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PY 413 Study Guide Exam 2

by: Caitlin Owens

PY 413 Study Guide Exam 2 PY 413

Caitlin Owens

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This study guide contains all in class lecture notes and chapter outlines.
Physiological Psychology
Dr. Gable
Study Guide
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This 23 page Study Guide was uploaded by Caitlin Owens on Monday March 7, 2016. The Study Guide belongs to PY 413 at University of Alabama - Tuscaloosa taught by Dr. Gable in Spring 2016. Since its upload, it has received 59 views. For similar materials see Physiological Psychology in Psychlogy at University of Alabama - Tuscaloosa.


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Date Created: 03/07/16
Physiological Psych Exam 2 Vision *50% of cortex is dedicated to visual processing *75% of sensory neurons dedicated to vision *electromagnetic radiation-emission of small particles(photons), visual receptors receive these photons very fast(speed of light) *benefit of light is we don’t have to be in direct contact, light travels in a direct/straight pathway eye & its connection to brain • orbits encompass and protect eyeball in skull-protection from lateral impact • eyelids (by blinking) protect from wind, dust, etc. • tear ducts help eyes stay moist which helps clear “gunk” from eyeball • pathway of light: sclera(white outer-covering of eye)àcorneaàpupil(lets light in; iris can change shape/dilate pupil)àaqueous humor/eye jellyàretina***** • accommodation-bending of light to reach retina; un-accommodation causes near/far sightedness, can be fixed with corrective lenses visual receptors:RODS & CONES • transduction-takes photons and turns them into neural impulse; physicalàchemical signal • 120 million rods, 6 million cones; 90% of brains input comes from cones • 1 million axons leave the retina • optic nerve runs from back of eye to visual/occipital cortex retina (info from back to front) • photoreceptors-back layer of retina • ganglion cells-transmit information out with optic nerve • bipolar cells-receive input from rods & cones; synapses info to amacrine cells and ganglion cells; impulses can skip these sometimes • horizontal cells-can also receive input from rods & cones; synapses information to bipolar cells; have inhibitory influence on bipolar cells-important for lateral inhibition • amacrine cells-receive info from bipolar cells; help transmit info to ganglion cells; important in shape processing why “backwards” formation? • 3 functional layers 1. stimulus reception (sensory input) 2. signal processing (bipolar, horizontal, amacrine) 3. signal transmission (ganglion) • rods & cones lie at back because they need nutrients from layer of epithelial cells at back of eye; this layer of epithelial cells also blocks/absorbs any extra photons not absorbed by rods & cones to keep light out of rest of nervous system light transduction • photopigments release energy when struck by a photon • dark current-cyclic GMP (cGMP) attached to sodium receptors; keeps them open- slightly depolarized in the dark • transduction occurs when light hits photopigments o Opsin proteins (Rhodopsin-located in rods) o When light is absorbed it breaks into Opsin & Retinal(vitamin A); this causes cascade of processes that changes cGMPàGMP closing sodium gate o In the dark, photoreceptors are more active; vision works on inhibitory transmission (glutamate release in dark, not light) § Functional argument: conservation of energy; in light 2/3 of day fovea (most important part of retina) • Process acute/detailed vision and color • Center of vision • Packed tightly with receptors-mainly cones • Free of blood vessels and ganglion cells • Each photoreceptor (mostly cones) gets very own bipolar & ganglion cell for direct line to the brain • 90% of visual input from the fovea • organisms that look down/up a lot have a second fovea (ex. mice, predatory birds) periphery of retina • rods have less detail/acuity but more light sensitivity • rods do not sense color • convergence of many rods to one ganglion cell theories of color vision • we only see small amount of wavelength, reason we aren’t blinded by radio waves • trichromatic theory(three colors)- 3 different kinds of cones; short wavelength cones (blue), medium wavelength cones (green), long wavelength cones (red); perception of different colors is activation of these cones • opponent-process theory- perceived color is result of paired opposites (ex. when green receptors are activated, red receptors are shut off); bipolar cells are excited by one wavelength but inhibited by another wavelength • retinex theory-cortex pulls info from retina to maintain color constancy limitations • explaining color constancy-light