Neuroscience and Substance Abuse: Brain Abnormalities and Addiction, Study notes of Biological Psychology

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PSYC 302: Biopsychology 11/27/07- Announcements:

1. Review Session today.
2. Final exam next Tues (12/4). Substance Abuse and Addiction Reward pathway-- Dopaminergic neurons have their cell bodies in the ventral tegmental area (VTA), and their axons extend into various brain areas, including the nucleus accumbens. The nucleus accumbens is part of a structure called the striatum that includes the caudate nucleus and putamen. Although it's a small structure, it's a very important "pleasure center." Olds & Milner- stuck an electrode accidentally in a rat's nucleus accumbens and they found that the rat would forego sleep and food to self-stimulate. Alcohol-- From a psychopharmacological perspective, alcohol inhibits the flow of sodium ions into neurons, making it a CNS depressant. Decreases serotonin (excitatory) activity and facilitates response by the GABA (inhibitory) receptors. It blocks glutamate (excitatory) receptors and increases dopamine (excitatory; key to the reward pathway) activity. Type I vs Type II- Type I is late onset, and so it appears to be less genetic in basis, and less severe than Type II, which is largely genetic. Type II alcoholism has greater concordance in monozygotic vs. dizygotic twins. Plus, there is a strong correlation between the occurrence of Typ II alcoholism in biological fathers and sons, even when the son is adopted and raised in a non-alcoholic family. One of the treatments for alcoholism is antabuse, which has a low adherence rate. The drug causes the user to become severely nauseated when they drink alcohol. Alcohol metabolism: alcohol ---> acetaldehyde ---> acetic acid Acetaldehyde is very toxic and causes nausea and vomiting. Methadone in the treatment of heroin addiction: Methadone is just a substitute opiate for heroin. When taken orally, it crosses the blood-brain barrier much more slowly than heroin, and so it produces its effects more slowly, including withdrawal, and it's far less addictive. BUT if you inject methadone, it

becomes pretty similar to heroin in its effects. Solution: Mix naloxone with methadone. Naloxone is an antagonist that blocks opiate receptors. But when it's taken orally, it's broken down in the stomach and rendered ineffective. If it's taken in any other way, it blocks the effects of methadone or any other opiate. DEPRESSION Is there a genetic component? There are two genes implicated in depression: One gene results in lowered serotonin production and the other gene increases the efficiency of serotonin reuptake. What are anatomical/structural differences in the brains of depressed individuals? Depressed people have less activity in the LEFT prefrontal cortex and more in the RIGHT. Drug treatments:

1. tricyclics (e.g. Tofranil)-- prevents the presynaptic neuron from reuptaking serotonin, dopamine and norepinephrine.
2. selective serotonin reuptake inhibitors (SSRIs; e.g., Paxil, Zoloft, Prozac)-- they block the reuptake of serotonin but not of other monoamines.
3. Monoamine oxidase inhibitors- Monoamines are a class of neurotransmitters that includes dopamine, serotonin, epinephrine, and norepinephrine. Monoamine oxidase (MAO) is an enzyme that breaks down these neurotransmitters. By blocking MAO, you leave the neurotransmitters in the synapse longer so that they exert a greater effect.
4. atypical antidepressants (Wellbutrine) inhibits dopamine and norepinephrine reuptake Comparing different treatments for depression, we see the following efficacy rates: Antidepressants- 50-60% Psychotherapy- 50-60% Placebo- 30% Electroconvulsive therapy (ECT; as seen in "Ordinary People" and "One Flew Over the Cuckoo's Nest"). Nobody knows exactly why it works. It has certain side effects, including memory loss, which can be minimized by administering the current only to the right hemisphere), and it has a high relapse rate. Depressed people have sleep maintenance insomnia (trouble getting back to sleep when they awaken) and enter REM more quickly. This suggests that they are "phase advanced", that their sleep-waking cycle has shifted so that their body temperature starts to decrease earlier in the day. In some cases, if you keep the patient awake for an entire night, their sleep-waking

cycle will return to normal and depression symptoms will decrease. Seasonal Affective Disorder (SAD)- phase delay in the sleep-waking cycle, meaning that sleep occurs later and temperature rhythms are altered so that temperature decreases happen later, as well. Bright full-spectrum light. Bipolar disorders- manic and depressive episodes Bipolar I-- The manic episodes are more severe, and can include restlessness, excitement, rambling thought, loss of inhibitions Bipolar II- much milder manic phases (hypomania), which include agitation and anxiety Treatments for bipolar: Lithium, carbamazepine (Depakote) and Valproate-- all block the synthesis of arachidonic acid (a precursor of cannabinoids in the brain), which is produced when the brain is inflamed. Lithium does not increase GABA activity, but the other two do. Since GABA is inhibitory, we assume that these drugs reduce manic symptoms by inhibiting brain activity. Valproate stimulates growth of axons and dendrites. Schizophrenia Acute-- sudden onset, good prospects of recovery ("Eden Express" by Mark Vonnegut) Chronic-- gradual onset, long-term course, harder to treat Two classes of symptoms of schizophrenia:

