New User Special Price Expires in

Let's log you in.

Sign in with Facebook


Don't have a StudySoup account? Create one here!


Create a StudySoup account

Be part of our community, it's free to join!

Sign up with Facebook


Create your account
By creating an account you agree to StudySoup's terms and conditions and privacy policy

Already have a StudySoup account? Login here

PSYC 220 Study Guide Exam 2

by: Lynde Wangler

PSYC 220 Study Guide Exam 2 PSYC 220

Lynde Wangler
GPA 3.836

Preview These Notes for FREE

Get a free preview of these Notes, just enter your email below.

Unlock Preview
Unlock Preview

Preview these materials now for free

Why put in your email? Get access to more of this material and other relevant free materials for your school

View Preview

About this Document

These are notes from all the lectures.
Meghan Jones
Study Guide
50 ?




Popular in Biopsychology

Popular in Psychlogy

This 17 page Study Guide was uploaded by Lynde Wangler on Thursday March 3, 2016. The Study Guide belongs to PSYC 220 at University of North Carolina - Chapel Hill taught by Meghan Jones in Spring 2016. Since its upload, it has received 43 views. For similar materials see Biopsychology in Psychlogy at University of North Carolina - Chapel Hill.

Similar to PSYC 220 at UNC


Reviews for PSYC 220 Study Guide Exam 2


Report this Material


What is Karma?


Karma is the currency of StudySoup.

You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!

