Final Flashcards
(121 cards)
1
Q
- What are endogenous rhythms? Describe circadian and circannual rhythms and why they are important for certain species. What external stimulus helps reset rhythms?
A
When animals generate rhythms that prepare it for seasonal changes.
Circadian – humans generate a 24-hr wake-sleep rhythm.
Circannual – about a year. Birds have this.
Sunlight is important for resetting rhythms.
2
Q
- What is the suprachiasmatic nucleus (SCN), where is it located and what is its role?
A
It’s the main driver of sleep and body temp rhythms. It’s located in the hypothalamus.
3
Q
a. Describe the retinothalamic path and what type of information it delivers to the SCN.
A
It’s a small branch of the optic nerve. Delivers info from the retina (vidual) to SCN.
4
Q
b. How could looking at a phone or tablet late at night affect sleep through the retinothalamic pathway?
A
Input from the retina comes from special ganglion cells who responds mostly yo short wavelength (blue) light. Phones etc. emit short-wavelength light and exposure late in the day can phase-delay the circadian rhythm.
5
Q
- What is the pineal gland and how does it affect sleep?
A
The pineal gland produces melatonin and modulates sleep patterns in both circadian and seasonal cycles.
6
Q
a. What hormone does the pineal gland secrete and how does it affect sleep cycles?
A
It releases melatonin which influences both circadian and circannual rhythms.
7
Q
- What is sleep?
A
A state that the brain actively produces. An alternation in consciousness with decreased response to stimuli.
8
Q
- What is a coma?
A
Extended period of unconsciousness. Low level of brain activity. Little to no respons to stmuli.
9
Q
a. What does it mean to be in a minimally conscious state?
A
Some deliberate movements (eye tracking), some attempt to communicate.
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Q
b. What does it mean to be in a persistent vegetative state?
A
Coma lasting more than a month. Less likely to recover consciousness the longer this lasts.
11
Q
- What is EEG and what does it do?
A
4 types of brainwaves associated with sleep. Records electrical potentials of neurons.
12
Q
- What is a polysomnograph?
A
Combination of EEG and recording of eye movements.
13
Q
- Describe the EEG wave pattern and any behavioral characteristics (e.g., muscle inhibition, eye movement, etc.) associated with the following stages of sleep:
a. Relaxed wakefulness:
A
steady series of alpha waves.
14
Q
- Describe the EEG wave pattern and any behavioral characteristics (e.g., muscle inhibition, eye movement, etc.) associated with the following stages of sleep:
b. Stage 1
A
theta waves. People at this stage can be awakened easily, but may deny that they were sleeping. May experience a vivid visual image, or psychological experiences such as feeling like you’re falling.
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Q
- Describe the EEG wave pattern and any behavioral characteristics (e.g., muscle inhibition, eye movement, etc.) associated with the following stages of sleep:
c. Stage 2:
A
Theta waves continue but sleep spindles (rapid, short burst of electrical activity) and K-complexes (large fluctuation in voltage) start to occur.
16
Q
- Describe the EEG wave pattern and any behavioral characteristics (e.g., muscle inhibition, eye movement, etc.) associated with the following stages of sleep:
d. Stage 3 & 4:
A
Delta waves. Sensory input to cortex is reduced, and neurons synchronize their activity. Can still process some info, but irrelevant stimuli is filtered out but parents can still hear their babies cry. Hard to wake up, disoriented when awakened.
17
Q
- Describe the EEG wave pattern and any behavioral characteristics (e.g., muscle inhibition, eye movement, etc.) associated with the following stages of sleep:
REM:
A
Show flurry of beta wave activity. Brain activity is high, but body is mostly paralyzed. Eyes dart back and forth rapidly beneath eyelids. Associated with dreaming.
18
Q
- What are PGO waves and with what stage of sleep are they associated?
A
High-amplitude electrical potentials. Associated with REM sleep.
19
Q
- Briefly describe how humans cycle through stages of sleep during the course of a night.
A
You start in stage 1 and slowly progress through states 2,3, and 4. First hours you don’t spend time in REM sleep but as time goes on you spend more time in REM sleep..
20
Q
- What neurotransmitter increases in activity during sleep?
A
Neurons that release GABA because it weakens communication between neurons.
21
Q
- What happens in the thalamus during sleep?
A
Neurons in the thalamus become hyperpolarized.
