retinal, and causes it to change conformation from bent to straight. o When retinal changes shape, rhodopsin changes shape. o That begins this cascade of events – there’s a molecule in green called transducin made of 3 dif parts – alpha, beta, gamma  Transducin breaks from rhodopsin, and alpha part comes to disk and binds to phosphodiesterase (PDE).  PDE takes cGMP and converts it to regular GMP. Na+ channels allow Na+ ions to come in, but for this channel to open, need cGMP bound. As cGMP decreases, Na channels closes.  As less Na+ enters the cell, rods hyperpolarize and turn off. Glutamate is no longer released, and no longer inhibits ON bipolar cells (it’s excitatory to OFF bipolar cells).  So bipolar cells turn on. This activates retinal ganglion cell which sends signal to optic nerve to brain. Photoreceptors (Rods and Cones)  A photoreceptor is a specialized nerve that can take light and convert to neural impulse.  Inside rod are optic discs, which are large membrane bound structures – thousands of them. In membrane of each optic disc are proteins that fire APs to the brain.  Cones are also specialized nerves with same internal structure as rod.  Rods contain rhodopsin, cones have similar protein photopsin.  If light hits a rhodopsin, will trigger the phototransduction cascade. Same process happens in a cone.  Differences: o 120 M rods vs. 6 million cones. o Cones are concentrated in the fovea. o Rods are 1000x more sensitive to light than cones. Better at detecting light – telling us whether light is present, ie. BW vision o Cones are less sensitive but detect color (60% Red, 30% Green, 10% Blue) o Rods have slow recovery time, cones have fast recovery time. Takes a while to adjust to dark – rods need to be reactivated. Photoreceptor Distribution in Retina  Where optic nerve connects to retina, blind spot – no cones or rods.  Rods are found mostly in periphery.  Cones are found throughout the fovea, and few in rest of eye.  If we zoom in on fovea – no axons in way of light, so get higher resolution. If light hits periphery, light has to go through bundle of axons and some energy lost. So at fovea light hits cones directly. Visual Field Processing  How our brain makes sense of what we’re looking at. Right side of body controlled by left side, vice versa. How does it work in vision?  All right visual field goes to left side of brain, all left visual field goes to right side of brain. Feature Detection and Parallel Processing  Color (cones, trichromatic theory of color vision), form (parvocellular pathway – good at spatial resolution, but poor temporal), motion (magnocellular pathway, has high temporal resolution and poor spatial resolution, no color)  Parallel processing – see all at same time. Sound (Audition) Auditory Structure – Part 1  Need 1) pressurized sound wave and 2) hair cell  Ex. In between your hands are a bunch of air molecules, and suddenly hands move towards each other, so space is a lot smaller.  Air molecules are pressurized and try to escape, creating areas of high and low pressure – known as sound waves o Sound waves can be far apart or close together o How close peaks are is the frequency. o Different noises have different sounds o You can listen to different frequencies at same time – if you add dif frequency waves together, get weird frequency. Ear has to break this up. Able to do that because sound waves travel different lengths along cochlea.  Hair cells – first hit outer part of ear, known as the pinna. Then go to external auditory meatus (aka auditory canal). Then hit the tympanic membrane (Eardrum) o As pressurized wave hits eardrum, it vibrates back and forth, causes these 3 bones to vibrate – malleus, incus, and stapes. o Stapes is attached to oval window (aka elliptical window). As it gets pushed, it pushes fluid and causes it to go around cochlea. At tip of cochea, it can only go back, but goes to the round window and pushes it out.  Reason doesn’t go back to oval window, is because in middle of cochlea is a membrane – the organ of Corti (includes the basilar membrane and the tectorial membrane). o Keeps happening until energy of sound wave is dissipated. Meanwhile hair cells in cochlea are being pushed back and forth and send info to auditory nerve. o General classification – from pinna to tympanic membrane is the outer/external ear. From malleus to stapes, middle ear. Cochlea and semicircular canals is the inner ear. Auditory Structure – Part 2  Focus on cochlea and inner ear  Let’s unroll the cochlea. Stapes – moving back and forth at same frequency as stimulus. It pushes the elliptical window back and forth. o There’s fluid inside the cochlea which gets pushed around cochlea, and comes back around. Organ of Corti splits cochlea into 2.  Cross section of Organ of Corti o Upper and lower membrane, and little hair cells. As fluid flows around the organ,c auses hair cells to move back and forth. o The hair bundle is made of little filaments. Each filament is called a kinocilium. o Tip of each kinocilium is connected by a tip link. o Tip link is attached to gate of K channel, so when get pushed back and forth they stretch and allows K to flow inside the cell. o Ca cells get activated when K is inside, so Ca also gets activated, and causes AP in a spiral ganglion cell which then activates the auditory nerve. Auditory Processing  Brain relies on cochlea to differentiate between 2 different sounds. o Base drum has low frequency, whereas bees have high frequency. o We can hear between 20-20000Hz. o Brain also uses basilar tuning – there are varying hair cells in cochlea. Hair cells at base of cochlea are activated by high frequency sounds, and those at apex by low frequency sounds.  Apex = 25 Hz, base = 1600 Hz.  Only certain hair cells are activated and send AP to the brain – primary auditory cortex receives all info from cochlea.  