Date Created: 03/03/16
PSYCH 220 Study Guide EXAM 2 PSYC 220 WEEK 5 Vision  Properties of Perception: perception occurs in the brain, whereas sensation occurs in the sensory organs (nose, ears, eyes, etc.); there are several levels of perception  Law of Specific Nerve Energies: Johannes Muller (1883), posited that each neuron is specific to each type of sensory information o Activity of olfactory nerves is interpreted as smell, photoreceptor activation light, etc. o Perception (rather than sensation) is dependent upon the frequency and patterns of firing  Eye Anatomy: o Cornea – first structure light passes through, immovable structure, does 80% of the focusing o Pupil – light enters eye through this opening o Lens – light is focused (20%), moveable structure that operates by accommodation o Retina – light is projected on the retina which consists of photoreceptors (rods and cones) and various other cells (horizontal, bipolar, amacrine, ganglion)  Retinofugal Pathway: photoreceptors bipolar  ganglion cells; bipolar cells also active amacrine cells which synapse with other bipolar cells; blind spot – occurs where there is an absence of photoreceptors where the optic nerve exits the eye  Types of Cells Within the Retina: Photoreceptors, HBAG (horizontal, bipolar, amacrine, and ganglion); light passes thought all other cells to the photoreceptors in the back of the retina and then information gets filtered forwards through other cells (backwards set up)  Fovea vs. Periphery: o Fovea – small area in the retina composed almost exclusively of cones; low neural convergence = high level of acuity each photoreceptor (cone) converges onto only one bipolar cell o Periphery – composed of rods primarily; high neural convergence = less visual acuity and higher sensitivity to light  Photoreceptors: o Rods – scotopic vision (night vision), lower acuity because of higher neural convergence, higher sensitivity to light, found in periphery and not in the fovea, provides contrast information (outlines of objects), outnumber cones by a lot o Cones – photopic vision (color vision), higher acuity because of lower neural convergence (in the fovea especially), less sensitive to light = mediates day time vision or when a lot of light is available, responsible for 90% of eyes’ input to the brain  Sensitivity vs. Acuity: sensitivity (to light) is the ability to detect objects; acuity is the ability to discern details about objects; pupil constriction = increases acuity; in settings with lower lighting, the pupil will dilate to allow more light to enter (increasing sensitivity to light) but decreasing acuity  Convergence of Input onto Bipolar Cells – bipolar cells can laterally inhibit one another to increase acuity  Electromagnetic Spectrum: visible wavelengths for humans about 400- 700nm; long – red, medium – green/yellow, short – blue, violet  Trichromatic Theory of Color Vision: posits that there are three types of cones (one for short, medium, and long wavelengths) and that nervous system perceives color based on comparing activity of the different receptors (the cones each have different opsins); good explanation at the photoreceptor sensation level  Opponent Process Theory of Color Vision (supported by afterimages) – good at the perception level; red-green, yellow-blue, black-white – we perceive colors in opposites; color coded by response of bipolar cells (more or less firing could mean red or green on that type of cell or blue or yellow for another type of cell); cells that are perpetually stimulated become fatigued so when it stops being stimulated by a certain wavelength of light, perception of the opposite color occurs (after images)  Illusory Square – perception of the square can’t be adequately explained by either theory visual perception depends on more than just activity of neurons in the retina  Retinex Theory: visual cortex compares information from different parts of the retina to determine the brightness and hue of a color for each area in your view visual perception (consciously or not) involves reasoning and inference (BLUE/BLACK or WHITE/GOLD dress example)  Color Deficiency (technically not “color blindness” even though we commonly refer to this characteristic in this way) – occurs when a gene that codes for one of the photopigments in the cone is altered; sex-linked characteristic on the X chromosome so males are more often affected PSYC 220 Week 6 Notes Chapter 5-6 Vision and Other Sensory Systems  Transduction – process through which nervous system converts light into electric signals  Photoreceptors – rods and cones (depolarized in resting state and releasing glutamate); photopigments consist of retinal bound to opsins light stimulation will cause the retinal to let go of the opsin and release energy (bleaching); opsins modify which wavelengths each receptor is sensitive to  Rhodopsin Activation – cGMP is the second messenger that is altered by the release of opsins; cGMP is abundant in the resting cell and keeps the Na+ channels open light activation causes enzymes to break down cGMP causing Na+ channels to close and the cell becomes hyperpolarized; this also decreases the release of Glutamate  Response of Rods to Light: o 1) rhodopsin molecule is inactive o 2) Na+ channels kept open by cGMP o 3) Na+ ions flow into the rods partially depolarizing them o 4) rods continuously release glutamate  Rods Response to Light: o 1) light bleaches rhodopsin molecules o 2) cGMP is broken down by enzymes and Na+ channels close o 3) Na+ ions cannot enter rods so rods become hyperpolarized o 4) glutamate release is blocked  Transduction-Bipolar Cells: light always hyperpolarizes photoreceptors but photoreceptors can excite or inhibit neurons o ON center bipolar cells – glutamate inhibits this type of cell; photoreceptor stimulation excites this type of cell; less glutamate release = less inhibition so the cell is excited o OFF center bipolar cells – glutamate excites this type of cell; photoreceptor stimulation inhibits this type of cell; less glutamate release = less excitation so the cell is inhibited  Transduction – Horizontal cells, Amacrine cells, and Ganglion cells: o Horizontal cells – receive information directly from photoreceptors and inhibit bipolar cells to further refine the information that is transmitted to the visual cortex o Amacrine cells – receive information from bipolar cells and synapse onto other bipolar cells (or ganglion cells); also to refine information in the visual system o Ganglion cells – glutamate always depolarizes ganglion cells; ganglion cells join to form the optic nerve where information is sent to the lateral geniculate nucleus (LGN) of the thalamus (though some projections extend to the superior colliculus and other