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Exam 3 guide.docx

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PSB 2000

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Exam 3 Highlighted stuff on exam! Sleep Study Questions 1) We discussed 3 possible functions of sleep in general; know those.  1)Energy Conservation, Restoration, Memory  2)Repair and restoration; growth hormone secreted, wound healing increased  3) Learning & memory consolidation • All of these may be true. • Sleep is useful for conserving energy while an animal is inactive. • Body temperature drops and metabolism slows down. • The brain is inactive and uses less energy. • It also makes the animal inconspicuous. • Sleep may also help to recalibrate the senses. • Gives neurons a chance to rebuild • Neurotransmitter production cant keep up with continuous activity • Monoamine neurotransmitters are depleted • Essential for wakefulness, mood, and attention • REM (rapid eye movement) sleep: also called paradoxical sleep because the brain waves are fast but the body is relaxed and the person doesn’t wake up easily. It is accompanied by rapid back and forth eye movements. • Show electroencephalogram (EEG) waves; NREM=nonREM A polysomnograph includes records of EEG, eye movements, and sometimes 2) We also discussed possible functions of REM sleep; know those. • Hypothesis 1: REM is important for memory consolidation & removal of useless connections • Yes: sleep deprivation can impair verbal or motor learning, but only when deprivation occurs in REM sleep; REM episodes increase following training, return to normal after tasks are mastered • No: MAOi’s and antidepressants decrease REM, but no memory problems in these people • Hypothesis 2: Brain development • Infants have LOTS of REM sleep (next slide) • Animals born more developed than humans have less REM sleep in infancy • Hypothesis 3: Just for “rapid eye movement” part of REM sleep…to get enough oxygen to corneas • But people w/o REM sleep don’t have eye problems 3) What are the different stages of sleep? In general, what is brain activity like in those stages? In what order do humans move thru these stages during a night of sleep? What do heart rate, breathing, blood pressure and temperature do during the different stages of sleep? • Stage 1: overall brain activity is high, but declining • Stage 2: brain activity still decreasing; see wave forms (K-complexes) which serve to protect a person from being awakened by a sudden stimulus • Stages 3 & 4: Slow wave sleep • Stage 4: thalamus stops relaying sensory info to cortex (unless extreme or relevant) • From 1  2 3 4  3  2  REM • Postural muscles of body are most relaxed…actually paralyzed (so deep sleep) • HR, BP and breathing are more variable than in SWS; more facial twitches 4) What is “paradoxical” about REM sleep? What neurotransmitters are involved? How is it related to dreams? • Its paradoxical because the right side of the brain shows up as having activity like its awake, while the left side of the brain shows up with no activity and as if its in a deep sleep. • REM sleep depends on the relationship between the NTs serotonin and acetylcholine • Ach “stimulates” REM sleep (activates cortex when awake too); 5-HT shortens it (so does NE…so people on drugs that increase serotonin and NE (like antidepressants, anxiolytics and aderall) may experience less REM sleep 5) When dreaming, what brain areas are very active, and which ones are inactive? What is the functional consequence of that (for example, the prefrontal cortex being inactive leads to poor memory and logic in dreams)? What are PGO waves? • Region of the hypothalamus that was important for slow-wave sleep is inhibited • Pons activates thalamus, cortex, eye movement center for REM sleep; also inhibits spinal motor neurons • PGO waves P-PONS G-GENICULATE O-OCCIPITAL CORTEX • PGO waves are high amplitude electrical potentials • PGO waves start in the pons  lateral geniculate nucleus of thalamus  occipital cortex 6) Know/understand some common sleep disorders: insomnia, narcolepsy, sleep apnea, periodic limb movement disorder (restless leg syndrome), REM behavior disorder, night terrors, sleep walking, sleep talking. 7) As we age, what changes about overall sleep and the amount of time spent in REM sleep, and what happens to the incidence of sleep disorders? 