Primary auditory cortex is also sensitive to various frequencies in dif locations.  So with basilar tuning, brain can distinguish dif frequencies – tonotypical mapping. Cochlear Implants  A surgical procedure that attempts to restore some degree of hearing to individuals with sensory narrow hearing loss – aka `nerve deafness` o They have a problem with conduction of sound waves from cochlea to brain. o Receiver goes to a stimulator which reaches the cochlea. Receiver receives info from a transmitter. Transmitter gets electrical info from the speech processor. Speech processor gets info from microphone. o Sound -> microphone -> transmitter (outside the skull) sends info to the receiver (inside). Then it sends info to the stimulator, into the cochlea, and cochlea converts electrical impulse into neural impulse that goes to brain. Somatosensation Somatosensation  Types of Sensation, Intensity, Timing, and Location  Types: Temperature (thermoception), pressure (mechanoception), pain (nociception), and position (proprioception)  Timing: Non-adapting, slow- adapting, fast-adapting.  Location: Location-specific nerves to brain Sensory Adaptation and Amplification  Adaptation is change over time of receptor to a constant stimulus – downregulation o Ex. As you push down with hand, receptors experience constant pressure. But after few seconds receptors no longer fire. o Imp because if cell is overexcited cell can die. Ex. If too much pain signal in pain receptor (capsaicin), cell can die.  Amplification is upregulation o Ex. Light hits photoreceptor in eye and can cause cell to fire. When cell fires AP, can be connected to 2 cells which also fire AP, and so on. Somatosensory Homunculus  Your brain has a map of your body –focus on pink area, the cortex.  This part of cortex is the sensory cortex – contains the homunculus.  Info from body all ends up in this somatosensory cortex.  If there was a brain tumor, to figure out what part it’s in neurosurgeons can touch dif parts of cortex and stimulate them. If surgeon touches part of cortex patients can say they feel it. Do it to make sure they aren’t removing parts in sensation.  This creates topological map of body in the cortex. Proprioception and Kinaesthesia  How can you walk in a pitch black room? You rely on your sense of balance/position –proprioception. o Tiny little sensors located in our muscles that goes up to spinal cord and to the brain. It’s sensitive to stretching. o Sensors contract with muscles – so we’re able to tell how contracted or relaxed every muscle in our body is.  Kinaesthesia is talking about movement of the body. Proprioception was cognitive awareness of body in space. Kinaesthesia is more behavioural. o Kinaesthesia does not include sense of balance, while proprioception does. Pain and Temperature  Pain = nociception, temp = thermoception  In order for us to sense temperature, we rely on the TrypV1 receptor. o Interestingly, this receptor is also sensitive to pain. o There are thousands of these in membranes. Heat causes a conformational change in the protein. o When cell is poked, thousands of cells are broken up, and releases different molecules that bind to TrypV1 receptor. Causes change in conformational change, which activates the cell and sends signal to brain.  3 types of fibres – fast, medium, slow. o A-beta fibres - Fast ones are thick and covered in myelin (less resistance, high conductance) o A-delta fibres -– smaller diameter, less myelin. o C fibres - small diameter, unmyelinated (lingering sense of pain).  Pain also changes conformation of receptors – capsaicin binds the TrypV1 receptor in your tongue, and triggers the same response. Taste and Smell Olfaction – Structure and Function  When you have a cold, you aren’t able to taste things very well. o When you eat, molecules travel up back of throat and some go into back of your nose. So you’re using your sense of smell in conjunction with taste. o If your smell is knocked out, you can’t taste things as well.  Smell is also known as olfaction  Area in nostril called the olfactory epithelium. Separating the olfactory epithelium from the brain is the cribriform plate. Above the plate is an extension from the brain – olfactory bulb – a bundle of nerves that sends little projections through cribriform plate into the olfactory epithelium, which branch off. o At end of each connection are receptors, each sensitive to 1 type of molecule. o Molecule travels into nose, binds one of receptors on nerve endings.  Zoom in on olfactory bulb o Imagine there’s olfactory cell sending projection to olfactory bulb. There are thousands of types of epithelial cells, each with dif receptor. Say this one is sensitive to benzene rings. o When it binds to receptor, triggers events that cause cell to fire. AP will end up in olfactory bulb. All cells sensitive to benzene will fire to one olfactory bulb – called a glomerulus. o They then synapse on another cell known as a mitral/tufted cell that projects to the brain.  The molecule binds to the GPCR receptor, G-protein dissociates and causes a cascade of events inside the cell. Binds to ion channel, which opens and triggers an AP. Pheromones  Why do dogs pee on fire hydrant? There are molecules released in the urine, which can be sensed by other animals through the nose – pheromones. o They’re specialized olfactory cells. o Cause some sort of response in animal smelling them. o Pheromone is a chemical signal released by 1 member of the species and sensed by another species to trigger an innate response. o Really important in animals, particularly insects – linked to mating, fighting, and communication.  