22
Q
- What are orexins?
A
Neuropeptide that regulates wakefulness and transitions among sleep stages.
23
Q
- What is insomnia?
A
Inability to sleep.
24
Q
- What is obstructive sleep apnea and how is it treated?
A
Breathing during sleep is disrupted or even stopped for short periods. Treated with continuous positive airway pressure (CPAP) device.
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16. What is narcolepsy? What is believed to be the underlying cause and how is it treated?
A rare, chronic brain disorder involving poor control of sleep/wake cycles. Lacks the hypothalamic cells that produce and release orexin. Can also be an autoimmune reaction where the immune system attacks part of the body.
Treatment – stimulant drugs such as Ritalin.
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17. What is REM Behavior Disorder? (study tip: how does it differ from sleepwalking or night terrors?)
Normal paralysis that accompanies REM sleep is disabled. Often unpleasant dreams with vocal sounds and sudden, often violent arm and leg movements.
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18. What is Somnambulism (sleepwalking)?
Behavior during slow-wave, non-REM sleep, typically within 1-2 hours after falling asleep. May appear awake, but disconnected from others. Usually not accompanied by dreaming.
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19. What are night terrors?
Intense anxiety, more severe than nightmares. Usually awakens screaming. Occur in non-REM sleep. Dream content (if any) is simple – like single image.
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20. List and describe two important functions of sleep (why we need it.)
Restoration – allows the body and brain to rest and repair itself. After physical activity, such as marathon, people sleep longer than usual.
Facilitation of learning – neural connections made during awake learning are strengthened during sleep.
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21. What changes in sleep after learning? Are there certain brain regions that are more active and is there a sleep stage we get more of versus other stages?
During times of increased learning, more REM occurs. Hippocampal activity in sleep correlates with degree of learning/memory.
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22. Why may dreaming be important for learning and memory? We discussed some evidence for this in class.
People who dream about a task while sleeping may be especially likely to perform better. It’s good for problem solving.
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23. What are some effects of sleep deprivation discussed in class? (Study tip: note what happens after a few hours, a few days, and what tends to occur with REM sleep).
Light effects; 3-4 hours – more sleepy. Bad mood. Decreased vigilance.
Larger effects; complex cognitive functions (prefrontal cortex). Preform worse on tasks involving assimilating information, planning strategies, innovative, insightful thinking, and working memory.
After 2-3 days: microsleeps – 2-3 second periods that subject may be sitting or standing, but eyelids droop and they are unresponsive to external stimuli.
Proceed more rapidly into REM as REM deprivation increases. REM rebound – more time spent in REM when deprivation is over.
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24. Why do we dream, according to the Activation Synthesis Theory?
Dreams are byproduct of mental processes produced by random brain activation/neural firing during REM sleep. Brain areas that normally interpret sensory input tries to make sense of the random activity by synthesizing it with stored memories. Sensory stimuli, such as sounds in the room, occasionally get incorporated into the dream.
PGO waves are internally generated info and originate from the brainstem. The brain processes these signals and interprets them in terms of information stored in memory. These activations can expand to activate higher-level neurons as well, evoking visual images, sounds, etc. creating dreams.
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25. Why do we dream, according to the Clinico-Anatomical Theory and how does it differ from the activation synthesis theory?
Like AS theory, sees dreaming as a result of stimuli generated within the brain, but less emphasis on pons, PGO waves or REM sleep. Stimuli generated within the brain are combined with recent memories. Dreams are a form of thinking that takes place under unusual circumstances.
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1. Can you tell whether a fetus in the first 6 weeks of development is male or female? Why or why not?
No because there are both Mullerian ducts (precursors to female internal structures) and Wolffian ducts (precursor to male internal structures).
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2. Briefly describe what happens if the fetus as a Y chromosome present (male) and or absent in terms of sex differentiation in fetal development.
If Y present, then SRY gene on this chromosome causes undifferentiated gonads to develop into testes.
Because females don’t have the SRY gene, undifferentiated gonads turn into ovaries.
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a. What develops from the Woffian ducts?
Male internal structures – seminal vesicles and vas deferens.
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b. What develops from the Mullarian ducts?
Female internal structures – oviducts, uterus.
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3. What is androgen insensitivity syndrome (AIS) and what happens during does it occur fetal sex differentiation?