1. Positive symptoms-- Psychotic cluster (delusions, hallucinations); disorganized cluster-- inappropriate behavior, emotional displays, bizarre behavior, thought disorder)
2. Negative symptoms-- flat affect, weak social interactions, problems with speech and working memory Is schizophrenia genetic? There is evidence for and against: FOR: greater concordance in dizygotic twins than in other siblings AGAINST: The concordance rate for monozygotic twins is only 50% Neurodevelopmental hypothesis-- Brain abnormalities that occur in prenatal or neonatal development. Evidence for this hypothesis:
3. A number of different neonatal complications have been linked to schizophrenia.
4. Schizophrenics show certain brain abnormalities a) decreased volume in the left temporar and frontal cortex b) larger ventricles c) smaller cell bodies, especially in the neurons of the hippocampus and right prefrontal cortex d) unlike most people, who have a larger planum temporale in the left hemisphere, schizophrenics have a larger right p.t. e) lower than normal left hemisphere activity
5. abnormalities in development have been shown to impair behavior in adulthood

People born in winter have a slightly higher risk of schizophrenia. Why? Possibilities: more complications in delivery in the winter time, influenza and other viruses occur most often in the winter Treatment Antipsychotic drugs (neuroleptics):

1. Phenothiazines --chlorpromazine (Thorazine)
2. Butyrophenones-- Haldol Block dopamine synapses. Dopamine hypothesis-- Schizophrenics have higher-than-normal dopamine activity Evidence in support of this hypothesis:
3. Drugs that block dopamine receptors reduce schizophrenic symptoms.
4. Repeated doses of amphetamines or cocaine can produce similar symptoms (stimulant-induced psychosis) Glutamate hypothesis-- Schizophrenics have lower-than-normal glutamate activity. Evidence in support of this hypothesis:
5. Brain imaging data have shown that schizophrenics have lower-than-normal glutamate levels in their brain, especially in the prefronal cortex and hippocampus.
6. PCP, which inhibits glutamate receptors, produces symptoms similar to schizophrenia, including hallucinations, thought disorder, and memory loss. REVIEW III-3f genetics-- there is greater concordance in monozygotic vs. dizygotic twins, and greater concordance in blood siblings than in adopted siblings hormones-- there is no correlation between levels of sex hormones in adults and sexual orientation, but there is evidence that males who are exposed to less testosterone levels early in life show more interest in other males, and that females exposed to higher levels of testosterone show interest in other females. prenatal environment-- mothers of homosexual sons recalled higher than average levels of stressful experiences during pregnancy; homosexual men tend to have older brothers. brain anatomy-- homosexual men have a larger anterior commissure than heterosexual men, which is closer in size to that of a woman; the SCN is larger for homosexual vs heterosexual men; and a part of the hypothalamus (the dimorphic nucleus) is smaller in homosexual men, closer in size to that of a woman.

III-13a Kanzi & Malika:

1. understand more than they can produce
2. use symbols to name and describe objects even when those objects are not present
3. request items they cannot see
4. can describe past events
5. can make original requests Using language in a creative manner and describing events not just in the present III-2f The first mechanism is hormonal before experience between the mother and infant can create a bond. Oxytocin is one such hormone that kicks in during the first few days of life. After that, the hormonal effect dissipates and bonding becomes experience- dependent. III-9f In the alarm phase of stress response, cortisol gets produced. Small to moderate amounts of it actually stimulate memory, activating the amygdala and hippocampus. This enhances memory consolidation and storage. But prolonged stress damages the hippocampus and impairs memory. III-9d
6. hippocampus size-- as people age, their hippocampus shrinks; but hippocampus size does not predict memory loss
7. rate of shrinkage-- this is correlated with memory performance; higher rate of shrinkage results in greater memory impairment.
8. less than average activity less in the hippocampus is related to memory performance (supported by data). 11/20/07- The visual system is wired such that the information from the right visual field in both eyes goes to the right hemisphere and left visual field to the left hemisphere. Split-brain patient-- Generally, these were patients who had severe epileptic seizures that crossed the midline of the brain, and so the corpus callosum was severed in these patients, along with the anterior commissure, to try and prevent the most seizures from crossing over. In split brain patients, the two hands sometime operate independently; some complex tasks that involved both hands or perhaps visual and auditory processing simultaneously could cause problems, but in general these patients are high-functioning and it's hard to know in most situations that they have a deficit.