source changes color, we perceive colors to be the same even though light can change them color vision deficiency (not “color blind”) • difficulty seeing certain colors • located on X chromosomes, more common in men (8%, less than 1% in women) • long/medium wavelength cones processed as same color pigment • blind spot-where ganglion cells & optic nerve exit the eye, no receptors here lateral inhibition • starts at the retina, moves to bipolar/horizontal cells • Hermann grid-explanation of lateral inhibition; more in the periphery • helps us see shapes more clearly visual system • ganglion cells/axons form optic nerve • optic chiasm-information coming from both sides of the visual field; left hand vision processed in right hemisphere & right hand vision processed in left hemisphere • information travels to sensory switchboardàthalamusàlateral geniculate nucleus (LGN)àprimary visual cortex(V1) • blindsight-no conscious reporting of vision, can respond to some visual stimuli unconsciously-could be because thalamus sends information to areas other than V1 • retinotopic mapping-V1 is retinotopically organized; info on retina is all sent to V1 like a projector primary visual cort ex • Hubel & Weisel (1959, 1998)-different columns in cortex respond to very specific features in visual stimuli • development-needs stimulation to develop o astigmatism-70% of infants have astigmatism, asymmetric curvature of the eyes, inability to respond to certain aspects of vision V2 area & beyond… • dorsal stream: “where” pathway-moves from V1 to parietal lobe, shows where and how to approach objects o telescope-dorsal stream moves up and helps find where objects are located • ventral stream: “what” pathway-moves toward temporal lobe and helps identify and recognize objects o microscope-look down and identify what you’re looking at • fusiform gyrus-area specific for facial processing in ventral stream; first to develop in infants; one of the most specialized parts of the brain • V4-responsible for color constancy-cortical process o color we see under different light sources is the same o #thedress-example of color constancy, blue and black • V5 (MT)-stimulus movement Sound psychophysics of hearing • Wavelength-measured in hertz (Hz)-waves per second o Pitch (ex. longer wavelengths, lower pitch)-comparative to color in light • Amplitude-measured in decibels-volume/loudness o Comparative to brightness in light sound transduction • Pinna-funnels/directs sound into ear canal, localizes sound • Tympanic membrane(ear drum)- vibrates with the sound, connected to hammer, anvil, and stirrup • Oval window-front of cochlea • Cochlea-fluid-filled area, basilar membrane contains hair cells o Transduction occurs at hair cells-specialized dendrites connected to neurons o Dendrites form axons to form auditory nerve which transports info to brain pathway: spiral ganglion neuronsàmedulla, inferior colliculiàmedial geniculate nucleus of thalamusàprimary auditory cortex(A1) in temporal lobe***** auditory cortex (A1) • Organization parallels to visual cortex-tonotopic mapping like piano keys pitch perception theory • Place theory-works well for high frequency sounds; different frequencies are processed by different neurons in different locations • Frequency theory-works well for low frequency sounds; patterns of neural firing match the frequency of a sound hearing • Amusia (tone deafness)-fewer connections between auditory and frontal cortex • Perfect pitch-can hear a note and identify it, can be learned through musical instrument playing • Conductive/middle ear loss- bones in middle ear fail to transmit sound well; individuals with this can hear themselves clearly but have trouble hearing others, can be linked to psychological disorders • Nerve/inner ear loss-more damaging, damage to cochlea causes certain frequencies to not be perceived • Tinnitus- high pitched frequency sound heard continuously, similar to phantom limb syndrome, disorganization of synapses in the cortex • Damage-decibels logarithmic; 23% 18-44 year olds, 29% 45-64 year olds, 43% 65+ have hearing damage sound localization • Sound shadow-best explains high frequency • Time of arrival-slight discrepancy in time between each ear receiving sound • Phase difference-sound waves, best explains low frequency Mechanical Senses vestibular sensation • allows us to maintain balance, position, movement o semi-circular canals o otoliths-particles of calcium carbonate-activate hair cells in basilar membrane somatosensation • skin is largest organ of the body • merkel disks- sense fine/gentle touch; women more sensitive than men because generally have a smaller surface area but same number of disks • meissner’s corpuscles- sense pressure on the skin • pacinian corpuscles-deep within the skin & joints, sense