areas)  Lateral Inhibition – stimulation of a single cone receptor excites the bipolar and horizontal cells; the horizontal cell inhibits the surrounding bipolar cells (important for defining edges)  Bipolar Receptive Fields – on-off center surround; distinct regions of excitation and inhibition; respond to specific orientations of bars of light  Retinal Ganglion Cell Receptive Fields: o Parvocellular  Small cell bodies, small receptive fields, mostly in or near fovea, responsible for detailed analyses of stationary objects, color- sensitive o Magnocellular  Larger cell bodies, larger receptive fields, distributed evenly throughout the retine, respond to movement and broad outlines of shape, not color-sensitive o Koniocellular  Small cell bodies, variable receptive fields, found throughout retina, color sensitivity and function varied  Hierarchical Processing – sensory receptors, bipolar cells, ganglion cells, LGN cells, simple cortical cells, complex cortical cells  Primary Visual Cortex – nasal visual field (closer to nose on each side) crosses over to opposite side of the brain while temporal retina (closer to lateral sides of head) remain ipsilateral; the LGN projects to the primary visual cortex (V1) aka striate cortex Blindsight is a condition in which some with damage to the V1 is still able to perceive the physical properties of light so when you throw a ball, they will move out of the way but not be able to tell why other than a random guess (but it must be more than this because they are able to do it a significant number of times)  Simple Cells in the Visual Cortex: fixed excitatory/inhibitory zones (more light in the excitatory zone = more excitation, whereas more light in the inhibitory zone = less of a response); responds to particular orientation of bar or edge- shaped light stimuli; more likely to respond to vertical or horizontal orientation than diagonals  Complex Cells in the Visual Cortex: located in V1 and V2; respond to a pattern of light in a particular orientation ANYWHERE within its large receptive field  End-stopped Cells in the Visual Cortex: similar to complex cells but include a strong inhibitory areas at one end of the bar-shaped receptive field (if any light hits that inhibitory zone, the cell reduces its response); responds best to bars moving in a particular direction at a certain orientation; MOTION detectors  Parallel Processing in the Visual Cortex: V1 projects to V2 V2 branches in several directions to parts of the parietal and temporal cortex ventral stream: WHAT pathway: through the temporal cortex / dorsal stream: WHERE/HOW pathway: through parietal cortex  Inferior Temporal Cortex: cells in the inferior temporal cortex respond to our perception of objects, not the physical features of a visual stimulus o Visual Agnosia – the inability to correctly name an object even when features of that object can be detected perfectly fine (someone might say “round” and “red” and “curved” when describing something but not be able to identify it as an apple) o Feature detectors – a person with this condition can still identify features with accuracy and lucidity o Prosopagnosia – inability to recognize faces  Specialization for Specific Visual Stimuli: o Parahippocampal (place area: PPA) cortex – images of places o Fusiform (face area: FFA) gyrus – faces (and emotionally relevant stimuli) o Adjacent to fusiform gyrus – bodies, biological motion o V4 – apparent or perceived color; color constancy  Motion Perception: o Area MT (middle-temporal cortex) – aka V5; sensitive to particular speeds and direction of stimulus, acceleration and deceleration, etc.; photographs that IMPLY movement (running, jumping, driving, etc.) o Area MST (medial superior temporal cortex) – more complex stimuli; dorsal: expansion, contraction, and rotation; ventral: objects moving relative to their backgrounds  Akinetopsia: motion blindness (trouble crossing street very common)  damage to area MT; can see objects but not discern movement; MT also receives some input directly from LGN (damage to V1 produces blindness, but in some cases MT has enough info to sense motion)  Development of the Visual System: o Most neurons within the visual system respond to corresponding areas in both eyes; retinal disparity – discrepancy between information from the left and right eye (necessary for depth perception); survival of appropriate synapses through the visual system is dependent on visual stimulation/input o Strabismus (“lazy eye”) – children attend to one eye or the other – treatment often includes wearing a patch over the unaffected eye to force them to attend to the affected eye Chapter 6 – Other Sensory Systems  Sensory Transduction from a Broad Perspective: Generator potential – graded potentials that convert an environmental stimulus of any kind to an electrical change sensory receptor cell (the first EPSP/IPSP; graded potentials)  Audition: sound waves are compressions or vibrations of air, water, or other media o Intensity (force per unit area, measured in decibels) or amplitude codes for loudness o Frequency (cycles per second, measured in Hz) codes for pitch  Fundamental frequency  Harmonics (multiples of fundamental frequency)  Timbre (dependent upon waveform)  Audition in Animals: o Humans – 20Hz to 20,000Hz (gradual decline with age) o Dogs – approximately 40Hz to 60,000Hz (dog whistles work for this reason) o Bats – approximately 20Hz to 120,000Hz echolocation o Mice – 1kHz to 90kHz (cannot hear the lower frequencies that humans can hear)  Structures of the Ear: o Outer Ear – funnels sound waves to the middle ear; consists of pinnae (outer recognizable structure) o Middle Ear – amplifies signal “biological microphone”  consists of tympanic membrane (ear drum), ossicles (hammer, anvil, and stirrup), oval window, *tensor tympani and stapedius – 200ms (these muscles contract to reduce sound within ear – this is why our voices do not sound ridiculously loud to us) o Inner Ear – consists of the cochlea, three parallel, fluid-filled canals  scala vestibule, scala media, and scala tympani, as well as the organ of corti (contains the hair cells)  Auditory Sensory Neurons have Preferred Frequencies:  Outer hair cells have lower thresholds of excitation for some frequencies  Pitch Perception: Place Theory: each area along the basilar membrane is tuned to a specific frequency of vibration; higher frequencies are coded for at the base of the basilar membrane while lower frequencies are at the apex this has to do with the shape of the membrane – the base is more narrow and stiff while the apex is wider and less rigid (imagine cords on a piano – the shorter ones are higher pitched whereas the longer ones are for lower pitches)  Pitch Perception: Frequency