When information is presented to the left hemisphere, which is the area where language processing happens, they can name objects they see but they difficulty drawing them. Objects to the right hemisphere show the opposite pattern. Left hemisphere is dominant for speech in more than 95% of right handers and in 80% of left handers; it is also better at language comprehension, although the right hemisphere has SOME language comprehension. The right hemisphere is better at visuopatial processing, and that includes drawing information. The left hemisphere is more likely to process detailed information about visual stimuli and the right hemisphere overall patterns. The left hemisphere has a larger planum temporale, which is a structure found in the temporal lobes and associated with language process. It's larger in the left hemisphere for 65% of people. Young children resemble split-brain patients in some ways, because the commissures in their brains are not fully developed yet. For example, and infant with one arm restrained will not reach across his/her body to grab an object. If you give toddlers two fabrics, one placed in each hand, and ask them to determine whether the fabrics are the same or different, they will have a hard time with the task, showing high error rates. Some people are born without a corpus collosum and they do much better than split- brain patients in a number of tasks involving auditory and visual processing, the use of both hands simultaneously, or language processing by the right hemisphere. The two hemispheres are less specialized, so that more language processing occurs in the right hemisphere and more visual/spatial processing in the left. Moreover, these individuals still have an intact anterior commissure and a hippocampal commissure, which allows the two hemispheres to communicate to some degree. In right handers, left hemisphere is dominant for speech. In lefties, you can have left- hemisphere dominance, right-hemisphere dominance, or a mixture of left and right. Language Processing (in animals and children) Kanzi/Malika are a type of bonobo called a bonobo. They use language in creative ways, they refer to events in their past and to objects that are not in their field of vision, and they refer to objects not just when they want or need them.

Why are they so much more advanced in language production than other animals that have been taught languages?

1. Bonobos may have more language ability than chimps.
2. Kanzi/Malika started young.
3. They may have learned from observing their mother. Alex the grey parrot- Give give spoken answers to spoken questions involving color, number, shape, and other characteristics of objects. Children- In the first five years, they go from a vocabulary of zero to several thousand words, but perhaps more significantly, they learn to use the grammatical rules of their language. The study of language acquisition had been dominated by behaviorists, who claimed that language was just a learned behavior, until Noam Chomsky introduced his ideas about nativism, which are based on the premise that children are born with a language acquisition device. In other words, language acquisition is hardwired so that children have an innate understanding of grammar, syntax, and other language-related rules. There is also the idea of a critical period in language acquisition: language is most easily acquired prior to a certain age. This point is somewhat controversial because there is evidence for and against a critical period. For: Children are much more likely than adults to learn a second language. Against: No sharp cutoff in terms of learning a second language. Two-year-olds are better than 4-y.o.'s, who are better than 6-y.o's. Language Deficits Broca's and Wernicke's aphasia-- Broca's aphasia affects language production whereas Wernicke's affects language comprehension. The story is more complicated: In Broca's aphasia, the patient has trouble with pronouns, prepositions, conjunctions, and articles. Patients with Wernicke's aphasia show anomia, or the inability to utter or remember certain kinds of words, mostly nouns and verbs. Dyslexia-- people who are born dyslexic have certain anomalies in brain structure:
4. Their planum temporale is more likely to be bilaterally symmetrical as opposed to being larger on the left side.
5. In some cases, they have more development of language-related centers in the right hemisphere compared to the left hemisphere.
6. Fewer connections of lnanguage-related brain areas. Theories that account for dyslexia:
7. Impairment in visual processing- This theory is not well-supported.