pressure and vibration • dermatome • αβ myelinated axons- transmits info from dermatome, located in spinal cord (sensory route is dorsal) • ventral posterior(VP) nucleus of the thalamus • primary somatosensory cortex-parietal lobe • hands, feet, and lips have greatest amount of real estate in somatosensory cortex pain • bare nerve endings • alpha delta fibers vs. c fibers o alpha delta fibers: myelinated, travel faster, transmits sharp pain o c fibers: unmyelinated, transmit dull/aching pain, 70% of pain transmitted here • nocieception vs. pain o nocieception is purely stimulus experience (nauseous perception) o brain creates pain and emotion tied to pain • mild pain-glutamate*** in spinal cord • pain can cause release of histamine, NGF and substance P**** • physical sensation-somatosensory cortex-remembers and responds to pain • other brain areas affected-thalamus, hypothalamus, amygdala, hippocampus o vision blurred-interrupts other sensory input when in pain o amygdala-remember pain & fear it o frontal cortex-while in pain, frontal cortex fixates on it and hard to ignore treating pain • opiates block release of substance P by closing gates in spinal cord and midbrain- specifically dull, aching pain • anti-inflammatory drugs: work on prostaglandins; aspirin and motrin (ex. advil, motrin) • local anesthetics- block sodium channels • non endorphin pain relief-gate control theory-stimulate sensory receptors around painful area to reduce pain and beat pain signal wimp theory! • receptor potentiation- when tissue gets damaged, it becomes enflamed which increases the pain receptors sensitivity • emotional pain resembles physical pain-cingular cortex activated in social and physical pain (social pain=break-up/social rejection) • acetaminophen (Tylenol) can reduce physical and emotional pain; reduces hurt feelings and social pain descending pain inhibition circuit • endorphins-endogenous morphines o periaqueductal gray area-where endorphins affect o endorphins block substance P • placebo administration, amygdala stimulation can trigger endorphin release internal mechanisms of relief • brain can reduce pain relief if it believes it is getting help; psychological ability itch • histamine causes itch; histamine related to sleep/wake cycles • pain blocks itch; heat/cool can stop itch, cool can reduce inflammation • morphine/opiates can cause itchiness because pain relieved • phantom pain-can show up in cortex following amputation-result of abnormal signals by sleeper receptors Chemical Senses *label-lined codes-vision & sound *chemical coding- taste & smell-one stimulus activates several neurons, largely depends on context taste • 5 primary tastes- sweet, salty, sour, bitter, umami (Japanese for delicious or savory taste; ex. soy sauce, MSG) o fat can influence taste of foods, thought of as a 6 taste o miracle fruit can alter taste buds-make sour things sweet • flavor perception-combination of taste and smell; endopiriform cortex • papillae-contain taste buds; each contains ~50 receptors, each receptor has ~10 taste buds taste transduction • saltiness-sodium ions in salt cross membrane, depolarizes cell to make neurons fire, very direct • sourness-acid closes potassium channels making neuron more likely to fire • sweetness, bitterness, umami- activates a g-protein to have a wider range of actions; toxic substances taste bitter tasting heat • capsaicin o pain receptors activated o not absorbed into body, passes right through o activates heat receptors in body and responds by inflammation o pepper spray is concentrated capsaicin taste pathway • taste receptors part of cranial nerves • form synapses at gustatory nucleus then travel to ventral posterior medial nucleus in thalamus • connected to amygdala-emotion related to taste • projections to hypothalamus-memory and motivator for food psychology of taste § adaption-idea that receptors fatigue from same stimuli o first bites of meal are the best § enhancement-combining 2 flavors into one o huge industry (ex. pumpkin spice, salted caramel) olfaction § olfactory epithelium(OE)-airborne chemicals come in contact with receptors in OE § cilia-hair-like projections that act as receptors/dendrites-transduction occurs here § triggers changes in g-proteins § particles of what you smell are in your nose-most direct sense-in contact with physical world § olfactory pathway: olfactory receptorsàneural impulseàolfactory nerveàolfactory bulb(brain) o smells critical for memory formation-located beside hypothalamus synesthesia § sensory information processed in wrong cortical areas o information interpreted as more than one sense § ex. sound as vision, numbers as colors Sensory Systems Book Outline {Sound} § sound waves-periodic compressions of air, water, or other media; vary in