8) What neurotransmitters are depleted during sleep deprivation? What are some of the symptoms of sleep deprivation? How might these be related? • Monoamine neurotransmitters are depleted. (Which are these?) • They are essential for wakefulness, mood, and attention. • 5HT = Serotonin • DA = Dopamine • NE = Norepinephrine • His = Histamine Deprivation results in poor reaction time, memory loss, mood imbalance, and hallucinations. Sensory Systems Study Questions: 1) What are the names of the receptors for each sensory system and where are they located? o Eye (retina)  photoreceptors (rods and cones) o Ear (cochlea)  hair cells o Nose (olfactory epithelium)  olfactory receptor cells o Mouth (tongue)  taste receptor cells o Skin  mechanoreceptors, nociceptors, thermoreceptors, chemoreceptors 2) What are some differences between rods and cones? o Rods: o Abundant in the periphery o Best for dim light o See black/white o Good sensitivity; not great for visual acuity o Cones: o Abundant in the fovea o Best for bright light o See color o Good for visual acuity; not great sensitivity 3) What is the speech banana? o The speech banana is called such due to its shape. When the sounds of speech or phonemes of all the world’s languages are charted in a diagram with one axis containing decibel levels (dB) and the other axis containing the frequency (Hertz or Hz), the shape is that of a banana. Generally, the graph known as an audiogram is charted with frequency levels (Hz) on the X-axis and the decibel levels (dB) on the Y-axis. o However, normal human hearing can occur with sounds outside of the Speech Banana. These sounds include ambient natural sounds such as a rustling of leaves in the wind or birds chirping. Man made sounds outside of the Speech Banana can include music and mechanical noises (i.e., automobiles, lawn mowers). How does this affect speech? If your high frequency sounds need to be louder for you to hear them, and the teacher is sitting there talking to you then there is a good chance you wont be able to perceive some of the sounds she is making, *Presbicusis- (age related hearing loss) So the problem is that were not hearing all of the sounds in speech anymore, so language compensation becomes more difficult. 4) What are important factors in determining the range of stimuli a species can respond to (ie, the frequencies of sounds, the wavelengths of light, etc)? In what other ways do different species differ from each other in terms of sensory systems? o Transduction determines range of stimuli o We can’t transduce all energy o Can only see small portion of electromagnetic radation (visual light) o Can only hear a small range of frequencies o Differs between species depending on  What they need to be sensitive to (predators; pretyetc)  Structure of receptor organ and receptor cells  Species differences also in terms of sensitivitiy and discrimination  Mice discriminate more odors than we do  Dogs are more sensitive to odors than we are 5) What is transduction? What type of cells are responsible for transduction? (How does transduction occur in hair cells and in photoreceptors?) • Answer to the latter (just so you don’t overthink it): receptors! o Transforming physical energy into the world into electrical energy in our bodies o Receptor cells o Hair cells: o sound waves travel thru outer and middle ear to cochlea causing a wave In the fluid within the cochlea o Fluid movement causes stereocilia to pivot back and forth o Pivoting stretches tip links, which are connected to K+ channels o K+ channels are opened and K+ enters cell, depolarizing it o •VG Ca++ channels open  neurotransmitter is released o NT depolarizes axon of auditory nerve  action potentials sent to brain! o Photoreceptors: o •Without light, receptors inhibit bipolar cells (the “dark current”) o •Light hyperpolarizes photoreceptor cells o •Receptors stop NT release o •Bipolar cells are disinhibited o •Bipolar cells stimulate ganglion cells  –By releasing an excitatory NT o •AP down optic nerve 6) What are labeled line coding and cross fiber patterning? What are examples of each from different sensory systems? o Labeled line: the specific axon carrying the information provides useful info in understanding the stimulus o –Frequency of very high frequency sounds (esp. if quiet) o –Primary taste o –Touch?  AN EXAMPLE: is how we know what primary taste we are tasting (sweet, salty, bitter, sour) o Cross fiber patterning: the pattern of activation across many receptors/axons gives the brain useful coding information o –Color (next)  most light is reflected light  when light hits an object, some is absorbed some reflected  more absorbed  darker looks  wavelengths that are reflected enter our eye  perception of color o –Discrimination w/in primary taste o –Sound frequency (especially if low-ish frequency or well above threshold) o –Olfaction • Example: is how we perceive color (3 types of cones of the colors we see). So now you just need to understand why those are appropriate examples. 