Theory – basilar membrane vibrates in synchrony with the sound stimulation of auditory nerve causes action potentials to be phase-locked to the sound – A 100Hz sound wave would cause 100APs/sec  Pitch Perception: Current Theory –> o Frequency Theory applies to low frequency sounds (<100Hz) o Volley Principle applies to higher frequency sounds (<4,000HZ) o Place Theory applies to super-high frequencies (>4.000Hz)  Path of Auditory Impulses: o SONIC MG o Superior olivary nuclei (binaural input – some information crosses over at this point, inferior colliculi, medial geniculate nuclei  Auditory Cortex: o Primary (A1) – tonotopic map o Anterior temporal cortex – “what” o Posterior temporal cortex – “where” o Superior temporal cortex – motion of sounds  Secondary Auditory Cortex – changes in sounds, complex stimulus, sound meaning  Sound Localization – intensity difference, time of arrival/latency difference, phase difference  Hearing Loss: o Conductive deafness – ear fails to convert vibrations into waves of fluid (cochlea still functional) o Nerve deafness (sensorineural hearing loss) – hair cells fail to respond to vibrations o Tinnitus – constant ringing in the ears causes by damage to cochlea o Traditional hearing aid vs. Cochlear implants  Vestibular System: consists of three semicircular canals, saccule and utricle, otoliths and hair cells; important for planning body movements and maintaining balance – where do you think information from the vestibulocochlear nerve goes?  Motion Sickness: sensory conflict theory; caused by movements in the inner ear that we cannot control  Somatosensation – sensory information travels up the dorsal column of the spinal cord and crosses over to the opposite half of the brain at the medulla oblongata  Somatosensory Cortex – Dermatome: each spinal nerve innervates a limited area of the body – its receptive field; somatosensory thalamus innervates a specific part of the somatosensory cortex PSYC 220 Week 7 Notes  Chapter 6: Other Sensory Systems  Stereocilia – cilia on hair cells are mechanically activated; connected by tip links that move to allow ions to flow into the hair cell  Auditory sensory neurons have preferred frequencies – threshold of excitation at a specific frequency will be lower than at others  Pitch Perception: o Place Theory – each area along the basilar membrane is tuned to a specific frequency of vibration; good for explaining higher frequency sounds o Frequency Theory – basilar membrane vibrates in synchrony with sound; stimulation of auditory nerve causes action potentials to be phase-locked to the sound; good for explaining lower frequency sounds but not so much for higher frequencies o Current Theory – frequency theory for low frequency sounds and volley principle for higher frequency sounds (overall pattern of firing represents the frequency); place theory can be applied to super-high frequency sounds  Path of Auditory Impulse: SONIC MG – 1. Cochlear nucleus, 2. Superior olivary nucleus, 3. Inferior colliculus, 4. Medial geniculate nucleus, and 5. A1/Auditory cortex  Auditory Cortex – Primary auditory cortex/A1; anterior temporal cortex = WHAT pathway; posterior temporal cortex = WHERE pathway; superior temporal cortex = motion of sounds o Secondary auditory cortex – changes in sound, complex stimuli, and meanings of sounds o Damage to Auditory cortex – simple pure tones can be heard even with complete removal of auditory cortices; there will, however, be deficits in hearing details of sounds in everyday life  Sound Localization – differences in intensity (whichever is louder will be perceived); time of arrival/latency difference (whichever is heard first will be perceived); phase difference and spectral filtering (pinnae of outer ear)  Hearing Loss: o Conductive deafness – ear fails to convert vibrations into waves of fluid; the cochlea is still functional o Nerve deafness – sensorineural hearing loss hair cells fail to respond to vibrations o Tinnitus – constant ringing in the ears caused by damage to cochlea o Traditional hearing aid – increases volume of sound; amplifies all sounds o Cochlear implant – improves hearing certain frequencies  Vestibular System: three semicircular canals (ampulla); saccule and utricle; otoliths and hair cells important for planning body movements and maintaining balance (information goes to the cerebellum)  motion sickness: sensory conflict theory (structures that are part of the vestibular system register movement but our eyes tell us that we are not moving our bodies in space)  Somatosensation: Receptor Location Responds to Free nerve ending Near base of hairs and Pain, warmth, and cold (unmyelinated or thinly elsewhere in skin myelinated axons) Hair-follicle receptors Hair-covered skin Movement of hairs Meissner’s corpuscle Hairless areas Sudden displacement of skin; low-frequency vibrations Pacinian corpuscle Both hairy and hairless Sudden displacement of skin skin; high-frequency vibrations Merkel’s discs Both hairy and hairless Light touch skin Ruffini endings Both hairy and hairless Stretch of skin skin Krause end bulbs Mostly or entirely in Uncertain hairless areas, perhaps including genitals  Sensory information travels up dorsal column of the spinal cord and crosses over at the medulla oblongata  Somatosensory cortex o Dermatome – each spinal nerve innervates a limited area of the body (think of it like a receptive field) o Somatosensory thalamus innervates a specific part of the somatosensory cortex  Pain: free nerve ending nociceptors: respond to chemicals released when tissue is injured, acids, and temperature; TRPV1: responds to mechanosensory pain and capsaicin o C fibes – unlyelinated; slow, aching pain; A delta fibers – myelinated; acute, sharp pain o Pain information travels up spinal cord via spinothalamic tract; information crosses in spinal cord so that it travels up the contralateral side o Somatosensory information is relayed from the ventral posterior nucleus of the thalamus to the primary somatosensory cortex – same as touch  Mild pain – glutamate  Strong pain – glutamate + substance P o Emotional pain – painful stimuli also travel through a pathway that goes through the reticular formation of the medulla and to the thalamus, amygdala, hippocampus, prefrontal cortex, and cingulate gyrus  Ways to Relieve Pain: 1. At the level of the spinal cord, 2. Descending inhibition o Opioids:  Can directly inhibit the release of substance P  Can trigger descending inhibition from the periaqueductal gray area to disinhibit GABAergic interneurons in the spinal cord (inhibiting neurons that would normally send the pain signal)  Endogenous (endorphins) vs. Exogenous opioids  Opioid mechanisms alter both physical and emotional pain  