amplitude (intensity) and frequency (# of compressions per second measured in hertz) o humans hear sounds from 15/20Hz-20,000Hz; children can hear higher frequencies than adults § pitch-related aspect of perception § timbre-tone quality or tone complexity o people communicate emotion by changes in pitch, loudness, and timbre; conveying info by tone of voice is prosody {Ear Structures} § outer ear: pinna-cartilage attached to each side of head, alters reflections of sound waves to locate source of sound, sound then travels to auditor canal § middle ear: tympanic membrane (ear drum)-vibrates the hammer, anvil, and stirrup which connect to the oval window § inner ear: oval window-membrane of the inner ear; cochlea-contains 3 fluid filled tunnels (scala vestibuli, scala media, scala tympani), auditory receptor hair cells respond to displacements of the fluid in the cochlea caused by vibrations from the stirrup to the oval window {Perception of Pitch} § place theory-basilar membrane like strings of piano and each section tuned to a specific frequency, each frequency activates hair cells only at specific place on basilar membrane and neurons respond based on which hair cells activated § frequency theory-basilar membrane vibrates in synchrony with a sound causing auditory nerve axons to produce action potentials at same frequency § current theory-modification of both theories § volley principle of pitch & discrimination-auditory nerve produces volleys of impulses for sounds up to 4,000 per second even though no individual axon approaches that frequency § amusia (“tone deafness”)-4% of people have it, do not detect minor changes in sound {Auditory Cortex} § primary auditory cortex (A1)-in superior temporal cortex o the “what”-sensitive to patterns of sound in the anterior temporal cortex o the “where”-sensitive to sound location in posterior temporal cortex and parietal cortex § development of auditory system depends on experience § damage to A1 does not produce deafness; cortex not necessary for hearing, just for processing the info; those with damage have trouble with speech and music but can hear simple sounds {Sound Localization} § time of arrival-sound coming directly from the side reaches closer ear faster, useful for sounds with a sudden onset § sound shadow-difference in intensity between the ears, head makes sound louder for closer ear § phase difference-useful for localizing sounds up to 1500 Hz, sound wave will strike each ear out of phase, best for low frequencies {Pain Relief} § opioid mechanisms-systems that respond to opiate drugs and similar chemicals to halt pain; opiates bind to receptors in spinal cord and periaqueductal gray area of midbrain to act on nervous system not injured tissue § gate theory-attempts to explain why some people withstand pain better than others- spinal cord neurons that receive messages from pain receptors also receive input from touch recpeptors and from axons descending from the brain; these other inputs close the gates for pain messages by releasing endorphins § placebo-drug with no pharmacological effect, those who receive placebos often times say they have/feel the effect they are suppose to have from the real drug Movement muscles & their movement § smooth-controls internal organs § skeletal (striated)-movement, connects skeleton/limbs § cardiac-heart, can propagate neural impulse from muscle fiber to muscle fiber, tissue lasts a lifetime o exercise causes greater blood flow to heart § muscles-individual fibers receive info from only one axon, axon can innervate multiple fibers § neuromuscular junction-synapse, where motor neuron synapses to muscle fiber o acetylcholine is neurotransmitter that causes muscles to contract muscle contraction § pull not push § neuron releases ach which depolarizes membrane by opening calcium channels; myosin extends to connect actin filaments § antagonistic (ex. biceps & triceps) skeletal muscle § fast-twitch-contract more quickly than slow-twitch; require anaerobic reaction-glucose but not oxygen; fatigue rapidly § slow-twitch-contract less quickly, require aerobic process so requires oxygen; non- strenuous exercise § intermediate fibers-in between fast/slow twitch reflexes § involuntary, consistent, and automatic § seen in infants: grasp reflex, Babinski reflex, rooting reflex § medical vs. lateral corticospinal tracts o medial-develops earlier, control of trunk and midline § ballistic movements-once initiated, cannot be altered § central pattern generators-rapid sequences of movement in a rhythmic pattern (ex. bird wing flapping, wet dog shaking) § motor program-innate or learned responses, no brain needed (ex. yawning) cerebral cortex § primary and secondary motor cortices o hands, feet, face, tongue have largest areas-dextrous movement