Specialized part of olfactory epithelium in animals – the accessory olfactory epithelium. It sends projections to the accessory olfactory bulb. o Within the accessory olfactory epithelium, you have the vomeronasal system. o In vomeronasal system, there are basal cells and apical cells. They have receptors at tips. o Triangle will come in and activate receptor on basal cell here. Basal cell sends axon through accessory olfactory bulb to glomerulus, which eventually goes to the amygdala. o Amygdala is involved with emotion, aggression, mating etc. o Humans have vomeronasal organ, but no accessory olfactory bulb. Gustation – Structure and Function  We have 5 main tastes, localized on the tongue – bitter, salty, sweet, sour, and umami (ability to taste glutamate).  Taste buds are concentrated anteriorly on the tongue. Taste buds can be fungiform (anterior), foliate (side), and circumvallate (back). o In each taste bud are the 5 receptor cells that can detect each taste. Each taste can be detected anywhere on the tongue. o Mostly on anterior part of tongue.  Each receptor has an axon, which all remain separate to the brain. And they all synapse on dif parts of the gustatory cortex. Known as the labelled lines model. o Ex. Glucose hits tongue, activates sweet cell (because it has sweet sensitive receptors), triggers cascade of events so cell depolarizes, and travels down axon to the brain. o Glucose binds GPCR, conformational change, G-protein dissociates, opens ion channels, cause cell to depolarize and fire an AP  Sweet, umami, and bitter cells GPCR receptors.  Sour and salty rely on ion channels. They bind to receptor directly, ex. NaCl binds to receptor and causes ion channel to open, and + ions outside flow in. Cell depolarizes and fires an AP.  What happens if we put salty receptor inside a sweet cell? Receptors in membrane bind to glucose. But let’s insert a salty receptor. Since axon from cell leads to brain, if NaCl comes in, it activates the receptor, + ions go inside, sweet cell depolarizes and fires AP, and brain interprets it as a sweet signal. Sleep and Consciousness States of Consciousness  Consciousness is awareness of our self and environment – dif levels of awareness can be induced by external factors such as drugs or internal mental efforts. Range from alertness to sleep.  Alertness – you’re awake  Daydreaming- feel more relaxed, not as focussed. Can also be light meditation (self-induced)  Drowsiness - just before falling asleep/after waking up. Can also be self- induced in deep meditation.  Sleep – not aware of world around you. EEGs can measure brainwaves. 4 main types – alpha, beta, delta, theta. o Each type oscillates at dif frequency o Beta (13-30Hz) – associated with awake/concentration. Increased stress, anxiety, restlessness. Constant alertness. o Alpha waves (8-13 Hz) – in daydreaming. Disappear in drowsiness but reappear in deep sleep. During relaxation. o Theta waves (7 Hz) – Drowsiness, right after you fall asleep. o Delta waves (0.5-3 Hz) - Deep sleep or coma. o In sleep, waves vary by stage. Sleep Stages and Circadian Rhythms  Your brain goes through distinct brain patterns during sleep. 4 main stages that occur in 90 min cycles.  First is non-rapid eye movement sleep (non-REM) – N1, N2, N3 o N1 (Stage 1)– Dominated by theta waves. Strange sensations – hypnagonic hallucinations, hearing or seeing things that aren’t there, ex. Seeing flash of light, or someone calling your name, doorbell, etc. Or the Tetris effect – if you play Tetris right before bed, you might see blocks. Also a feeling of falling – hypnic jerks. Theta waves. o N2 (Stage 2) – deeper stage of sleep. People in N2 are harder to awaken. We see more theta waves, as well as sleep spindles and K- complexes.  Sleep spindles help inhibit certain perceptions so we maintain a tranquil state during sleep. Sleep spindles in some parts of brain associated with ability to sleep through loud noises.  K-complexes supress cortical arousal and keep you asleep. Also help sleep-based memory consolidation. Even though they occur naturally, you can also make them occur by touching someone sleeping. o N3 (Stage 3) – slow wave sleep. Characterized by delta waves. Where walking/talking in sleep happens.  REM (rapid-eye movement) stage. Most of your other muscles are paralyzed. Most dreaming occurs during REM sleep, so paralysation inhibits actions. Most important for memory consolidation. Combination of alpha, beta, and desynchronous waves, similar to beta waves seen when awake. o Sometimes called paradoxical sleep, because brain is active and awake but body prevents it from doing anything. o Waking up during REM sleep prevents memory formation of the dream.  Cycle through these 4-5 times per sleep, each one 90 times. Order within cycle goes from N1 -> N2 -> N3 -> N2 -> REM. How long each stage lasts depends on how long you’ve been asleep and your age.  Circadian Rhythms – why you get sleepy in afternoon. They’re our regular body rhythms across 24-hour period. Controlled by melatonin, produced in the pineal gland. o Control our body temperature, sleep cycle, etc. o Daylight is big queue, even artificial light. o Also change as you age – younger people are night owls, but older people go to bed early. Dreaming  Everybody dreams during REM sleep. Can tell someone is dreaming because eyes are moving rapidly under eyelids, and brainwaves look like they are completely awake.  Activity in prefrontal cortex during REM sleep is decreased – part responsible for logic. Why things in our things that defy logic don’t seem weird.  Sigmund Freud o Dreams are our unconscious thoughts and desires that need to be interpreted. Little scientific support.  