Someone have XY chromosomes and produces normal amounts of androgens (including testosterone). Lack receptors that allow cells to responds to androgens – develops external female anatomy. Usually doesn’t know until puberty. Breast develop. Hibs broaden, but no mens (never developed ovaries. Physically, she develops as a female.
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4. What does it mean to be intersex, and how can this occur in males? How can this occur in females? How can it affect behavior in childhood?
True hermaphrodite (rare) has some testicular and ovarian tissue. May be fertile as either male or female, not both.
More common type: intermediate appearance of anatomy due to atypical hormone pattern during development.
Genetic male with low levels of testosterone may lead to more female appearance.
Genetic female exposed to more testosterone may be partly musicalized.
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5. What is congenital adrenal hyperplasia (CAH) and how does it affect development and subsequent behavioral interests in childhood and adulthood?
CAH is overdevelopment of adrenal gland from birth – affects girls.
In genetic male, extra testosterone causes no problem.
In a genetic female, various degrees of masculinization of external genitals. Ovaries and other internal organs are less affected.
Brains during prenatal development exposed to more testosterone compared to other girls, so behavior is somewhat masculinized. Tendency to play more with boys’ toys vs other girls, but less than boys.
Adolescence and beyond: interest of more rough sports, fewer style magazines, more likely to enter male-dominated occupations.
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6. What are steroid hormones?
Sex hormones. Estrogens and androgens.
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7. Briefly describe the roles of these three sex hormones: androgens (including testosterone) estrogens and progesterone.
Androgens: more in males.
Estrogen: more in females.
Progesterone: another predominantly female hormone. Prepare uterus for implantation.
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8. What is the difference between organizing effects and activating effects of hormones? Give 1-2 examples of each type of effect.
Organizing – produce long-lasting structural effects. Determines whether the body develops male or female genitalia. Breast development (girls), changes in voice and facial hair (boys).
Activating – more temporary. Influences sex drive. Pregnancy; emotional arousal, aggressive behavior, learning/cognition.
Organizing effects set stage for activating effects.
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9. What are the effects of exposure to high levels of testosterone for females in utero in terms of genital development and behavioral interests later in childhood?
Elevated preference for boys’ toys at age 3.5. Tens to spend more time than average playing with toy trains.
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10. What is the medial preoptic area, and how does it affect male sexual behavior (Hint: a certain neurotransmitter is involved).
Located in hypothalamus. Crucial site in the control of sexual behavior in males. Dopamine.
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11. How may testosterone affect single vs. multiple mate preference?
Men and women with higher testosterone levels are more likely than average to seek additional sex partners, even after they marry or establish a long-term relationship.
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12. What are some behavioral changes (including mate preferences) in females that are a result of hormone fluctuations during the menstrual cycle?
Women tend to be more drawn to masculine features during time of ovulation. Women shown videos or photos of men and asked to choose preference for short term relationship – more likely to choose man perceived as more athletic, competitive and assertive.
Hormones associated with fertility move women’s mate preferences toward men who look and act more masculine.
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13. The brain-behavior differences between men and women are relatively few when we think of all aspects of behavior. However, what are some of the few differences that have been shown?
several brain areas are relatively larger in men, and other relatively larger in women. But most individuals show a mix (male-typical patterns in some ways and female typical patterns in others).
These minor differences does not explain why men and women behave differently.
But women tend to be better than men at recognizing emotional expressions, even very subtle ones. If women given testosterone, they temporarily lose this advantage, particularly when trying to recognize anger. Testosterone may interfere with attention to emotional expression.
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14. According to evolutionary theory, what are the mate-selection preferences, on average for men versus women?
Women are more likely to seek good provider, more cautious in dating (avoids men who act interested and then leave).
Men tend to have a preference for younger partner (women are more fertile in younger years) and men stay fertile into old age.
In cultures where women have more educational, employment opportunities, more likely to choose partner closer in age rather than choose based on wealth.
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15. According to evolutionary theory, what are male/female differences with respect to jealousy? If men and women experience infidelity in reality, are their responses the same or different?
Men tend to be more jealous of partner’s possible infidelity. Stronger desire to confirm that the children (his genes) he supports are his own. (women give birth – there is no question!)
Men more upset about sexual infidelity. Women more upset about emotional infidelity. But both men and women who have actually gone through it say they were more upset about emotional infidelity.
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16. What is the difference between sex, gender, gender role, and gender identity?