conscious movement § readiness potential-activity in motor cortex before we consciously decide to move § conscious decision to move occurs ½ second after activity in motor cortex basal ganglia *** § subcortical structures in the forebrain-caudate nucleus, putamen, globus pallidus § works on inhibitory processes § basal ganglia causes a movement by ceasing to inhibit it § critical for automatic behaviors/habits § key structure in movement disorders parkinson’s disease § motor symptoms: tremors, rigidity, loss of balance and coordination § neural symptoms: substantia nigra deteriorates, decreased excitation from thalamus to cortex § causes: exposure to neurotoxins (ex. herbicides, pesticides, carbon monoxide) § exercise can reduce age causing deterioration § treatment: o L-dopa- precursor to dopamine that can cross blood brain barrier; causes many negative side effects o deep brain stimulation huntington’s disease § motor symptoms: writhing, grimacing, arm jerks, facial twitches § neural symptoms: cell loss in striatum of cortex because of overstimulation § genetic-huntingtin gene § treatment-reduce dopamine, experimentation with anti-glutamate drugs multiple sclerosis § motor symptoms: tremors, impaired coordination § neural symptoms: deterioration of myelin sheath Movement Book Outline {Muscles} § three types: o smooth-control digestive system & organs o skeletal/striated-control movement of the body in relation to the environment o cardiac-control the heart § each muscle fiber receives info from only one axon, but a given axon may innervate more than one muscle fiber; allows for more precise movement in certain muscles § neuromuscular junction-synapse between a motor neuron axon and a muscle fiber; axon releases acetylcholine to excite muscle to contract § antagonistic muscles-opposing sets of muscles (ex. flexor and extensor) § fast-twitch fibers-fast contractions and rapid fatigue because anerobic-using reactions that do not require oxygen at the time but need oxygen for recovery § slow-twitch fibers-less vigorous contractions and no fatigue; aerobic-use oxygen during movement {Muscle Control} § proprioceptor-receptor that detects position or movement of a part of the body; detect stretch/tension of a muscle and send messages that enable spinal cord to adjust its signals § stretch reflex-when muscle is stretched, spinal cord sends a signal to contract it reflexively; caused by a stretch does not produce one § muscle spindle-proprioceptor parallel to the muscle that responds to the stretch o negative feedback-when a muscle and its spindle are stretched, the spindle sends a message that results in a muscle contraction that opposes the stretch § golgi tendon organs-proprioceptors that respond to increased muscle tension; act as a brake against an excessively vigorous contraction § refelexes-consistent automatic responses to stimuli; involuntary because insensitive to reinforcements, punishments, and motivations § ballistic movement-executed as a whole; once initiated it cannot be altered {Sequences of Behaviors/Movement} § central pattern generators-neural mechanisms in the spinal cord that generate rhythmic patterns of motor output; important for speaking, writing, dancing, etc. § motor program-fixed sequence of movements; in humans yawning and certain facial expressions are programmed {Cerebral Cortex} § primary motor cortex-precentral gyrus of the frontal cortex; direct electrical stimulation of this area elicits movement o axons extend to the brain stem and spinal cord which generate the impulses that control the muscles § cerebral cortex important for complex actions such as talking or writing § motor cortex orders an outcome and leaves it to the spinal cord and other areas to find the right combination of muscles {Planning a Movement} § posterior parietal cortex-monitors position of the body relative to the world; first area to become active in planning a movement § supplementary motor cortex-important for planning/organizing a rapid sequence of movements; essential for habitual actions § premotor cortex-most active immediately before a movement; receives info about the target the body is directing its movement and current position and posture-info necessary to direct movement to target § prefrontal cortex-active during delay before a movement, stores sensory information relevant to movement, and important for considering outcomes of movement o damage to this area would cause disorganized movement (ex. showering with clothes on) {Mirror Neurons} § mirror neurons-active both during preparation for a movement and while watching someone else perform the same/similar movement o important for understanding, identifying, and imitating others {Connections from BrainàSpinal Cord} § messages from brain must