2. Impairment in auditory processing-- There is evidence of less-than-normal response to certain speech sounds.
3. Problems connecting visual and auditory information.
4. Differences in attention-- Dyslexics don't shift their attention from one target to the next in the same way that "normal" individuals do, and when they focus their visual attention directly on a word, they are more likelty to process a word or letter that is 5- degrees to the right of their focal point. ATTENTION Does the brain exert more effort to attend to a salient (ie. relevant) stimulus or to tune out a distractor stimulus? Research has shown that the brain is more active when attending to a salient stimulus compared to a non-salient stimulus, but that brain areas are not necessarily more active in tuning out some types of irrelevant stimuli over others. See example in Fig 14.18 on p. 443 Deficits in attention Spatial neglect-- Tendency to ignore the left side of visual space and of the body, directing attention to the right. If a patient with neglect is asked to cross out all of the H's that make up a larger letter "E", they will only cross out the ones on the right. However, if asked, they will correctly identify the letter as an E, suggesting that their deficit is NOT one of visual processing. How to deal with these deficits:
5. You can teach patients with neglect to look left, but the benefit will be short-term.
6. You can have them cross their arms and that tends to improve their awareness of their left side and specifically of their left arm.
7. You can have them turn to the left when looking or hearing something on their left side. Attention deficit hyperactivity disorder (ADHD) is a disorder that is characterized by hyperactivity, impulsiveness, temper flairs, difficulty being organized, and problems both inhibiting and disinhibiting attention. People with ADHD show specific patterns of performance on certain tasks:
8. Choice delay task-- Do you want the smaller reward now or the bigger one later? The vast majority of people ADHD go for immediate gratification.
9. Stop signal task-- You see a signal and are asked to press a button unless you get the "stop" signal ("Don't press the button"). People with ADHD are less likely to be able to stop the button press in response to the stop signal.

3. Attentional blink-- You see a string of letters and you have to respond to a letter that is a different color than the rest. Then, you have to report whether or not a particular letter such as an R appeared after that colored letter. "Normal" people tend to miss the R if it appears 100-700 ms after the colored letter. For people with ADHD, this "attentional blink" lasts much longer--well over a second. Brain Differences: People with ADHD have:
4. Smaller brain volume (95% of normal)
5. Smaller right prefrontal cortex
6. Smaller cerebellum The main drug treatment for ADHD has been the use of stimulants, such as Ritalin (methylphenidate) and Aderrall (amphetamine). 11/13/07- Learning & Memory Classical conditioning- Pair a conditioned stimulus (CS) with an unconditioned stimulus (UCS) to produce a conditioned response (CR) Operant conditioning- A reinforcer changes the probability of a certain behavior. Is there a specific brain area or brain change associated with learning? Karl Lashley-- Search for the "engram," which is the physical representation of learning. Lashley's research generated two principles:
7. Equipotentiality-- All parts of the cortex are equally involved in learning, and any part could substitute for another.
8. Mass action-- The cortex works as a whole and the more cortex is involved in a task, the better. Two faulty assumptions:
9. The cortex is the best or only brain area to study if we understand learning.
10. All kinds of memory and learning are the same physiologically. Possible sites of engram:
11. The cerebellum has a structure called the lateral interpositus nucleus (LIP); in classical conditioning, cells in the LIP show greater activation for the conditioned

stimulus once conditioning has happened.

2. The prefrontal cortex, which maintains a high level of activity during certain kinds of learning task, such as the delayed response task, which requires the individual to respond to a stimulus that was presented sometime in the recent past. Since the advent of cognitive neuropsychology (the study of cognitive deficits caused by damage to specific brain areas): Patient HM-- Because of severe epilepsy, HM had parts of his medial temporal cortex removed, including the hippocampus. Anterograde vs. retrograde amnesia-- Retrograde amnesia is when your memory less is for events occurring prior to your brain damage; anterograde is memory loss for events after your injury (i.e., the inability to lay down new memory traces). HM shows severe anterograde amnesia. Short-term memory (STM) vs. long-term memory (LTM)-- STM has a capacity of 7 plus- or-minus 2; LTM has a possibly infinite but unknown capacity. Duration: STM lasts about 30 seconds at the most; LTM lasts a lifetime. Forgetting: once something is forgotten from STM, it's lost; but information forgotten from LTM can be recovered. Baddeley & Hitch-- STM is overly simplistic, because--among other things--it focuses on auditory processing (STM has an acoustic code). New concept: working memory, which includes: a) a phonological loop-- stores auditory info b) visuospatial sketchpad-- stores visual info c) central executive-- directs attention to a specific stimulus and determines which items of information will be stored in working memory. HM has intact STM or working memory but damaged LTM. Procedural vs. declarative knowledge-- Procedural knowledge is "knowing how" (knowledge of how to carry out specific tasks); declarative knowledge is "knowing that" (knowledge of facts) HM has intact procedural knowledge but impaired declarative knowledge. Episodic vs. semantic memory-- Episodic memory is memory for specific events in your life; semantic memory is knowledge of basic facts that are "disembodied" (you do not necessarily remember the context in which you learned those facts). HM has a little bit of semantic memory but no real episodic memory. He can't form new memories of events in his life, but he can learn an occasional fact.