Evolutionary biology o Threat simulation, to prepare for real world. o Problem solving o No purpose  Other o Maintain brain flexibility o Consolidate thoughts to long-term memory, and cleaning up thoughts. People who learn + sleep retain more than those who do not sleep. But role of REM is unclear. o Preserve and developing neural pathways. Because infants constantly developing new neural networks spend most of time in REM sleep. Dream Theories – Freud and Activation Synthesis Hypothesis  Do our dreams have a meaning? Sigmund Freud’s theory of dreams says dreams represent our unconscious feelings/thoughts. Like an iceberg. o 1. What happens? Manifest content. Ex. Monster chasing you o 2. What is hidden meaning? Latent content. Ex. Job pushing you out. o Can help us resolve and identify hidden conflict.  Activation Synthesis Hypothesis o Brain gets a lot of neural impulses in brainstem, which is sometimes interpreted by the frontal cortex. o Brainstem = activation, and cortex = synthesis. o Our brain is simply trying to find meaning from random brain activity. Therefore might not have meaning. Sleep Disorders  People with sleep deprivation might be more irritable and have poorer memory. Could be dangerous when it comes to flying airplanes or driving cars. o Also more susceptible to obesity – body makes more cortisol, and the hunger hormone. o Can also increase your risk for depression. REM sleep helps brain process emotional experiences, which can help protect against depression (not certain). o Can get back on track by paying back “sleep debt”  How much is enough sleep? 7-8 hours for adults. Varies with age and individual. Babies need a lot more.  More serious form – insomnia (persistent trouble falling asleep or staying asleep). Various medications but taking them too long leads to dependence and tolerance. o Exercising or relaxing before bed can help  Other end of spectrum is narcolepsy – can’t help themselves from falling asleep. Various fits of sleepiness, going into REM sleep. Can occur any time. 1 in 2000. o Indications it’s genetic, and linked to absence of alertness neurotransmitter.  Sleep apnea – 1 in 20 people. People with it are often unaware. Stop breathing while sleeping – body realizes you’re not getting enough oxygen, wake up just long enough to gasp for air and fall back asleep without realizing. Can happen 100x/night! o Don’t get enough N3 (slow-wave) sleep. o Snoring is an indication, or fatigue in morning.  Sleepwalking/sleep talking – mostly genetic, occur during N3 and are harmless. Occur more often in children (have more N3). Breathing-Related Sleep Disorders  Sleeping problems can arise from brain, airways, or lungs/chest wall.  Obstruction to airways causes problems breathing at night o Air going into nose/mouth reaches the lungs. Tissues around neck may block this airflow – snoring/gasping/pauses in breathing. Called an apnea (absence of airflow). o Called obstructive sleep apnea, very common and gets worse as people get older. o People are tired/sleepy and unrefreshed when they wake up. o 5+ apneas an hour (measured by polysomnography)  In the brain, called central sleep apnea. Presence of apneas without obstruction. Problem with the control system for ventilation. o Cheyne-Stokes breathing (period of oscillations, then flat, etc.) pattern in polysomnography  In lungs or chest wall, hyperventilation can occur (high pCO2, low pO2). Caused by medication/obesity. Chronically elevated pCO2 can lead to right- sided heart failure. Hypnosis and Meditation  Hypnotism usually involves getting person to relax and focus on breathing, and they become more susceptible to suggestion in this state – but only if they want to. More alpha waves in this stage – an awake but relaxed state. o Some use hypnosis to retrieve memories, very dangerous because memories are malleable. Can create false memories. o 2 theories for how it works: Dissociation Theory (hypnotism is an extreme form of divided consciousness) and the Social Influence Theory (people do and report what’s expected of them, like actors caught up in their roles) o Refocused attention, so sometimes it’s used to treat pain. Reduced activity in areas that process sensory input. Although it doesn’t block it out, it might inhibit attention o that inhibit.  Meditation – training people to self-regulate their attention and awareness. Can be guided and focused on something in particular, like breathing, but meditation can also be unfocussed – mind wanders freely. o More alpha waves than normal relaxation in light meditation. o In deep meditation have increased theta waves in brain. o In people who regularly go to deep meditation, increased activity in prefrontal cortex, right hippocampus, and right anterior insula – increased attention control (goal of meditation). o Can be helpful for people with ADHD, or in aging. Drug Dependence Psychoactive Drugs: Depressants and Opiates  3 main categories of psychoactive drugs: depressants, stimulants, hallucinogens  Depressants are drugs that lower your body’s basic functions and neural activity, ex. Heart rate, reaction time, etc.  The most popular depressant is alcohol. o Think more slowly, disrupt REM sleep (and form memories), removes your inhibitions  Barbiturates – used to induce sleep or reduce anxiety. Depress your CNS. o Side effects are reduced memory, judgement and concentration, with alcohol can lead to death (most drugs w/ alcohol are bad)  Benzodiazepines are the most commonly prescribed suppressant. Sleep aids or anti-anxiety o Enhance your brain’s response to GABA. They open up GABA-activated chloride channels in your neurons, and make neurons more negatively charged. o 3 types: short, intermediate, and long-acting. Short and intermediate are usually for sleep, while long acting are for anxiety.  Opiates are used to treat pain and anxiety. Ex. Heroine and morphine. NOT a depressant. o Used to treat pain because they act at body’s receptor sites for endorphins. o Different class than depressants, even though overlapping for anxiety, rest act on GABA receptors while opiates act on endorphin Rs. o Lead to euphoria, why taken recreationally Psychoactive Drugs: Stimulants  Stimulate or intensity neural activity/bodily functions.  