Sex – biological status of being male or female
Gender – psychological differences between males and females
Gender role – behavior that is typically associated with being male or female. Can be culturally defined
Gender identity – major part of sense of self and whether you think of yourself as being female or male.
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17. What happened in the case of David Reimer, and what does that tell us about the effect of environment on gender identity?
That nature plays a big role in gender identity.
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19. What are the current recommendations when treating those who are intersex or those who identify as the gender opposite of their sex?
Be completely honest with the person and family. Do nothing without their consent. At first. Identify the child as male or female based on predominant external characteristics. Raise the child as consistently as possible but be open to varying gender-typical interests and sexual orientation. Do not perform surgery unless the person makes an informed request in adulthood.
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20. People who differ in sexual orientation also differ in other behaviors, such as how they give directions. What are these differences, and how are gay men alike or different?
Men – give directions in terms of distances and N S E W.
Women – give directions in terms of landmarks
Gay men – tend to refer to landmarks and are better than straight men at remembering landmarks.
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21. What is prepulse inhibition, and how is it the same/different among women who identify as lesbian?
```
It’s stronger in gay women than in straight women.
Prepulse inhibition (PPI) is a phenomenon in which a weak acoustic auditory stimulus inhibits a startle response induced by the subsequent presentation of a loud sound.
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22. When examining the data on sexual orientation of twins and other siblings, what does that tell us about the influence of genes, environment or both?
If an identical twin is gay, probability for the other twin is increased. Less so for fraternal twins.
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23. What are some of the biological theories of homosexuality in men discussed in class?
Mother’s immunity theory – said homosexuality is higher among men with older brothers, even if reared separately. With each pregnancy, mother develops greater immune response to a protein produced in male fetus. Mothers immune cells may alter brain development of the fetus.
2D:4D ratio – said length of the index finger divided by length of ring finger on same hand.
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24. What is the one biological theory of homosexuality in women discussed in class? (Includes discussing the 2D:4D ratio)
2D:4D ratio – said length of the index finger divided by length of ring finger on same hand. Gay women have lower digit ratio on average than straight women.
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25. What is the 3rd interstitial nucleus of the anterior hypothalamus (INAH-3) and what has previous research shown with respect to differences in heterosexual and homosexual males?
Men’s cells in this area have more androgen receptors. 2x as large in heterosexual men as in women.
Study about this area post-mortem - larger in straight men, smaller in gay men and more similar to straight women.
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26. What are 3 evolutionary theories as to why the trait of homosexuality persists?
1. Genes for homosexuality maintained by kin selection – help care for relatives’ young.
2. Same genes might also affect other relatives differently, increasing relatives’ probability of reproducing.
3. Not DNA or genes themselves, but something in the environment that activates or inactivates these gene(s). As an embryo develops, sex-related genes are turned on and off in response to fluctuating levels of hormones in utero, produced by both mother and child. This “tug of war” benefit the fetus, keeping male or female development on a steady course even amid spiked in hormones.
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1. Describe the two branches of the autonomic nervous system. Which one is associated with the “fight or flight” response and how does it affect the feeling of emotion?
Sympathetic division: the accelerator. Functions in actions requiring quick responses. Initiates fight or flight response.
Parasympathetic division: the brake. Promotes calming of the system to return to regular function.
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2. What does the James-Lange Theory state about how we experience emotion?
Autonomic arousal and skeletal actions occur first. You feel afraid because your heart is racing and you’re running away.
Cognitive aspect comes first, then an action/response, then the feeling aspect of emotion.
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3. What is pure autonomic failure and how does it affect emotional experiences?
Automatic nervous system is unable to regulate heartbeat and other organ activities. Someone with this condition does not react to stress with changes in heart rate, blood pressure or sweating. They do experience emotions, but much less intensely.
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4. What do studies on Botox and facial expressions tell us about what hinders or enhances the emotions we experience?
Botox blocks transmission at synapses and neuromuscular junctions. Those getting botox have weaker emotional responses when watching emotional scenes, and are less likely to identify subtle emotions of others.
Feeling a body change is important for feeling an emotion.
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5. What is the behavioral activation system (BAS)?
Increased activity of the left frontal and temporal lobes and low autonomic arousal. The “go” system. Leads an individual to approach stimuli in pursuit of reward.
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6. What is the behavioral inhibition system (BIS)?