Inescapable pain – system shuts down  Gate Control Theory: the same spinal cord neurons that receive input for pain also receive input for touch touch inputs might “close the gates” for pain (explains natural inclination to rub something that has been hurt)  Other Ways to Relieve Pain: o Acetaminophen, Cannabinoids, Capsaicin – excessive buildup of calcium damages mitochondria, rendering the receptors temporarily nonfunctional, stress-induced analgesia (opioid dependent); Pain relief methods also attenuate emotional pain  Placebos and Neuropathic Pain: placebo – a drug or procedure with no direct pharmacological effects  most can be blocked with an opioid receptor antagonist (naloxone); have greater effect on emotional or anticipated pain o Neuropathic pain – akin to synapse strengthening as we learn pain synapses in the spinal cord can be sensitized or strengthened to cause neuropathic pain (activity-dependent and difficult to treat) Chemical Senses  Taste: salty, sour, bitter, sweet, umami  Labeled-line coding versus pattern coding (across-fiber coding)** generally considered to be pattern coding that results in most flavor perception (which results from a combination of taste and smell)  Taste Receptors – papillae taste buds taste cells/receptors; microvilli extend from the taste receptor cell into a tiny pore where they can come into contact with tastants  Do We Have Individual Taste Receptors for each Taste? – miracle berries (cells are switched); adaptation and cross-adaptation; researchers can manipulate perceived taste by manipulating neuronal firing in the gustatory cortex (this indicates that patterns of firing result in perception of tastes, rather than individual cells for each taste)  Taste Receptors: o Salty – sodium ions from salty food enter through sodium channels; TRPV1 allows potassium to enter the cell o Sour – detects presence of acid; allows H+ ions to enter the cell o Sweetness – T1R1 and T1R2 proteins combine to be sensitive to sweet chemicals o Bitter – one on any 30T2R proteins (a lot more options than sweet) o Umami – sensitive to dietary amino acids other than glutamate; variant of metabotropic glutamate receptor – sensitive to the amino acid glutamate  Taste Coding in the Brain – input goes to the Nucleus of Tractus Solitarius (NTS), which also sends projections to the pons; 7 , 9 , and 10 cranial nerves  Olfaction – important for selecting food, mates, and avoiding danger; behavioral responses to smell are often unlearned and very robust  Olfactory receptors – about 350 receptor proteins form metabotropic olfactory receptors that are sensitive to a small range of chemically similar odors (rodents have >1000) o Each olfactory neuron extends an axon to a specific glomerulus in the olfactory bulb o Olfactory bulb sends axons to primary olfactory cortex, amygdala, hypothalamus, and orbitofrontal cortex  A Few More Points about Olfaction: anosmia – inability to smell; more common among men; phantosmia – no cortical input creates false olfactory sensations; usually bad ones; women are more sensitive to smell on average; cells extending into olfactory bulb are unmyelinated; adaptation of olfactory cells is relatively quick  Pheremones – vomeronasal organ is separate from olfactory receptors (in humans, it is small with no functional receptors); subconscious responses occur to chemicals that we cannot perceive as olfactory sensation (men find sweaty women sexy while women find sweaty men scary; women’s menstrual cycles sync up)  Polymodal Neurons and Synesthsia – the experience when stimulation of one sense evokes a perception of that sense and another (ex. seeing numbers in color; smelling colors; etc.) o Polymodal neurons in different cortical areas? o Genetic predisposition (for synesthetes) Chapter 7 Movement  Muscles: smooth, skeletal/striate, cardiac  Neuromuscular Junction: synapse between a motor neuron axon and one muscle fiber; motor neurons release Ach; antagonist muscles allow for contraction and relaxation (flexor and extensor muscles)  Types of Skeletal Muscles: fast twitch fibers – fast contractions, rapid fatigue, anaerobic (sprinters); slow twitch fibers – less vigorous contractions, virtually no fatigue, Aerobic (distance runner) o Nervous system will conserve muscle strength in times of strenuous activity  Proprioception: required for coordinated movements; muscle spindle – responds to stretch; golgi tendon organ – responds to contraction (excites interneurons that inhibit muscle contraction); proprioceptors send info to brain and spinal cord (how heavy do you perceive an object to be? vs. how heavy do you expect an object to be?)  Units of Movement: reflexes – involuntary, unlearned, and resistant to change; central pattern generators – rhythmic patterns of motor output (wet dog shake) o Motor Programs – fixed sequences of movements that are established before an act occurs; conserved across species  Feedback from proprioceptors fine tunes movement during execution (yawning – debatable)  Cerebral Cortex – axons from the motor portions of the cerebral cortex extend through the brainstem and spinal cord to reach the muscles; significant amount of overlap in the portions of cortex that innervate any given muscle (motor cortical areas generate outcomes)  Motor Areas of the Cerebral Cortex: o Primary motor cortex – elicits movements, organized topographically o Posterior parietal cortex – planning and monitoring positions of the body relative to the world o Supplementary motor cortex – inhibiting habits o Premotor cortex – acquiring target and body positions needed for a movement immediately before a movement; movement initiated by external stimuli o Prefrontal cortex – calculating outcomes of a given movement  Mirror Neurons – active during a given movement and while observing another person perform the same movement; empathy? Social learning?; do mirror neurons cause imitation and social behaviors or do they result from them???  