Range from caffeine to cocaine, amphetamines, methamphetamines, and ecstasy. In between is nicotine.  Caffeine (inhibits adenosine receptors) can disrupt your sleep. Nicotine also disrupts sleep and can suppress appetite. o At high levels, nicotine can cause muscles to relax and release stress- reducing neurotransmitters (to counteract hyper alertness). o Both physiologically addicting. o Withdrawal symptoms from both. Like anxiety, insomnia, irritability.  Cocaine is even stronger stimulant – releases so much dopamine, serotonin, and norepinephrine that it depletes your brain’s supply. Intense crash and very depressed when it wears off. o Regular users can experience suspicion, convulsions, respiratory arrest, and cardiac failure.  Amphetamines and methamphetamines also trigger release of dopamine, euphoria for up to 8 hours. o Highly addictive o Long-term addicts may lose ability to maintain normal level of dopamine Hallucinogens  These drugs cause hallucinations, altered perception.  Many types of hallucinations. Some even have medical uses.  Ecstasy – synthetic drug both a stimulant and hallucinogen. o Increases dopamine and serotonin and euphoria. Also stimulates the body’s NS. Can damage neurons that produce serotonin, which has several functions including moderating mood. o Causes hallucinations and heightened sensations, ex. artificial feeling of social connectedness.  LSD – interferes with serotonin, which causes people to experience hallucinations. o Hallucinations are visual instead of auditory  Marijuana is also a mild hallucinogen. Main active chemical is THC, which heightens sensitivity to sounds, tastes, smells. o Like alcohol, reduces inhibition, impairs motor and coordination skills. o Disrupt memory formation and short-term recall. o Stays in body up to a week. o Used as medicine to relieve pain and nausea  Some hallucinogens are used for PTSD treatment. Allow people to access painful memories from past that’s detached from strong emotions – so they can come to terms with it. Drug Dependence and Homeostasis  Homeostasis is how you maintain temperature, heart beat, metabolism etc.  If you take amphetamines, body quickly tries to lower HR and get back to normal. Brain is smart about this. o If regular drug user, might take it at same time of day. o If you’re cocaine addict, your brain starts to recognize external cues like room, needles, etc. and knows it’s about to get big dose of drug. Brain tells body to get head start – lowers HR before you take drugs. Why you need higher dose over time.  What would happen if you get those cues and don’t get the drug? You get a crash.  If you’re in a new location but take same level of drugs, might get overdose. Routes of Drug Entry  Oral, injection, inhalation,  Oral is ingesting something, one of slowest routes because goes through GI tract – half hour.  Inhalation is breathing or smoking, because once you inhale goes straight to brain – 10 seconds.  Injection- most direct, intravenous means goes right to vein. Takes effects within seconds. Can be very dangerous.  Transdermal – drug is absorbed through skin, ex. Nicotine patch. Drug in patch has to be pretty potent, released into bloodstream over several hours.  Intramuscular – stuck into muscle. Can deliver drugs to your system slowly or quickly. Quick for example is epipen. Or vaccines, slowly.  Faster route of entry = more addictive potential. Reward Pathway in the Brain  When you first experience pleasure, brain releases neurotransmitter called dopamine. Produced in the ventral tegmental area (VTA), in the midbrain. o VTA sends dopamine to the amygdala, nucleus accumbens (controls motor functions), prefrontal cortex (focus attention and planning), and hippocampus (memory formation). o NAcc, amygdala and hippocampus are part of the mesolimbic pathway.  Different stimuli active circuit to dif degrees.  VTA releases dopamine and receptors uptake dopamine – amygdala says this was enjoyable, hippocampus remembers and says let’s do it again, and nucleus accumbens says let’s take another bite. Prefrontal cortex focuses attention to it.  At same time dopamine goes up, serotonin goes down, partially responsible for feelings of satiation. Less likely to be satiated or content.  Increased genetic risk.  Biological basis comes from animal models – ex. Rats and drug experiment, rats keep increasing dosage. Or if sick drug + favorite food = avoids it, addictive drug + fav food = wants more.  Addiction takes over rational mind. Tolerance and Withdrawal  Tolerance means you get used to a drug so you need more of it to achieve the same effect. o Ex. Just took cocaine, lots of dopamine in synapse. Post-synaptic neuron has receptors for dopamine. Long-term stimulation can lead to brain shutting down some receptor; therefore same amount of drugs won’t cause same high. Called tolerance.  If you go through period of not having the drug, you experience withdrawal symptoms. o Things less strong as cocaine won’t give you as strong of an effect, so dopamine levels decrease and you feel depressed, anxious, etc. (varies). o Will do whatever it takes to get that high. o Once you’ve built up tolerance, need drug to feel “normal” again. o However, with time and effort brain can reverse back. Substance Use Disorders  Drugs include alcohol, tobacco, cannabis, opioids (heroin/morphine), stimulants (cocaine), hallucinogens (LSD), inhalants, and caffeine  We have to consider what happens when drugs enter the body and when they exit. 2 different processes: intoxication and withdrawal. o Intoxication refers to behavioural and psychological effects on the person, drug-specific. Ex. “drunk” or “high” o Withdrawal is when you stop after using for prolonged time.  