What is the relationship between the hippocampus and memory?

1. Hippocampus size: There is not a good correlation between hippocampus size and memory loss in older adults, but there is a correlation between the extent of memory loss and the rate of shrinkage of the hippocampus.
2. Hippocampus activity- Evidence of increased activity in the hippocampus during memory tasks, and there is an especially strong correlation between verbal memory and hippocampus activity. What kind of memory is associated with the hippocampus?
3. Declarative memory, especially episodic memory. Damage to the hippocampus tends to impair performance on certain kinds of memory tasks, such as delayed matching-to-sample tasks (Example: "Concentration" game show).
4. Spatial memory. Rats with damage to their hippocampus have problems on a radial maze task, in which they have to locate the arm of maze that has a food reward at the end of it. Impaired rats will keep going down the arms where they already found food, suggesting that they don't remember where they've been. They also struggle with the Morris maze task, in which they have to navigate through water to locate a platform.
5. Configural learning-- Learning that specific stimuli (e.g., shaped objects) are associated with specific outcomes. Example: you get a reward if you choose the circle over the square. Types of memory damage:
6. Korsakoff's syndrome-- Caused by brain damage due to thiamine (a type of B vitamin) deficiency for very long periods of time, usually related to alcoholism. Severe alcoholics will use alcohol as their primary energy source, and will suffer nutritional deficiencies as a consequence. Symptoms of Korsakoff's: retrograde and anterograde amnesia, confusion, apathy, and extensive confabulation (make up stuff), usually about the events in their lives.
7. Alzheimer's-- Better procedural than declarative memory, and they show deficits in both implicit and explicit memory. Progressive, leading gradually to more sever memory loss and confusion, as well as delusions, restlessness, sleeplessness, loss of appetite, hallucinations. Is Alzheimer's disease genetic? Evidence for: Link between Alzheimer's disease and chromosome 21. People with Down's syndrome almost always get Alzheimer's if they live long enough, and a specific gene on chromosome 21 has been linked to early-onset Alzheimer's.

Evidence against: Half of all Alzheimer's patients have no family history (i.e., no known relatives with the disease). Environmental factors such as diet have been linked to some extent to Alzheimer's. Smoking and drinking coffee reduce your likelihood of having the disease. Mechanism of Alzheimer's onset involves the metabolism of amyloid proteins in the brain. A normal amyloid protein has 40 amino acids, and in Alzheimer's, a form of the protein is produced that has 42 amino acids. These proteins produce a type of deposit called plaques that are the result of the degeneration of axons and dendrites. A separate protein called a tau protein produces tangles, which are the result of damage to cell bodies. Current methods of treatment: 1 Drugs that stimulate acetylcholine receptors or that prolong acetylcholine release delay the onset of memory deficits.

2. Drugs that stimulate cannabinoid receptors can slow the progression of the disease.
3. Drugs that block amyloid production (antioxidants).
4. Immunization-- Introduce amyloid 42 into young people's bodies, they will produce antibodies to destroy it (because it's seen as a foreign protein). 11/6/07- CH.11: Reproductive Behavior Menstrual Cycle
5. After the end of a menstrual cycle, the anterior pituitary releases follicle-stimulating hormone (FSH), which promotes the growth and release of a follicle in the ovary. The follicle contains the egg, as well as nutrients and hormone systems. It produces estradiol (form of estrogen).
6. Toward the middle of the cycle, the follicle produces more FSH receptors (which trigger more hormone release), which causes an increase in the release of estradiol.
7. The increased release of estradiol causes an increase in the release of luteinizing hormone (LH) from the anterior pituitary, which triggers the release of the egg from the follicle.
8. The remnant of the follicle releases progesterone, which prepares the uterus for implantation of the fertilized egg and which inhibits the release of more LH.
9. Toward the end of the cycle, levels of LH, FSH, estradiol, and progesterone all decline. If the egg is not fertilized, the lining of the uterus is cast off and the cycle begins again.