reach medulla and spinal cord which control the muscles § corticospinal tracts-paths from the cerebral cortex to the spinal cord; lateral and medial tracts § lateral corticospinal tract- pathway of axons from primary motor cortex, surrounding areas, and the red nucleus (a midbrain area that is responsible for controlling arm muscles) to their target neurons in the spinal cord o aka pyramidal tract- in bulges of the medulla called pyramids, lateral tract crosses to the contralateral side of the spinal cord o controls movements in peripheral areas (ex. hands and feet) § medial corticospinal tract-pathway of axons from many parts of cerebral cortex, midbrain tectum, reticular formation, and vestibular nucleus (brain area that receives input from vestibular system) to both sides of the spinal cord o controls muscles of the neck, shoulders, and trunk therefore bilateral movements such as walking, turning, bending, standing up, etc. {Cerebellum} § contains more neurons than the rest of the brain combined and a huge number of synapses § important for tasks requiring timing and certain aspects of attention § cerebellar damage symptoms: clumsiness, slurred speech, inaccurate eye movements (resembles those of alcohol intoxication) § responds to sensory stimuli even in the absence of movement and responds to violations of sensory expectations § cellular organization-cerebellar cortex receives input from spinal cord, sensory systems by cranial nerve nuclei, and the cerebral cortex § arrangement of neurons in cerebellar cortex-neurons are arranged in precise geometrical pattern with multiple repetitions of the same unit o purkinje cells-flat cells in sequential planes parallel to one another o parallel fibers-axons parallel to one another and perpendicular to planes of purkinje cells; action potentials in parallel fibers excite purkinje cells which then transmit inhibitory messages to cells in the nuclei of the cerebellum and the vestibular nuclei in the brainstem, which in turn send information to the midbrain and thalamus {Basal Ganglia} § group of large subcortical structures in the forebrain including caudate nucleus, putamen, and globus pallidus § dorsal striatum-caudate nucleus and putamen together-receives input from cerebral cortex and substantia nigra and sends output to globus pallidus which sends output to the thalamus which relays it to the frontal cortex o direct pathway-enhances selected movement o indirect pathway-inhibits inappropriate competing movements; essential for learned performance § role of basal ganglia is to regulate vigor of movement, especially in self-initiated spontaneous movements; also important for learning new habits {Conscious Decisions & Movement} § readiness potential-activity produced by motor cortex before any voluntary movement; begins ~500ms before the movement § brain activity responsible for movement begins before the conscious decision {Parkinson’s Disease} § symptoms: rigidity, muscle tremors, slow movements, and difficulty initiating physical and mental activity; early symptoms include loss of olfaction and psychological depression § immediate cause is the gradual loss of neurons in the substantia nigra and therefore a loss of dopamine-releasing axons n the striatum which casuses decreases in inhibition of the globus pallidus which increases inhibitory output to thalamus § more common in those with exposure to toxins in rural areas § MPTP-chemical in a drug similar to heroin that the body converts to MPP+ which accumulates and destroys neurons that release dopamine § L-dopa-precursor to dopamine that crosses the brain barrier; most common treatment o treatment does not slow the continuing loss of neurons and it produces unpleasant side effects {Huntington’s Disease} § severe neurological disorder that causes arm jerks and facial twitches; then tremors spread to other parts of the body and develop into writhing; disorder associated with gradual, extensive brain damage in basal ganglia and cerebral cortex; psychological disorders stem from this disease § 1 in 10,000 people in the US; diagnosed between the ages of 30 and 50 § results from autosomal dominant gene § huntingtin-protein that codes for Huntington’s disease, mutant form produces harm only inside neurons in the brain Sleep biological clock § human circadian rhythms § zeitgeber: “time giver”-sunlight is most important, tides, meals, arousal, exercide suprachiasmatic nucleus (SCN) § part of hypothalamus § retinohypothalamic pathway-small part of optic nerve travels here o melanopsin-photopigment stimulated,; ganglion cells use this instead of rods and cones o melatonin is a hormone released by the pineal gland 2/3 hours before bedtime, influenced by light § damaged SCN causes inconsistent body rhythms midbrain structures