Can result in substance-induced disorders. Could be disorders of mood (mania/depression), anxiety, sleep, sexual function, psychosis (loss of contact with reality).  Which can lead to substance use disorders. Causing real degree of impairment in life, at work, school, or home. o How do you know? By looking at their usage. Are they using increasingly large amounts, stronger cravings, more time recovering from it, failing to cut back, affecting obligations at work/home/school? o Second factor is presence of withdrawal. o Also tolerance.  With caffeine, can’t develop substance-use disorder. Treatments and Triggers for Drug Dependence  Treatments address physiological + psychological symptoms.  To treat, detox. But sometimes require strong medications to address symptoms. o Ex. Opiates such as heroine act at neural receptor site for endorphins to reduce pain and give euphoria. Methadone activates opiate receptors, but acts more slowly, so it dampens the high. Reduces cravings, eases withdrawal, and can’t experience the high because receptors are already filled. o For stimulants like tobacco, medications replace nicotine by delivering low levels of nicotine through patch, or deliver chemicals that act on nicotine receptors in brain. In this case prevents release or reuptake of dopamine. Help reduce cravings. o For alcoholics, meds block receptors in reward system of alcohol. Also reduce symptoms of withdrawal. Important to prevent relapse during this early stage by minimizing negative symptoms.  Inpatient treatments require residence at a hospital or treatment facility, outpatient means they can live at home and come in for treatment.  Cognitive behavioural therapy (CBT) addresses both cognitive and behavioural components of addiction. Recognize problematic situations and develop more positive thought patterns and coping strategies, and monitor cravings. o Long-lasting!  Motivational interviewing involves working with patient to find intrinsic motivation to change. Very few sessions and can be doorway for patient to engage in another treatment.  Group meetings such as AA involve 12-step program – acceptance, surrender, and active involvement in meetings. o Evidence they’re helpful.  Relapse is when patient can slip and go back. More addictive substances make relapse more likely. Why it’s hard for people to stay clean. Attention Divided Attention, Selective Attention, Inattentional Blindness, and Change Blindness  Attention is a limited resource – doing 2x at once you end up switching between tasks rather than doing them simultaneously. This is divided attention.  When you switch you’re exercising your selective attention – like a flashlight on your attention. At any given moment illuminating one area of interest. o 2 types of cues that can direct our attention – exogenous (don’t have to tell ourselves to look for them, ex. Bright colors, loud noises, “pop- out effect”) and endogenous (require internal knowledge to understand the cue and the intention to follow it, ex. A mouse arrow, or the cocktail party effect). o Cocktail party effect – ability to concentrate on one voice amongst a crowd. Or when someone calls your name.  Inattentional blindness – we aren’t aware of things not in our visual field when our attention is directed elsewhere in that field.  Change blindness – fail to notice changes in environment. Theories of Selective Attention  How do we filter out the unimportant information?  Shadowing task – left ear hear one thing, right ear another thing. Told to repeat everything said in one ear and ignore the other. We can learn about how selective attention works by seeing what they filter out in other ear. 3 theories  1) Broadbent’s Early Selection Theory o All info in environment goes into sensory register, then gets transferred to selective filter right away which filters out stuff in unattended ear and what you don’t need to understand it (accents etc.), and finally perceptual processes identifies friend’s voice and assigns meaning to words. Then you can engage in other cognitive processes. o Some problems – if you completely filter out unattended info, shouldn’t identify your own name in unidentified ear. Cocktail party effect.  2) Deutch & Deutch’s Late Selection Theory o Places broadband selective filter after perceptual processes. Selective filter decides what you pass on to conscious awareness. o But given limited resources and attention, seems wasteful to spend all that time assigning meaning to things first.  3) Treisman’s Attenuation Theory o Instead of complete selective filter, have an attenuator – weakens but doesn’t eliminate input from unattended ear. Then some gets to perceptual processes, so still assign meaning to stuff in unattended ear, just not high priority. Then switch if something important.  Still debate about which theory is best. The Spotlight Model of Attention and Multitasking  Spotlight model of attention. Selective attention – takes info from 5 senses, but don’t pay attention to everything. o Aware of things on an unconscious level – ex. Priming, where exposure to one stimulus affects response to another stimulus, even if we haven’t been paying attention to it. o We’re primed to respond to our name. Why it’s a strong prime for pulling our attention.  Resource model of attention – we have limited resources in attention. o Both models say something about our ability to multitask – not very good at it. Supported by research study.  