Towards the end of pregnancy, the female secretes large amounts of estradiol, prolactin, and oxytocin. Prolactin is necessary for milk production, but all three are important for stimulating maternal behavior. Men have vasopressin, which helps with bonding with both one's mate and offspring. Emotion What is it? It is some combination of cognition, behavior and feeling state. Behavior includes psychophysiology. James-Lange- Autonomic arousal and skeletal muscle movements come first; the interpretation follows. According to William James, we experience fear when we observe ourselves running from the bear. Facial efference- Output of facial muscles affects our mood. Schachter & Singer- The body cannot differentiate arousal based on any two emotions. Only by interpreting situational cues do we define and label that undifferentiated arousal as a specific emotion. Is arousal necessary for emotion? No. Patients with pure autonomic failure, who have no changes in heart rate, bp, perspiration during psychological stress, still report the same emotions as anyone else. Is arousal sufficient for emotion? No. You can autonomic arousal without emotion. For example, let's do jumping jacks! Some folks claim that emotions evolved out of physiological responses. The classic example is DISGUST: Disgust activates the insula, which is the primary taste area in the cortex, and the olfactory bulb, which processes smell. In fact, both of those areas are close to the amygdala, which is one of the primary emotion centers in the brain. Fear-- escape from danger Anger-- to defend oneself from an attacker Disgust-- to protect us from something toxic

Prefrontal cortex (specifically the orbitofrontal cortex)- Related to emotional decision making in which we weigh risks and rewards. Iowa Gambling Task-- The player chooses cards from $50 and $100 decks and the objective is to collect as much money as possible. The decks have occasional penalties associated with specific cards. It turns out that the $100 decks have greater penalties and result in overall losses, whereas the $50 decks result in overall gains. Patients with damage to the OFC cannot delay short-term gratification long enough to receive the long-term gains, and so they keep playing the $100 decks. Aggressive Behavior Is it genetic or environmental? There is evidence for both: Genetic-- Monozygotic twins resemble each other much more in terms of violent behavior than do dizygotic twins or non-twins. Those resemblences are more likely to be true in childhood and adolescence, however. Also, adopted children more closely resemble their biological vs. their adoptive parents in terms of criminal record and other signs of aggression. Environment-- The resemblence between twins goes down with age. Also, prenatal environmental plays a role in aggressive behavior. Women who smoke during pregnancy are more likely to have male offspring who engage in violent behavior. In the genetic corner is testosterone levels. Testosterone levels are significantly higher in men imprisoned for violent crimes compared to control subjects, but these effects are small. Serotonin turnover-- the rate with which serotonin is released and resynthesized in the brain. There is evidence that low turnover is correlated with aggressive behavior:

1. Suicide rates are highest in the spring, when serotonin turnover is lowest.
2. Serotonin levels in the brain predict a number of violent behaviors, including juvenile delinquency, suicide attempts, and convictions for violent crimes.
3. People fed diets low in tryptophan show a tendency to aggressive behavior, as do people who have low levels of tryptophan hydroxylase, an enzyme that is important for the synthesis of serotonin from tryptophan. Amygdala-- Enhances the startle response. The amygdala gets input from pain fibers, vision and hearing. And its output goes to the hypothalamus, which controls autonomic response. It also has axons that project to the prefrontal cortex, which controls approach/avoidance behavior (risk/reward assessment).

Kluver-Bucy syndrome-- The monkeys with amygdala damage become placid and tame. They are not afraid of stimuli that would normally induce fear, such as fire and snakes and large animals. They also don't react normally to other monkeys' threat gestures. In humans, facial expressions of other people are important emotional cues. We recognize angry expressions faster if they are directed at us and fearful expressions faster if they are directed to our side. The amygdala shows a greater response to fearful expressions directed towards us and to angry expressions directed toward our side. Why? Those stimuli are more ambiguous and require more ffort to process. So, the amygdala is trying to interpret emotional stimuli. People with amygdala damage report normal emot5ions but have a hard time processing subtle emotional cues, and they are more likely to pay attention to irrelevant cues in an emotion-inducing situation than normal individuals. Benzodiazepines (including valium) interact with the amygdala. They bind to GABA recpetors in the amygdala, hypothalamus, midbrain, and some cortical areas. GABA is an inhibitory neurotransmitter. By binding to the receptor, BDZs cause GABA to bind more tightly to the receptors. Because GABA is inhbitory, the net effect is to turn off fear-related responses. STRESS Hans Selye-- general adaptation syndrome; the body responds to stressors in three stages:

1. alarm-- increases sympathetic arousal
2. resistance-- the body repairs damage created in teh alarm phase, and the adrenals secrete corticosteroids such as cortisol, which functions to increase blood sugar levels.
3. exhaustion-- the nervous system and immune system no longer have the energy to function properly. HPA axis (hypothalamus, pituitary and adrenal)
4. hypothalamus releases corticotrophin releasing factor (CRF)
5. this triggers the anterior pituitary to release ACTH (adrenocorticotropic hormone)
6. this triggers the adrenals to release cortisol The adrenals also secrete epinephrine and norepinephrine, which stimulate sympathetic arousal The effects of stress on the immune system are as follows:
7. During the resitance phase, there is an increase in immune activity.