7) (What is the rate law?) o Rate of action potentials directly related to intensity of stimulus 8) What is the role of the (1) brainstem and spinal cord, (2) thalamus, and (3) cortex, in processing sensory stimuli? o •Brainstem/spinal cord o These are useful for organizing reflexes to sensory stimuli (knee jerk reflex, withdrawal reflex, blinking and maybe tearing when something touches your eye, startle response, etc) o –Reflexes  •Withdrawal  •Pupil constriction  •Conjugate lateral gaze  •Chewing & salivating  •Acoustic reflex o •Thalamus o –Filter/relay  as you know, is an important relay and filter for sensory info;  Each sensory system gets its own thalamic nucleus o •Cortex o Necessary for Conscious perception of the stimulus & high level evaluation  •Each sensory system gets its own primary sensory cortex o –Organization:  •Tonotopic, somatotopic, retinotopic 9) What do the terms somatotopic, tonotopic, and retinotopic mean? o Somatotopy is the point-for-point correspondence of an area of the body to a specific point on the central nervous system. Typically, the area of the body corresponds to a point on the primary somatosensory cortex o tonotopy (from Greek tono- and topos = place) is the spatial arrangement of where sounds of different frequency are processed in the brain. o Retinotopy describes the spatial organization of the neuronal responses to visual stimuli. In many locations within the brain, adjacent neurons have receptive fields that include slightly different, but overlapping portions of the visual field. 10)What is the trichromatic theory of color vision? What are after images and why do they occur? o •three kinds of receptors for human color vision (color cones) o • each type of cone is maximally sensitive to a different set of wavelengths (short, medium and long wavelengths) o • color is perceived through the relative rates of response of each cones any response by any one cone is ambiguous (CNS must process relative activity across all cones)…this is why we don’t see color well in the dark… perception of color relies on cross-fiber patterning and only 1 type of photoreceptor is active in the dark (rods) o afterimage o •Pigment in blue cones is selectively adapted or fatigued o •Look at white or gray surface…only unadapted cone pigments are active (green and red) o •Combo of green and red perceive yellow o 11)How are sensation and perception different from each other? Know examples from the auditory and visual system, and from aspects of pain perception. Last slide! o •Amplitude and loudness o •Frequency and pitch o •Pain o •Visual system in general! o Sensation occurs at the level of the sensory receptors; perception happens at the level of the brain, specifically at cortex. There is a positive correlation b/t sensation and perception, but the reality is that perception is just the nervous systems best guess of the sensory stimulus…sometimes we miss things and other times even make things up! Emotion and Agression 1) What is the James-Lange theory of emotion? What predictions does it make? What research supports this hypothesis? o •James-Lange theory  –Event  appraisal  action  emotional feeling o –Predictions:  •People w/ weak skeletal responses (paralyzed) should feel less emotion… NO  •People w/ weak autonomic responses (pure autonomic failure) should feel less emotion…YES (still feel emotions, but not as strongly as before)  •Enhancing someone’s responses should increase emotion... YES  –Short of breath  think suffocating  panic attack  panic disorder??  –Make person “smile”  show them something potentially funny  think it’s funny  Exceptions: depression isn’t cured by smiling; smiles aren’t necessary for the feeling of happiness 2) Are emotional expressions learned or innate? o •Innate, unlearned o •Way of communicating!! o •People in different cultures (even isolated environments) use same patterns of movements of facial muscles to express various emotions o •Blind versus sited children: same expressions o •Therefore biologically determined, but can be modulated  Men tend to not express as much emotion; women tend to increase amount of emotional expression 3) •What is the role of imitation in understanding emotions? o •Imitation seems to be innate  Maybe for empathy: see an emotional expression  imitate it  feel it 4) •What are some brain areas involved in emotion? What are some examples of the right hemisphere being more responsive to emotional stimuli? 5) •Personality o –More activity in left frontal cortex  happier, outgoing, fun-loving o –More activity in right hemisphere  socially withdrawn, less satisfied w/ life, prone to unpleasant emotions o •Limbic system  –traditionally thought of as emotion center  –Amygdala especially…more later… o •Insular cortex  –lights up a lot, especially when experiencing (or recognizing on someone else) disgust.  –Also fear. o •Right hemisphere more responsive to emotional stimuli  Activity in R amygdala (more than L) when listen to laughter or crying  Pay attention to emotional expression on face: R (more than L) temporal cortex  Damage to R temporal cortex: difficulty identifying others’ emotional states  People w/ L hemisphere damage outperformed other groups on knowing when people were lying or telling the truth  Inactivate R hemisphere: can remember facts surrounding emotional events, but not the emotion itself 6) •How is the prefrontal cortex involved in emotion? What is the general interaction b/t the prefrontal cortex & the amygdala? How is serotonin involved? o •cortex  –Strong response to all emotions  –Different emotions seen all over, esp. frontal & temporal lobes, and sometimes different emotions activate same regions  –Some cells respond mainly to pleasant pics, others to unpleasant pics; haven’t seen cells specific to differet types of unpleasantness (fear vs. anger) o •Prefrontal cortex, cingulate gyrus and amygdala all active when contemplating a moral decision.  We tend to make decisions based on how they “feel”; reason thru them (justify them) later o •Inability to anticipate unpleasantness leads to bad decision making (includes lack of autonomic arousal in anticipation of bad outcome)  Man w/ prefrontal cortex damage: No emotion, made bad decisions, could predict outcome, couldn’t predict feeling resulting from outcome  2 young adults w/ prefrontal damage in infancy: Never learned moral behavior; stole, lied & abused w/o guilt o •So the amygdala gives you this knee-jerk, aggressive reaction to scary or anger-provoking stimuli. o •Your prefrontal cortex puts the breaks on that reaction, in part by helping you understand how you would feel after such a response. o •Serotonin is excitatory to prefrontal cortex. o 7) •What types of emotions are the amygdala especially important for? What kinds of stimuli activate the amygdala? What are some behavioral/cognitive consequences of damage to the amygdala? Know the experiment about the resident and intruder hamsters, and the activation of the amygdala in those hamsters. o •Receives highly processed sensory information (vision, audition, olfaction, somatosensory; from cortex) o •Output to  –hypothalamus for autonomic response  –Prefrontal cortex to control approach and avoidance  –Midbrain, then pons, then spinal cord for startle reflex o •Associates appropriate emotional response with extrapersonal objects o •Associates drive with appropriate target o Amygdala activated when:  •Looking at photos of something frightening, or someone looking fearful  •Judging someone’s “goodness” or “badness” or when responding even to the name of someone widely known to be very bad or seeing words that denote threatening situation  •Trying to discern complicated emotional stimuli  –Fear directed at you or anger directed away from you are hard to discern  •Looking at someone else whose expression is fear or anger, even if observer isn’t conscious of presentation  –Brief presentation of image, or  –Cortical blindness  During fear conditioning o •Hamster in cage:  –Introduce another hamster (intruder) home hamster eventually attacks  –Take out intruder …wait…put in another intruder  home hamster attacks quicker  –During that time, increased activity in amygdala o •Or if stimulate amygdala, prime the hamster to attack o •Why don’t we attack? PFC o –Prefrontal cortex puts the breaks on a knee-jerk response initiated by the amygdala o DAMAGE to amygdala:  •Still feel emotions  •Impairment in processing emotional info when it is complicated or subtle or ambiguous  •Impairment in focusing on emotional details as opposed to other details  •Trouble recognizing arrogance, guilt, anger, surprise, admiration & flirtation  •Trouble rating “trustfulness” in another person  •Especially difficult to recognize fear  Why? Don’t focus on eyes (which express fear), just mouth (which expresses happiness) and nose o 8) •What do twin studies and adoption studies tell us about the role of heredity in aggressive behavior? o Role of heredity (& environment) in violence: Twin studies and adoption studies suggest genetic influence in violent behavior o o •Adolescent delinquent behavior: dizygotic (fraternal) = monozygotic (identical) therefore more environmental contribution  BUT o •Adult crimes: monozygotic > dizygotic therefore more genetic contribution  sooo….. o •Probably adults have more control over their environment, therefore magnifying the influence of the genetic contribution  interesting: o •Adopted kids: aggressive behaviors are most pronounced with biological parents w/ criminal records and dysfunction in adoptive family o 9) •What is the potential contribution of (1) smoking while pregnant, (2) low serotonin turnover, and (3) high testosterone to aggressive behavior? o •Smoking during pregnancy is correlated with increased likelihood of son to be arrested for violent criminal activities in adolescence and early adulthood  –Effect especially strong if mom smoked & had complications during delivery  –Do women who smoke while pg. raise their kids differently? Use other drugs? Have poor diet?  –Animal studies show that prenatal nicotine exposure impairs brain development o low serotonin turnover  •Mice: less serotonin turnover = more aggressive  –Isolate male mice for 4 weeks  increase aggression & decrease serotonin turnover (amount of serotonin used & replaced)  –Juveniles have lower serotonin turnover and more aggressiveness  •Male monkeys in natural environment: lowest serotonin turnover = most aggressive, most injured, earlier death  •Female monkeys w/ low serotonin turnover also more likely to get injured and die earlier  •Why would evolution select for this?  –Maybe selects for intermediate amount of aggression (b/c too much fear is also bad)  –Or high-risk, high-payoff: risk dying young, but if live become dominant (and therefore mate more; or a female would get more food for herself and her offspring)  •Low serotonin turnover in:  –People w/ history of violent behavior (including arson and other violent crimes) o •Adolescents w/ history of aggressive behavior: those w/ lowest turnover more likely to get in trouble again in next 2 years o •People released from prison: lower serotonin turnover = increased probability of more convictions for violent crimes  –Attempted suicides by violent means o •more common when serotonin turnover is lowest o •Survive one attempt  low turnover predicts more likely to try again in next 5 years o High Testosterone  MALES  •Animals: males fight over mates, females fight to defend their young  •Men fight more than women; 15-25 years of age is most common for male violence  –Hey, that’s also when testosterone is at highest level!  •“Chemical castration” in sex offenders  heterosexual and homosexual attacks disappear along w/ sex drive  •Alcohol along with testosterone seems to increase aggressiveness  –No effect of alcohol in subordinate monkeys who “hadn’t learned to be aggressive”.  •Testosterone doesn’t compel violent behavior; can be related to it o FEMALES  •Also mediated by testosterone (organizational and activational)  •Females get prenatal androgens from brother, especially if b/t 2 males  Rodents: 2M females more likely to exhibit interfemale aggressiveness  Humans: 1M female (girl w/ twin brother): increased aggressiveness, no difference in teenage T levels, so organizational effect of T (or growing up w/ brother)  •CAH girls: higher levels of aggression  •Alters autonomic responses in women, decreases ability to recognize facial expression of anger, increases response in amygdala to image of angry face 10)•Is the role of testosterone due to organizational or activational effects of the hormone? o See previous 11)•What are some aspects of a face that are important in recognizing the emotion it is expressing? 12)•What brain region is important in the expression of disgust? Why that brain region? o Insular cortex  Lights up a lot, also has to do with fear  Disgust.avoid, similar to fear 13)•What is different about the normal brain compared to the psychopathic brain? o •Normal subjects:  –Autonomic signs of emotional conditioning  –Activation in amygdala, insula, & part of prefrontal cortex o •Psychopathic subjects: no signs of conditioned emotional response, little brain activation 14)•By the way, evolutionarily, what is the general role of aggression? In other words, what is the most common cause of aggression (think of intermale aggression, specifically)? o Maybe selects for intermediate amount of aggression (b/c too much fear is also bad) o Or high-risk, high-payoff: risk dying young, but if live become dominant (and therefore mate more; or a female would get more food for herself and her offspring) Organizing and Activating Effects of Hormones 1) •Know the 3 classes of sex steroid hormones and their synthesis pathway. Know examples of each class (ie, testosterone is an androgen). o 3 Classes of sex steroid hormones  Androgens: testosterone, DHT  Estrogens: Estradiol  Progestins: progesterone 2) •Know the differences between organizational and activational effects of hormones. What are some examples of each type of effect in men and in women? o Organizing:  Occur mostly during sensitive periods in development (well before birth in humans)  Effects are generally permanent  Determine whether brain and body will develop male or female