Increased activity of right frontal and temporal lobe. Inhibits behavior that might lead to danger or pain, stimulates emotions.
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7. How does the BAS and BIS systems relate to emotional aspects of personality?
???
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8. Recall the Trolley and Footbridge dilemmas discussed in class. Why do people respond differently to these two hypothetical scenarios?
Most would pull the switch, fewer would push a person. Emotional component of interacting with another increases difficulty.
Emotional areas more active in footbridge dilemma, while rational thinking areas more active in trolley dilemma.
People with more autonomic arousal least likely to push.
In deciding right vs. wrong, we seldom work it out rationally. We sometimes call this our gut.
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9. Describe Bechara’s Card Experiment. What does this study tell us about the role of emotions in decision-making?
4 decks of cards, subjects chose one card at a time from any deck. Each card revealed a gain or loss of money. Subjects began to realize that two decks were “good” and two were “bad”. After about 25 draws, subjects were able to tell which decks were good and bad.
Some part of the brain was picking up on the expected return from the decks before they were consciously aware of it, this happened at draw 13. Conscious knowledge of the situation was not required for making advantageous decisions.
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10. Describe how the relationship between emotions and decision-making are affected in people with damage to the prefrontal cortex.
Blunts emotions, can also impair decision making. People with damage often make impulsive decisions without considering the consequences (including how they feel after a possible mistake). End to make choice quickly and calmly in the Trolley and Footbridge dilemmas, when most people find the choice emotionally unacceptable.
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11. Describe how the following factors may be associated with violent or aggressive behaviors:
a. Testosterone:
high testosterone more common among men convicted of violent crimes than those convicted of less violent ones (but difference is small). Those with higher testosterone tend to be more aggressive for both men and women. Does not mean that testosterone causes violent crimes.
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11. Describe how the following factors may be associated with violent or aggressive behaviors:
b. Serotonin turnover
the amount of serotonin that neurons release and replace. In mice: social isolation for 4 weeks increased aggression and decreased serotonin turnover. Effect greatest in genetic strains associated with aggressiveness.
In monkeys: those with lowest serotonin turnover were most aggressive, more likely to attack larger monkeys and incurred the most injuries.
In humans: low serotonin turnover in people with a history of violent behaviors. The relationship between low serotonin turnover and aggression is small.
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11. Describe how the following factors may be associated with violent or aggressive behaviors:
c. The low activity form of the MAOA gene
associated with aggression. It is X-linked gene, so far more men than women have only this type of gene. May contribute to the greater prevalence of violent behavior in men vs women.
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12. Are any of the above factors sufficient to cause violent behavior? Explain why or why not.
No. Low serotonin is weakly associated with increased aggression.
Low activity MAO gene is associated with violence only when there is also a history of childhood mistreatment.
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13. What is the Moro Reflex?
Newborns tendency to arch back, extend his arms in response to feeling sudden loss of support. Loud noises.
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14. What is the Startle Reflex?
Closely related to moro reflex. Auditory info travels to the medulla, then directly to an area in the pons that commands tensing of the muscles (especially neck) and blinking of eyes.
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a. How does fear learning (what can happen in classical conditioning) affect the startle reflex?
After conditioning, classical conditioning becomes a fear signal. Presenting the fear signal just before a sudden loud noise increases the startle response.
A stimulus previously associated with pleasant stimuli becomes a safety signal that decreases startle.
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b. What area of the brain is important for enhancing the startle reflex?
Amygdala
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15. What is the amygdala’s role in processing fear? (Hint: to what other areas of the brain does it send information?)
There are different and separate pathways through the amygdala. Fear of pain, fear of predators, fear of aggressive members of own species, paths for changes in breathing and heart rate, avoidance of unsafe places, path responsible for “freezing” in presence of danger.
Sends info to hypothalamus, PFC, thalamus and midbrain.
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16. How is the amygdala involved in fear learning and fear generalization to other stimuli?
It’s important for learning what to fear, but it also generalizes well. In classical conditioning with shock, rat will learn to fear other associated stimuli. Also true for humans: after trauma, one can become fearful in a wide variety of situations. Amygdala’s motto: better safe than sorry.
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a. What problems can fear generalization pose for people who have experienced a traumatic event?
???
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17. What is the “low and high road” (two pathways) in processing fear, and how might that affect behavior?
???
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18. What are the effects of amygdala damage in both animals and humans?