2. During the exhaustion phase, energy gets directed towards glucose metabolism and away from protein synthesis, including the synthesis of immuno-proteins. 10/30/07- Sex hormones- Organizing effects-- At a sensitive/critical period, hormones determine whether or not the brain body will develop male or female characteristics. Activating effects-- At specific points in the life cycle, when a hormone temporarily activates a certain response. The default setting for humans is female. Unless testosterone is released at a critical period, the individual will have the secondary sexual characteristics of a female. Sex and gender-- Sex is simply your genetic makeup (XX or XY), but gender is far more complex because it's due to a combination of factors, including cognition. Gender has to do with how individuals perceive themselves. Sexual variations- Hermaphrodites-- a small percentage of newborns have a combination of male and female genitalia or genitals that are somewhere in-between. Pseudohermaphrodites are more common (1 in 2000 individuals)-- There is enough ambiguity at birth to make a proper identification of sex difficult. Androgen insensitive males-- Androgen refers to male hormones, including testosterone. Genetically male but has the secondary sexual characteristics of a female, more or less. Generally, these individuals have broader shoulders and narrower hips than the prototypical female, and no body hair whatsoever. A tribe in the Dominican Republic that is fairly isolated geographically and so is susceptible to intermarriage. A genetic anomaly has occurred in that population, a group of individuals who are called "huevo-doces." These people have a deficiency in an enzyme that converts testosterone to dihydrotestosterone, which is what signals the production of secondary sexual characteristics. At puberty, other enzyme systems kick in. When that happens, these individuals go from being girls to men. congenital adrenal hyperplasia (CAH)-- overdevelopment of the adrenal glands from birth. This causes larger-than-normal levels of testosterone in the body. Genetically, the individual is female, but the effect is one of masculinizing the external genitals.

10/23/07-

Announcements:

1. Midterm 2 next Tuesday CH.10: Internal Regulation Homeostasis-- Self-regulation. There is a set point, which is the point at which a variable needs to be held (e.g. an ideal temperature) and the body regulates the variable to hit that set point. Thermostat-- When the temperature drops below the set point, the heat turns on, and when it goes above it, the AC turns on. Body Temperature Animals' body temp is determined by certain factors: a) ambient temperature; b) physiological mechanisms--sweating, panting, licking, shivering, decreasing blood flow to the skin surface and extremities, fluffing fur; behavioral mechanisms-- finding a warm or cool place; clothing; activity; huddling/cuddling. Why 37C (98.6)? Much above that temperature, the proteins in our bodies denature. Much below that temperature, muscle fibers don't operate at their peak. Brain areas associated with temperature regulation are the preoptic area and anterior hypothalamus (POA/HA). Fever- Why do we get a fever? Benefits: It keeps bacteria from growing at the higher temperatures because the bacterial proteins denature. Risk- A fever above 39C can be harmful, and above 41 can be deadly. Thirst- Vasopressin- secreted by the posterior pituitary and raised bp by constricting blood vessels; this conserves water; and increases pressure for a given blood volume. It is also known as antidiuretic hormone (ADH) because it allows the kidneys to reabsorb water from urine, which in turn makes the urine more concentrated. Two kinds of thirst:
2. Osmotic thirst-- this comes from eating salty foods, which causes sodium ions to build up in the blood and the extracellular fluid. The sodium buildup causes water to move from the inside of the cell to the extracellular fluid. Neurons in two brain structures called the OLT subfornical orgal, which line the third ventrical, detect water loss and signal to the hypothalamus that there is a need for more hydration.