Multitasking/divided attention o What about talking on phone or texting while driving? Maybe not multitasking, just switching spotlight back and forth. o What about singing to radio? o Task similarity – ex. Listening to radio while writing a paper. Better to listen to classical music, because harder to multitask with similar tasks. o Task difficulty – harder tasks require more focus. o Practice – activities well practiced become automatic, or things that occur without need for attention. Whether task is automatic or controlled (harder). Memory Information Processing Model: Sensory, Working, and Long-term Memory  Information processing model proposes our brains are similar to computers. We get input from environment, process it, and output decisions. o First stage is getting the input – occurs in sensory memory (sensory register). Temporary register of all senses you’re taking in. o You have iconic (what you see, lasts half a second) and echoic (what you hear, lasts 3-4 seconds) memory  Working memory is what you’re thinking about at the moment. Magic number 7 – can hold 7 +/- 2 pieces of info at a time. Why phone #s are 7 digits long. o Explains the serial position effect (primacy and recency effects) o Visual + spatial info are processed in the visuo-spatial sketchpad, while verbal info (any words + numbers in both iconic and echoic memory) is processed in the phonological loop. o What about visual + verbal info? Need coordination of the two – the central executive fills that role. Creates an integrated representation that stores it in the episodic buffer to be stored in long-term memory. o The dual coding hypothesis says it’s easier to remember words associated with images than either one alone. Can use the method of loci – imagine moving through a familiar place and in each place leaving a visual representation of topic to be remembered.  Final stage is long-term memory. Capacity is unlimited. 2 main categories: explicit (declarative) and implicit (non-declarative). o Explicit are facts/events you can clearly describe. Anytime you take vocabulary test or state capitals you’re using semantic memory (has to do with words). So remembering simple facts. Second type is episodic memory (event-related memories). o Implicit memories involve things you may not articulate – such as riding a bicycle, procedural memories. o Other is priming – previous experiences influence current interpretation of an event. Encoding Strategies  Encoding is transferring sensory information into memory.  If you want to remember more than 7 things, need to process that info so it stays in long-term memory.  1. Rote rehearsal – least effective technique. You say same thing over again.  2. Chunking – we group info we’re getting into meaningful categories we already know.  3. Mnemonic Devices – imagery (crazier the better), pegword system (verbal anchors like words that rhyme with the number – 1 is gun), method of loci (tying info to locations), acronym  4. Self-referencing – think about new info and how it relates to you personally. Also preparing to teach – learning it as if to teach it to someone else (putting more effort into understanding + organizing info)  5. Spacing – spreading out studying to shorter periods. Retrieval Cues  Priming – prior activation of nodes/associations, often without our awareness. Ex. hearing apple and asked to name word starting with A  Context – the environment you encode and take the test. Scuba divers who learned and tested on same place scored better than learned in one place and took test in another. But not always the case, if you can’t take test in same place studying in different places gives you dif cues for retrieval – so multiple cues that will help you.  State-dependent – your state at the moment. Ex. If you learn something while drunk you’ll remember next time you’re drunk. Or combining a mood with an advertisement – next time you’re in that mood will remember the product. Retrieval Cues: Free Recall, Cued Recall, and Recognition  Anytime you pull something out of long-term memory, you’re engaging in retrieval.  Free recall - no cues in recalling. Better recalling first items on a list (primacy) as well as last few (recency). Harder in middle. Curve is called the serial position curve/effect  Cued recall – give you “pl” for “planet”. Get more retrieval cues, tend to do better than free recall.  Recognition – best out of the 3 tests. Present two words, and say which one you heard. Memory Reconstruction, Source Monitoring, and Emotional Memories  Brain doesn’t save memories exactly. Every time we retrieve a memory we change it in small ways, according to our goals/mood/environment. Or due to our own desires. If gap brain fills it in with something desirable.  Sometimes information we retrieve is based on a schema (mental blueprint containing common aspects of world), instead of reality.  False information – inaccurate recollections of an event.  Misleading information – observed video of car crash, and asked how fast cars were going. Some people got word “hit” and some got “smash”. If people received “smashed”, more likely to say there was glass on the ground. o When people recall information they often forget the information’s source – an error in source monitoring, ex. angry with someone but forgot it happened in a dream. Or recognize someone but don’t know from where.  Emotional memories can be positive or negative, but highly vivid memories are called flashbulb memories – even if they seem as real as life, still susceptible to reconstruction. Long Term Potentiation and Synaptic Plasticity  Brain doesn’t grow new cells to store memories – connections between neurons strengthen. Called long-term potentiation, one example of synaptic plasticity.  Neurons communicate using electrochemical signals – through synapse. Pre- synaptic neurons release neurotransmitters on post-synaptic neurons, allowing Na and Ca to flow in. Dif in charge between outside and inside is the potential.  