Lateral Corticospinal Tract (Pyramidal)  Medial Corticospinal Tract (extrapyramidal) – axons from all motor areas of the cerebral cotex; axons go to both sides of the spinal cord and body (bilateral movements)  Cerebellum – balance and coordination (aim, timing, and adjusting); integrates input from somatosensory, vestibular, and auditory systems with muscle coordination; skilled movements damage causes ataxia (loss of coordination) and decomposition of movement o Purkinje cells – flat and arranged in sequential planes; lots of dendritic branching; parallel fibers are perpendicular to the purkinje cells and excite them sequentially  Basal Ganglia – caudate nucleus, putamen, globus pallidus; spontaneous, self-initiated behaviors; guide amplitude and direction of movement; necessary for habit formation  Direct vs. Indirect Pathway: o Direct pathway – enhancement of select movements; net excitation o Indirect pathway – inhibition of inappropriate movements; net inhibitory  Readiness Potentials – brain’s readiness potential begins to rise in preparation for the movement and then a person reports making a conscious decision about the movement and then the movement starts  Movement Disorders: o Damage to motor cortex – paralysis/plegia of voluntary movements on contralateral side of the body; hemiplegia; paresis or hemiparesis o Damage to supplemental motor areas – apraxia (inability to carry out complex movements despite no other visible deficits in motor movements) o Myasthenia gravis o Muscular dystrophy o Amyotrophic lateral sclerosis (ALS) Lou Gehrig’s Disease  Parkinson’s Disease: rigidity, muscle tremors, and slow movements; loss of DA input to striatum; exposure to toxins (MPTP), genetic contributions; treatment  L-dopa  Huntington’s Disease: gradual, extensive neuronal death starting in the basal ganglia; tremors, chorea (jerky movements); associated with depression, sleeplessness, memory impairment, anxiety, hallucinations, delusions, poor judgement, drug abuse; significant genetic contribution (Huntingtin) PSYC 220 Week 8 Chapter 8 (Voice Thread) Wakefulness and Sleep  Endogenous Rhythms: exogenous (sunlight, social influences, societal influences) vs. endogenous (circannual and circadian rhythms) stimuli controlling behavior o Circadian rhythms also exist for other behaviors – eating, urination, hormone secretion, metabolism, drug sensitivity, and mood  Setting the Biological Clock: o Time giver – Light, exercise, arousal, meals, and temperature o Jet lag and phase shifts o Shift work o Strong link to mood; depression o Stress?  Suprachiasmatic Nucleus: (of the hypothalamus) drives biological rhythm retinal ganglion cells feed the retinohypothalamic path which provides light into to the SCN (melanopsin is the photopigment used) o How does blindness affect biological clock?  Per and Tim – proteins that promote sleep and inactivity; produced in highest concentrations at night; pineal gland releases meatonin 2 or 3 hours before bed  Sleep as an Active Process State Brain Activity Responsiveness Duration Sleep Moderate Moderate Hours decrease decrease Coma Low level, remains Little to none Typically weeks, steady then death or recovery Vegetative state Alternation No awareness of Months or years; between sleep and surroundings, but 50% chance of low-level arousal autonomic regaining response to pain consciousness in first 6 months Minimally Alternation Occasional periods Months or years conscious (one between sleep and of comprehension level above VS) low-level arousal of surroundings Brain death none none Until life support is removed  Stages of Sleep: relaxed vs. awake o Alpha waves (8-12Hz); relaxed and awake o Stages 1 & 2 – brain activity decreases, irregular low voltage waves; Stage 2 – sleep spindles and K complex o Stages 3 & 4 – slow wave sleep; heart rate and brain activity decrease; slow large amplitude waves indicate highly synchronized neuronal activity  Rapid Eye Movement (REM) Sleep: marked by irregular, low voltage, fast waves (increased, asynchronous activity); PGO waves – high amplitude electrical potentials (pons, lateral geniculate, and occipital cortex); heart rate, breathing, and BP more variable o Body muscles are more relaxed in this stage than others; biological clock – amount of REM sleep is more related to time of day than amount of time that you have been sleeping  Brain Mechanisms of Sleeping and Waking: o GABAergic inhibition induces “sleep” at a local level o Pontomesencephalon induces wakefulness via acetylcholine and glutamate signals to hypothalamus, thalamus, and basal forebrain o Locus Coeruleus induces wakefulness via norepinephrine signals to cortical areas in response to meaningful events o Hypothalamus induces wakefulness via histamine release throughout the brain  Orexin/Hypocretin: from lateral and posterior nuclei of hypothalamus o Extend to basal forebrain, other areas o Necessary for staying awake o Normally levels rise throughout the day o Blocking orexin receptors induces drowsiness  Sleep Disorders: insomnia, sleep apnea, narcolepsy, periodic limb movement disorder, night terrors, and sleepwalking  Sleep and Energy Conservation: o Hypothesis – sleep evolved to conserve energy o Evidence for – virtually every species more efficient at some time of the day; body temp decreases by 1-2C; muscle activity decreases; sleep duration increased during food shortage o Nervous system can adapt to changing needs; some species of dolphins – don’t sleep for first couple of weeks after giving birth; migratory birds – hunt all day, fly at night  Sleep and Memory: neurons that fired during wakefulness fire during sleep; same patterns, but faster firing; amount of activity correlated with improvement in skill o Weeding out unused connections – weakening of synapses occurs during sleep; synapses that aren’t weakened stand out  Dreams: o Activation-Synthesis Hypothesis – brain’s effort to make sense of sparse and distorted information (sense of falling) o Clinico-Anatomical Hypothesis – when cortical activity is decreased, our thoughts from other brain areas are free to generate images without constraints (thinking under unusual conditions) Chapter 9 Internal Regulation  Homeostasis: physiological mechanisms maintain acidity, saltiness, water level, oxygenation, temperature, and energy availability within the body; homeostasis around a set point (a single value that the body works to maintain) through negative feedback mechanisms o Allostasis – homeostasis around an adjusted set point  Temperature Regulation: o Thermoregulation – basal metabolism (energy used to maintain constant body temperature); why would we want to maintain a constant (warm) body temperature?; ectothermic vs. endothermic; temperatures below freezing or above 109F are life-threatening  Mechanisms of Thermoregulation: Physiological – shivering, sweating, constriction/dilation of blood vessels, accelerated respiration  Brain Areas Important for Temperature Regulation: Preoptic area (POA) and anterior hypothalamus (AH)  Immune Function and Temperature: fever is adaptive change in the body’s temperature set point; Pathway of activation: leukocytes release small proteins called cytokines 1)attack infection, 2) stimulate release of prostaglandins from hypothalamus to induce fever Temperature receptors in the skin Temperature receptors in brain and other organs POA/AH  Infection immune response prostaglandins and histamine  POA/AH – controls shivering, sweating, heart rate, blood flow to skin, metabolism in brown adipose tissue, etc.  