Rats with damaged amygdala showed no increased startle. There a parasite that reproduces only in cats. Cat poops on the ground, rat burrow in the ground. Parasite enters the rat, damages amygdala. Then the rat just walks up to the cat. Cat eat rat. Parasite lives on in the cat. Circle.
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19. Panic disorder is associated with a decrease in activity of which neurotransmitter?
GABA
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20. What are benzodiazepines, and how do they work to decrease anxiety?
Valium, Xanax etc. They bind to the GABA receptor. When injected into the amygdala, decreased learned shock-avoidance behaviors in rats.
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21. What are some adverse effects of using benzodiazepines?
With prolonged use, can have rebound anxiety.
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22. What factors that are believed to place a person at risk for developing PTSD?
Genetic variability, environmental risks, and incident trauma.
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23. What are some psychotherapeutic treatments for anxiety disorders and PTSD discussed in class? How do they work?
Systematic desensitization – gradual exposure to feared object, in hopes of extinction.
Prolonged exposure – therapy to treat PTSD
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24. What is Behavioral Medicine?
Practice that emphasizes the effects of emotion and behaviors on health. We have a lot of evidence that stress, emotions and other experiences influence people’s illnesses and patterns of recovery.
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25. What is Psychoneuroimmunology?
Studies how stress and psychological factors alter the immune system and how, in turn, the immune system influences the central nervous system.
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26. What is stress?
a type of response that typically involves an unpleasant state, such as anxiety or tension and a perceived imbalance between the demands of the environment and the individual’s resources.
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27. What is a stressor?
Events, situations interpreted as threating to an individual and which elicit physiological and behavioral responses.
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28. What does Yerkes-Dodson Law state about the relationship between stress and performance?
Performance increases with stress, but only up to a point. When levels of stress become too high, performance decreases.
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29. The following two systems are activated when one is faced with a stressor. Describe each and how they affect the response to stress.
a. Sympathetic Nervous System:
Fast acting. Rapid preparation for flight or fight response.
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29. The following two systems are activated when one is faced with a stressor. Describe each and how they affect the response to stress.
b. HPA-axis (know what “HPA” stands for
Hypothalamic-pituitary-adrenal axis. Slower acting. Takes over for more sustained response. Dominates response to prolonged stressors.
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30. How does stress affect the immune response?
Stress decreases leukocyte production and function. Study: healthy volunteers paid to be exposed to cold virus. High stress before exposure led to worse cold symptoms and higher viral counts than those who were less stressed. Major life changes (losing a job or getting a divorce) has greatest impact on immune system.
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31. How does chronic stress affect memory?
There are lots of cortisol receptors on the hippocampus. They help inhibit stress responses. Memory formation is optimal when cortisol levels are mildly elevated.
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32. What are some effective ways for coping with stress?
Be unsympathetic, deep breathing, biofeedback, meditation, active problem solving, social support.
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1. What neurotransmitter is released during reinforcement of a behavior?
Dopamine
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2. What is the nucleus accumbens and its role in establishing reward/reinforcement?
It’s a part of the basal ganglia. It’s where dopamine is released. Central area associated with pleasure.
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3. Nearly all abused drugs affect which neurotransmitter system(s)?
Dopamine and norepinephrine systems.
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4. What does Olds & Milner’s study tells us about addictive behaviors and how they persist even in the face of negative consequences?
That people continue to do drugs no matter of the consequences. They pay a high price for their rewards.
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5. How is the reward circuit “high-jacked” in addiction and how does this affect decision-making for those with active addiction?
The nucleus accumbens gets altered by a lot of exposure to addictive substances. It becomes more responsive to drug and associated cues and less responsive to other types of reinforcements. It also disrupts activity in the prefrontal cortex (lessens ability to restrain impulses).
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6. What is the serotonin transporter? How is the gene that regulates serotonin transporter implicated in one’s risk for clinical depression?
It’s protein regulating reabsorption of serotonin after its release into the synapse.
People with two “short” forms of gene at increased risk of depression in face of major life stressors (loss of job, divorce etc.)
People with two “long” forms were at lower risk.
The gene itself did not cause depression, but magnified reaction to stressful events.
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7. People with depression tend to have one hemisphere more active than another. Describe how hemispheric dominance may be a risk factor for depression.
They tend to have decreased activity in the left prefrontal cortex and increased activity in right prefrontal cortex.