of wakefulness § reticular formation o pontomesencephalon-critical for wakefulness. ach and glutamate, widespread excitatory effects § locus coeruleus-stimulates brain by releasing norepinephrine hypothalamus and wakefulness § releases histamine § releases orexin-prevents brain from switching to sleep § preoptic area-manages sleep debt basal forebrain and sleep § releases inhibitory neurotransmitter GABA-helps calm us down § adenosine-builds up throughout the day to make sleepy, caffeine is adenosine antagonist functions of sleep 1. conserve energy 2. avoid predators why do we sleep? § restorative theory-repairs and maintains § growth theory-sleep to grow (babies & puberty) § memory consolidation & learning theory-perform motor/memory tasks after sleep biology of dreaming § very little input from sense organs during sleep-supressed VI, active inferior parietal cortex-visual special perception § motor cortex suppressed § active hypothalamus & amygdala- emotional content of dreams § suppressed prefrontal cortex-critical for working memory § lucid dreaming-we can influence and control dreams to some extent function of dreaming § activation synthesis hypothesis-brain tries to make sense of information § memory-culling § day dreaming- spend ½ of waking time day dreaming, brains default network activated when unegaged in conscious tasks sleep disorders § insomnia § sleep apnea-physiological-breathing stops temporarily, machine creates positive pressure to help keep breathing § narcolepsy-lack of orexin-fall asleep randomly, unpurposefully § catoplexy-loss of motor control-limpness § night terrors-wake up with sense of anxiety & terror-non REM sleep Wakefulness & Sleep Book Outline {Biological Clock} § zeitgeber(“time-giver”)-stimulus that resets the circadian rhythm; light, tides, exercise, arousal, meals, and temp of environment § suprachiasmatic nucleus (SCN)- a part of the hypothalamus; main driver of rhythms for sleep and body temperature; circadian rhythms produced here § retinohypothalamic path- path from the retina to the SCN that alters the SCN’s setting o input to the path comes from special retinal ganglion cells with their own photopigment called melanopsin o responds to overall average amount of light not to instantaneous changes in light § pineal gland-regulated by SCN, releases the hormone melatonin which influences both circadian and circannual rhythms; melatonin secreted mostly at night making us sleepy {Stages of Consciousness} § sleep-state that brain actively produces characterized by decreased response to stimuli § coma-extended period of unconsciousness caused by head trauma, stroke, or disease § vegetative state-alternates between periods of sleep and moderate arousal; aroused state shows no awareness of surroundings or purposeful behavior § minimally conscious state-occasional brief periods of purposeful actions and a limited amount of speech comprehension § brain death-condition with no sign of brain activity and no response to any stimulus {Stages of Sleep} § polysomnogragh-combination of EEG and eye-movement records § alpha waves- frequency of 8-12 per second, characteristic of relaxation not of all wakefulness § Stage 1-brain activity less than relaxed wakefulness but higher than other sleep stages § Stage 2 o sleep spindle-12-14Hz waves during a burst that lasts at least half a second; results from oscillating interactions between cells in thalamus and cortex o K-complex-sharp wave associated with temporary inhibition of neuronal firing § Stage 3-4-heart rate, breathing, brain activity decrease and slow, large-amplitude waves become more common o slow-wave sleep (SWS)-indicate that neuronal activity is highly synchronized; sensory input to cerebral cortex is greatly reduced and cells synchronize activity § paradoxical sleep-deep sleep in some ways and light in others (term for non-human species) § rapid eye movement (REM) sleep-synonymous with paradoxical sleep; increased neuronal activity and increased relaxation of postural muscles o believed that dreams occur here o (NREM) non-rem sleep-stages other than REM {Brain Structures of Arousal & Attention} § reticular formation-structure that extends from medulla into forebrain; some neurons have axons ascending into brain and descending into spinal cord o pontomesencephalon-part of reticular formation that contributes to cortical arousal; axons extend into forebrain releasing Ach and glutamate; maintains arousal during wakefulness and inc it in response to new or challenging tasks § locus coeruleus-small structure in the pons, emits bursts of impulses in response to meaningful events, especially those that produce emotional arousal; axons here release norepinephrine which inc activity of most active neurons and dec activity of less active