characteristics o Activating:  Occur any time in life, when a hormone temporarily activates a response  Effects last as long as hormone is present…thus generally temporary  Includes menstrual cycle in women, sexual excitement in men (and in women…there are some data…) 3) •What is the chromosomal difference between males and females? What is the region of the Y chromosome that is important for male development, and how/why does that trigger male development? What does it mean that “the default development pattern is female”? male XY female XX o SRY= sex determining region of Y chromosome o SRYmale development o No SRY female development o An individual’s sex is determined by the presence or absence of the Y chromosome. (default is female, presence of SRY gene signals male development factor) o Specifically, the SRY gene tells the gonads to develop into testes. o The testes release testosterone, and male development relies heavily on the presence of this testosterone as well as one of its metabolites, DHT. o So an individual’s sexual development could be altered by manipulating testosterone levels… 4) •How can a male be feminized/demasculinized or a female masculinized? o The “default” development pattern is female o w/o androgens or the ability to respond to androgens (androgen receptors), the individual develops as a female o SO, things that block androgen activity during a critical period of development can be feminizing/ demasculinizing in a genetic male  castration  lack of androgen receptors  drugs that block effects of testosterone (including marijuana, alcohol, haloperidol & cocaine) o To a much lesser extent, estrogens (including environmental estrogens) can alter the male pattern of development.  prostate gland (which stores sperm & releases it during intercourse) is especially vulnerable. o The critical period for organizing effects of hormones in rats is right around birth. o Testosterone at this time will masculinize genetic females in terms of behavior*, anatomy, and neuroanatomy o *If given T again again as adult, she will mount a receptive female (more later) o Males have larger sexually dimorphic nucleus (image to left) o Also, female hypothalamus generates cyclic pattern of hormone release (causing menstrual cycle). Male hypothalamus & masculinized female hypothalamus doesn’t 5) •Understand how hormones affect sexual behavior and know some evidence for those effects in rats and in humans. o Alter activity in certain brain regions  change the way the brain responds to certain stimuli. A few examples:  T and probably E decrease pain and anxiety  Decreases in T & E associated w/ memory problems  E stimulates growth of dendritic spines in hippocampus  E increases production of dopamine & serotonin receptors in nucleus accumbens, PFC, olfactory cortex, other cortical regions o •In terms of sexual behavior, hormones change activity in some brain regions & change sensitivity of penis, vagina and cervix. 6) •In what pattern do testosterone levels change in males? Do they also fluctuate in females? If so, in what pattern? o Sexual excitement highest when T is highest (15-25 yr old)  Higher T levels  more “partner-seeking” even if married  Decrease T  decrease sexual activity  Decrease T to control sex offenders  But T (alone) doesn’t cause these behaviors!  Sex offenders have average T levels, except child molesters whose T levels are especially high  Oxytocin also important in sexual behavior o •Fun fact: Viagra works by prolonging effects of nitric oxide (NO)  T increases release of NO  NO facilitates hypothalamus neurons important for sexual behavior & increases blood flow to penis 7) •What hormones are involved in the menstrual cycle? What are hormone levels (low, medium, high) when a woman is periovulatory? You do not need to know any details of the menstrual cycle beyond these questions. However, if is always good to have such knowledge of how the body functions! What changes in behavior do we see during the periovulatory phase? o Hypothalamus + pituitary + ovaries = menstrual cycle (more in Inquiring Minds slides)  Depends on 4 hormones: luteinizing hormone (LH), follicle-stimulating hormone (FSH), estrogen, progesterone o Certain changes when periovulatory  Periovulatory means that E is high, P is beginning to rise, T is as high as it gets in females; this is the few days surrounding ovulation.  More likely to initiate sexual behavior  Find erotica more pleasant and arousing  Prefer more masculine looking men and men who seem “athletic, competitive, and assertive, and who did not describe self as having a nice personality” for “short-term sexual relationship”  Lap dancers earn most tips (b/c feel/a
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