Eye gaze when solving a verbal problem can indicate which hemisphere is dominant. Most gaze to the right indicating that left hemisphere is dominant. Individuals with depression gaze to left.
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8. Briefly describe the 4 main types of antidepressants and how they affect neurotransmitters:
a. Tricyclics:
block transporter proteins that reabsorb serotonin, dopamine, and norepinephrine back into the presynaptic neuron. Also help with certain forms of chronic pain.
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8. Briefly describe the 4 main types of antidepressants and how they affect neurotransmitters:
b. Selective Serotonin Reuptake Inhibitors (SSRIs):
similar to tricyclics, but only affects serotonin reuptake. Less side effects than tricyclics but same effectiveness.
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8. Briefly describe the 4 main types of antidepressants and how they affect neurotransmitters:
c. Monoamine Oxidase Inhibitors (MAOIs):
blocks MAO, an enzyme that metabolizes serotonin, dopamine and norepinephrine into inactive forms. Oldest antidepressant, no longer first line.
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8. Briefly describe the 4 main types of antidepressants and how they affect neurotransmitters:
d. Atypical Antidepressants
everything else. More common one is buproprion (Wellbutrin or Zyban) which inhibits reuptake of dopamine and to some extent norepinephrine.
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9. Mr. D has severe depression and another, patient, Ms. T, has mild depression. For whom do you think antidepressants would be most effective?
Mr. D
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a. While it is still not fully clear, what are some theories as to how antidepressants might reduce depression in these patients?
Brain derived neurotrophic factor (BDNF) – helps synaptic plasticity, learning, forming new neurons in hippocampus. Lower BDNF in depression. Some evidence that antidepressants increase BDNF.
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b. What are some other biological treatments that may be more effective for Mr. D? What are other therapies that may be effective for Ms. T? (Hint: we briefly discussed psychotherapy, ECT, and deep brain stimulation)
Exercise increase BDNF, so helps depression.
CBT is most effective. Antidepressant medication often helpful in combination.
ECT: under general anesthesia, small electric currents through brain triggers brief seizure. Seems to cause changes in brain chemistry than can quickly reverse symptoms of certain mental illnesses. Effective for severe depression that is not responsive to other treatments.
DBS: used to treat Parkinson’s, but also used for severe depression or OCD that hasn’t responded to other treatments.
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10. Bipolar disorder is believed to be the result of a disruption in what neurotransmitter system?
Glutamate system.
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11. What are the kinds of medications used to treat Bipolar Disorders and how are they thought to work?
Mood stabilizers – reduce the number of a certain type of glutamate receptor (AMPA) in the hippocampus Also blocks arachidonic acid which is produced during brain inflammation.
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12. Briefly, what is the difference between positive and negative symptoms in schizophrenia and for which type of symptoms are antipsychotic medications most effective?
Positive symptoms are things that are added that normal people don’t experience, ex. Hallucinations.
Negative symptoms are things that are taken away, ex. Loss of motivation.
Medication reduce positive symptoms, but not negative symptoms.
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13. Which neurotransmitter system is thought to be affected in schizophrenia and in what way?
Hyperactive dopamine systems
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14. What are some other brain differences that have been observed among those with schizophrenia and those without the disorder?
Ventricles are enlarged in people with schizophrenia. Other brain regions show abnormal activity, possible problem of connection between brain regions.
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15. What is the viral theory of the development of schizophrenia?
Antibodies found in blood of people with schizophrenia vs in those unaffected. More people with schizophrenia born during late winter and early spring months. Second semester = flu season. Mothers of those with schizophrenia more likely to have contracted influenza during 2nd trimester. During 2nd trimester, lots of brain development occurring.
Trauma or pathogens may interfere with organization of brain regions.
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16. Briefly describe the two types of antipsychotics, what neurotransmitter system they affect, and potential problems with use (the latter will apply more to one type over the other):
a. Typical antipsychotics:
First generation. Developed in 1950’s for psychosis, schizophrenia. Problems: sleepiness, potentially permanent movement disorders.
block receptors in the brain’s dopamine pathways.
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16. Briefly describe the two types of antipsychotics, what neurotransmitter system they affect, and potential problems with use (the latter will apply more to one type over the other):
b. Atypical antipsychotics
Second generation. Less likely to cause motor control problems.
block receptors in the brain’s dopamine pathways.