Water Regulation: o Osmotic Thirst – a drive for water that helps restore the normal state of osmotic pressure  Osmotic pressure – the tendency of water to flow across a semipermeable membrane from the area of low concentration to an area of high concentration to an area of high concentrations o Hypovolemic thirst – thirst based on volume, animal desires salty water (pure water would dilute body fluid further)  Osmotic Thirst: Set point for concentration of all solutes in mammalian body fluids is 0.15M; Osmotic thirst occurs when osmotic pressure drives water out of the cell; cells in the stomach detect high levels of sodium; neurons detect their own loss of water o Greater concentration of solutes outside the cell than inside water flows out of the cell, equalizing the solute concentration and shrinking the cell  Osmoreceptors – increase solute concentration of interstitial fluid causes osmoreceptors to lose water and shrink in size  change in firing rate of axon  Osmotic Thirst – osmoreceptors located around the third ventricle; OVLT – organum vasculosum laminae terminalis; SFO – subfornical organ; info from OVLT & SFO to hypothalamus paraventricular nucleus & supraoptic nucleus o Control vasopressin release from posterior pituitary o OVLT & SFO  Hypothalamus (PVN & SON) posterior pituitary  vasopressin (ADH) constricts blood vessels and enables kidney to reabsorb water from urine  Hypovolemic Thirst: loss of fluids via bleeding, diarrhea, or excessive sweating; need to restore lost salts, not just water; drop in extracellular volume detected by baroreceptors; no change in osmotic pressure (salts and ions are lost with the water)  SFO then sends signals o hypothalamus to realease more vasopressin and increase drinking  Sodium-Specific Hunger: animal with hypovolemic thirst increases its preference for slightly salty water (developes automatically when sodium reserves are low); aldosterone produced by adrenal glands in response to low sodium (causes kidneys, salivary and sweat glands to retain salt); aldosterone and angiotensin II (can activate taste receptors, nucleus of tractus solitarius (NTS), other salty appetite regions in brain Chapter 9 Internal Regulation Continued  Feast vs. Famine: redundant and complex homeostatic mechanisms guide hunger because we need to monitor and maintain a wide range of nutrients (20 amino acids, carbohydrates – sugars and starches, minerals, vitamins)  The Human Digestive System: o Carnivores – get all the vitamins they need from their prey o Herbivores and Omnivores – social learning; taste (sweet=good, salty and sour=sometimes, bitter=harmful, familiarity) o One trial taste aversion learning – taste is a very potent stimulus in Pavlovian conditioning procedures  Feeding Regulation – oral factors (chewing gum); tasteless diet (liquid diet study); taste-only diet (sham-feeding experiments)  Feeding Regulation: Short Term o Stomach distension is the first signal for short-term satiety (preventing nutrients from passing to the small intestine did not interfere with short-term feeding o Hormone release in the duodenum (OEA, CCK) o Glucose is the principal fuel for cells in the body o Insulin – promotes conversion of glucose into glycogen for short term storage; enables glucose to enter cells; signals satiety o Glucagon – promotes conversion of glycogen back to glucose o Surplus sugars are stores as lipids in adipose tissue  Feeding Regulation: High Insulin o High insulin levels that persist even when there is plenty of glucose entering cells prepare the body for hibernation; no glucagon to balance the use of glucose stores with intake – store much more than you need to such that the cells don’t get as much glucose as normal; can we really blame our autumn weight gain on the holidays?  Diabetes: o Type I – lack of insulin production o Type II – insensitivity to insulin  Feeding Regulation: o Leptin – produced by fat cells, signals that you have plenty of nutrition  Leptin sensitivity declines as a result of pregnancy and obesity o Ghrelin – synthesized and released by cells of the stomach, signals appetite o PYY 3-36 – synthesized and released by cells of the intestines, signals satiety  Hypothalamic Regulation of Feeding: o Arcuate nucleus (AR)  Hunger-motive neurons – NPY neurons  Satiety-motive neurons – POMC neurons o Paraventricular nucleus (PVN)  Inhibited by hunger neurons  Excited by satiety neurons o Lateral hypothalamus  Inhibited by PVN  Output increases feeding  Hypothalamic Regulation of Feeding: NPY neurons are anxiolytic! Less stress hunger will be inhibited ; GABA, NPY, and AgRP inhibitory signals (two kinds of neurons in the lateral nucleus of the hypothalamus); cortical output – attentional biases to food  Hunger Signals: o 1. Inhibitory signal from arcuate nucleus to the PVN o 2. Inhibiting the inhibitory signal from the PVN to the LH  Results in disinhibition  Think of this as the “ releasing the brake” example o 3. Increase in eating behavior (because you are hungry)  Satiety Signals: o 1. Excitatory signal from arcuate nucleus to the PVN o 2. Increase the inhibitory signal from the PVN to the LH  Results in inhibition of the LH o 3. Decrease in eating behavior (because you are NOT hungry)  Lateral Hypothalamus: many pathways o NTS (taste and salivation); Cerebral Cortex (ingestion & swallowing; taste, smell, sight of food); Pituitary gland (insulin production); autonomic (digestive secretions)  Hypothalamic Regulation of Feeding: o Ventromedial hypothalamus is linked to satiety; activity in this region reduces eating behavior; lesions in these region lead to more frequent meals and increased insulin production  Obesity: significant genetic contribution, heritability (Prader-Willi syndrome – high blood levels of ghrelin); obesity was once evolutionarily adaptive; diet and exercise o Other treatments: appetite control (leptin, cannabinoids, PYY 3-36), increased metabolic rate (thyroid hormones); inhibition of fat; reduced reward; gastric bypass surgery  Need to adjust set point  Obesity/Eating Disorders: Over-Activity in Brain Areas Relative to Addiction: activation abnormalities higher in Obesity/Eating Disorders (relative to addiction); Putamen, insula, hippocampus, and temporal cortices  Obesity: Changes in Reward Circuitry: decreased response to receiving a milkshake in caudate for obese subjects (compared to those who are lean); Decreased activation in the caudate is negatively correlated with BMI  Anorexia-Nervosa and Bulimia Nervosa: o Anorexia-nervosa: net consumption of very little food o Bulimia-nervosa: alternate between periods of overeating and strict dieting (net consumption more variable) o Body dysmorphic disorder o Social pressures…but can’t be the whole story