With repeated stimulation, the same pre-synaptic neuron converts into greater post-synaptic neuron – stronger synapse, and when it lasts longer called long-term potentiation. This is learning! Decay and Interference  Decay – when we don’t encode something well or don’t retrieve it for a while, we can’t at all anymore. Connections become weaker over time. Initial rate of forgetting is high but levels off over time. o Ebbinghaus was first investigator of decay. Found his rate of forgetting very fast, but if he remembered it after initial stage it levelled out.  Just because you can’t retrieve something doesn’t mean it’s completely gone – relearning. Even if Ebbinghaus couldn’t reproduce everything, took less time to learn list second time around. Called savings.  Works with procedural skills too – ex. With piano.  Sometimes interference is the problem though – 2 types: retroactive (new learning impairs old info, ex. Writing new address) and proactive (something you learned in past impairs learning in future, ex. New password). Aging and Cognitive Abilities  Stable – implicit memory (ex. riding a bike), and recognition.  Improve – semantic memories improve around age 60, so older adults have better verbal skills. Also crystallized IQ (ability to use knowledge and experience). Also emotional reasoning.  Decline – recall, episodic memories (forming new memories is difficult, old memories stable), processing speed, and divided attention. Also prospective memory (remembering to do things in future) is decreased. Alzheimer’s Disease and Korsakoff’s Syndrome  Excessive forgetting can be problematic.  Dementia is forgetting to point of interfering with normal life – results from excessive damage to brain tissue, ex. From strokes. o Most common form is Alzheimer’s Disease. Neurons die off over time. Earliest symptoms are memory loss, attention, planning, semantic memory, and abstract thinking. As it progresses, more severe language difficulties and greater memory loss, emotional stability and loss of bodily functions. Cause is unknown – have buildup of amyloid plaques in brain.  Korsakoff’s Syndrome – caused by lack of vitamin B1 or thiamine. Caused by malnutrition, eating disorders, and especially alcoholism. o Thiamine converts carbohydrates into glucose cells need for energy. Imp for neurons. o Damage to certain areas causes poor balance, abnormal eye movements, confusion, and memory loss. At this stage called Wernicke’s encephalopathy – precursor to KS. If diagnosed in time can prevent further damage. If untreated, will progress to Korsakoff’s. Main symptom is severe memory loss, accompanied by confabulation (patients make up stories to fill in memories). o Treatment is healthy diet, abstain from alcohol, take vitamins, and relearn things.  Retrograde amnesia is inability to recall info previously encoded, anterograde amnesia is inability to encode new memories. Cognition Piaget’s Stages of Cognitive Development  Piaget argued children weren’t miniature adults. Believed they actively construct their understanding of world as they grow.  0-2 years – children are said to be in the sensorimotor stage (smell, hearing, touch etc. + active). Also develop object permanence – don’t realize objects still exist if they can’t see them. Can also use accommodation to acquire knowledge about novel experiences.  2-7 years (approx.) – Preoperational stage. When children are going to develop/engage in pretend play. Very egocentric – no empathy.  7-11 years – Concrete operational stage. Learn idea of conservation. Can do test to find out if they’re in this stage – take 2 glasses with same amount of water, pour one into short fat glass and other into tall skinny glass, and ask child which one has more. Before this stage will say tall glass, but once they reach concrete operational stage, have same amount of water. Also begin to learn empathy.  12+ - Formal operational stage – reason abstract consequences, and reason consequences. Where sophisticated moral reasoning begins to take place. Problem Solving  We are excellent problem solvers. Well-defined (clear) and ill-defined (more ambiguous starting/ending point) problems.  Methods o 1. Trial + error – not the most efficient. o 2. Algorithm – logical procedure of trying solutions till you hit the right one. o 3. Heuristics – mental shortcut to find solution quicker than other 2, ex. Focusing on one category of solutions.  Means-end analysis – we analyze main problem and break it down into smaller problems, and reduce differences between problem and goal.  Working backwards – start with goal and use it to suggest connections back to current. Used in mathematical proofs. o 4. Intuition – relying on instinct. High chance of error.  Fixation – getting stuck on a wrong approach. What happens might be insight – that aha moment. Or can let problem incubate – insight comes after some time.  Type I error = false positive, type II error = false negative Decision Making  You use heuristic shortcuts to make a decision – it’s a quick decision rule/rule of thumb, ex. putting hand on shoulder when someone is sad.  Availability method – using examples that come to mind. Helpful, but our memories don’t match real state of the world.  Representativeness – a heuristic where people look for the most representative answer, such as if person matches a prototype. But can lead to a conjunction fallacy, which means co-occurrence of two instances is more likely than a single one (ex. Feminist bank teller vs. bank teller – actually more likely she’s just a bank teller, but people tend to think the probability of 2 events occurring together is higher than the probability of one alone).  Availability vs. representativeness – availability = actual memories in mind, representativeness = not thinking of exact memories, thinking of a prototype of idea.  Biases that prevent us fr


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