neurons § hypothalamus o one axon pathway releases histamine which enhances arousal and alertness throughout the brain o one axon pathway, mainly from the lateral and posterior nuclei, releases orexin-a peptide neurotransmitter-important for staying awake especially towards the end of the day o lateral hypothalamus regulates cells in the basal forebrain which provides axons extending throughout thalamus and cerebral cortex-some axons release Ach which is excitatory and inc arousal, important for sharpening attention {Inhibition of Brain Activity} § during sleep, neurons in the thalamus become hyperpolarized, decreasing their readiness to respond to stimuli and decreasing the information they transmit to the cortex § during sleep, axons that release neurotransmitter GABA inc their activity interfering with the spread of info from one neuron to the other o sleep depends on GABA-mediated inhibition so sleep can be local within the brain § somnambulism-“sleep walking” § lucid dreaming {Sleep Disorders} § insomnia-inadequate sleep-can be caused by noise, temp, stress, pain, diet, medications, and neurological or psychiatric conditions § people fall asleep while their temperature is declining and awaken while it is rising; can be affected by phase delay and phase advance § sleep apnea- Impaired ability to breathe while sleeping; caused by genetics, hormones, old-age deterioration of the brain mechanisms that regulate breathing, or obesity § narcolepsy-condition characterized by frequent periods of sleepiness during the day, affects 1/1,000 people; symptoms: attacks of sleepiness during the day, occasional cataplexy, sleep paralysis, hypnagogic hallucinations; cause related to inability of hypothalamic cells to produce orexin § periodic limb movement disorder-characterized by repeated involuntary movement of legs and sometimes arms during sleep § REM behavior disorder- vigorous movement during REM periods, apparently acting out their dreams; inadequate inhibitory transmission may be responsible for this Internal Regulation Book Outline TEMPERATURE regulation {Homeostasis & Allostasis} § homeostasis-regulation of biological processes that keep the body variables as a set point-single value that the body works to maintain § negative feedback-processes that reduce discrepancies from the set point; something causes a disturbance, and behavior proceeds until it relieves the disturbance § allostasis-the adaptive way in which the body anticipates needs depending on the situation, avoiding errors rather than just correcting them {Controlling Body Temperature} § basal metabolism-energy used to maintain a constant body temperature while at rest § poikilothermic-amphibians, fish, and most reptiles; body temp matches environment temp; lack physiological mechanisms of regulating body temp § homeothermic-mammals and birds, use physiological mechanisms to maintain a nearly constant core temperature despite changes in temp of environment {Brain Mechanisms} § preoptic area/anterior hypothalamus-send output to hindbrain’s raphe nucleus, which controls the physiological mechanisms such as shivering, sweating, changes in heart rate and metabolism, and changes in blood flow to the skin THIRST…water makes up 70% of human body {Mechanisms of Water Regulation} § vasopressin-hormone released by posterior pituitary that raises blood pressure by constricting blood vessels, inc pressure helps compensate for the dec blood volume o also known as ADH (antidiuretic hormone) because it enables the kidneys to reabsorb water from urine and therefore make urine more concentrated § mammalian body fluids remain at a nearly constant level of 0.15M and any deviation activates mechanisms that restore concentration of solutes to set point {Osmotic Thirst} § osmotic thirst-a drive for water that helps restore normal state o osmotic pressure occurs when solutes are more concentrated on one side of the membrane than on the other § brain detects osmotic pressure and sodium content of blood by the OLVT and subfornical organ (SFO)-receptors around the third ventricle § OLVT and SFO relay info to parts of the hypothalamus including the supraoptic nucleus and the paraventricular nucleus (PVN) which controls the release of vasopressin § lateral preoptic area controls drinking {Hypovolemic Thirst} § thirst based on low volume; occurs after bleeding, diarrhea, or sweating § angiotensin II-constricts blood vessels, compensating for the drop in blood pressure; helps trigger thirst and detect blood pressure through receptors in large veins; indicates low blood volume § aldosterone-hormone produced by adrenal glands causing the kidneys, salivary glands, and sweat glands to retain salt; indicates low sodium HUNGER


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