Buy Material

Are you sure you want to buy this material for

50 Karma

Buy Material

BOOM! Enjoy Your Free Notes!

We've added these Notes to your profile, click here to view them now.


You're already Subscribed!

Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'

Why people love StudySoup

Jim McGreen Ohio University

"Knowing I can count on the Elite Notetaker in my class allows me to focus on what the professor is saying instead of just scribbling notes the whole time and falling behind."

Janice Dongeun University of Washington

"I used the money I made selling my notes & study guides to pay for spring break in Olympia, Washington...which was Sweet!"

Steve Martinelli UC Los Angeles

"There's no way I would have passed my Organic Chemistry class this semester without the notes and study guides I got from StudySoup."

Parker Thompson 500 Startups

"It's a great way for students to improve their educational experience and it seemed like a product that everybody wants, so all the people participating are winning."

Become an Elite Notetaker and start selling your notes online!

Refund Policy


All subscriptions to StudySoup are paid in full at the time of subscribing. To change your credit card information or to cancel your subscription, go to "Edit Settings". All credit card information will be available there. If you should decide to cancel your subscription, it will continue to be valid until the next payment period, as all payments for the current period were made in advance. For special circumstances, please email


StudySoup has more than 1 million course-specific study resources to help students study smarter. If you’re having trouble finding what you’re looking for, our customer support team can help you find what you need! Feel free to contact them here:

Recurring Subscriptions: If you have canceled your recurring subscription on the day of renewal and have not downloaded any documents, you may request a refund by submitting an email to

Satisfaction Guarantee: If you’re not satisfied with your subscription, you can contact us for further help. Contact must be made within 3 business days of your subscription purchase and your refund request will be subject for review.

Please Note: Refunds can never be provided more than 30 days after the initial purchase date regardless of your activity on the site.