2. Hypovolemic ("low volume") thirst- this comes from a loss of fluids, which can occur through sweating, bleeding, vomiting, diarrhea. There are two mechanisms in the body for detecting loss of blood volume
3. Receptors in the veins signal the kidneys to release renin, which is a precursor to angiotensin II (this hormone is similar to vasopressin in function; among other things, it constricts blood vessels and increases blood flow).
4. Subfornical organ detects lower blood volume. Sodium-specific thirst: When you have osmotic thirst, you can quench that thirst by drinking pure water, but when you have hypovolemic thirst, you need to add electrolytes. Sodium-specific thirst occurs when you dilute sodium and other ions in your blood stream. When sodium reserves are low, the adrenal glands secrete aldosterone, which causes the kidneys, salivary glands, and sweat glands to retain salt. HUNGER The factors that determine food selection:
5. Types of enzymes available in the digestive system. Lactase--an enzyme that helps in the digestion of lactose in dairy products
6. Imitation-- learn from those around us
7. Taste-- We tend to select sweet foods, avoid bitter foods, and eat salty and sour foods in moderation.
8. Learning-- We learn to reinforcement the consequences of eating certain foods. The factors that affect hunger:
9. Oral factors--if we don't taste, chew, and swallow our food, we tend to find it unsatisfying.
10. Stomach/intestines-- distension of the stomach sends messages to the brain about the stretching of the stomach (vagus nerve) and about the contents of the stomach (splanchnic nerve). Between the stomach and small intestine is the duodenum, which releases the hormone CCK. This hormone acts to limit meal size by closing the sphincter between the stomach and duodenum. CCK also signals fullness to the hypothalamus.
11. Blood glucose levels- trigger the secretion of insulin by the pancreas. Insulin allows glucose to enter the cells. Insulin levels increase after a meal, and this increase tends to sginal fullness. Brain areas associated with hunger: Lateral hpothalamus-- controls insulin secretion and facilitates feeding behavior. An animal with damage to that area refuses food and water.

VMH- Damage to this area leads to overating and weight gain because the individual or animal will eat normal-sized meals but more frequently. VMH has something with fullness but regulates the frequency rather than the size of the meal. PVN-- Inhibits the lateral hypothalamus and thus limits eating and drinking. Damage to this area result in much larger than normal meals. Arcuate nucleus-- there are two sets of neurons in this nucleus; one signals fullness and the other signals hunger. The output of this structure connects to the PVN. Genetic evidence for obesity: Twin and adoption studies REVIEW SESSION II-7e. Indicate which cortical structures process auditory information Primary auditory cortex-- superior temporal lobes Secondary auditory cortex-- surrounds the primary auditory cortex II-7d. Explain the volley principle No single auditory receptor can fire at a rate compatible with the highest frequency sounds. So, instead of one receptor firing 10,00 times, you could have 10, receptors firing at one time, and the effect would be the same. A volley is a synchronized firing of receptors (or cannons). II-9f Explain why there seems to be so much specialization among olfactory receptors. There are thousands of smells, and unlike tastes, which reduce to combinations of five basic flavors, there are no known basic or fundamental smells that serve as the "building blocks" for other smells. II-9c Explain how you would prove the existence of the five kinds of taste receptors Cross-adaptation- If you puts drops of a certain flavor, like sweet, on the right receptors, eventually you get adaptation, which means that the receptors become fatigued. But then if you introduce a different flavor, the receptors will be able to taste it "fresh," indicating that there is NO cross-adaptation. II-9j Compare the VNO of adult humans with that of other mammals. The vomeronasal organ (VNO) is associated with the detection of pheromones. In humans, it is relatively small compared to other mammals. II-18d

Discuss the role of leptin in regulating eating behavior. Leptin is a peptide that is produced by the body's fat cells. It signals the brain in a more long-term ways whether to eat more or less. It's more of a mechanism that indicates whether or not there are famine conditions. When leptin levels are high, animals eat less and become more active. Ghrelin is a peptide that is associated with fullness. Eating causes a decrease in ghrelin levels. In people with certain types of obesity, ghrelin levels are much higher in the bloodstream than they are in normal individuals. Sodium hunger = sodium-specific thirst *supertaster- someone with a highly developed sense of taste II-13a Give examples of endogenous circannual and circadian rhythms Circannual-- migratory pattern Circadian-- sleep and wakefulness II-4a Offer two possible explanations for the phenomenon of blindsight:

1. Weiskrantz-- Even though area V1 is damaged, other brain areas that process visual information are intact.
2. Gazzaniga-- There are tiny islands of healthy tissue intact in and around V1. II-3a Give a brief overview o the mammalian visual system The optic nerves, which are the set of axons coming off the receptors in the retina, meet at the optic chiasm, where half go to the left hemisphere and the other half to the right hemisphere. Most of the axons go to the lateral geniculate nucleus (LGN) in the thalamus, which sends its output to the visual cortex, starting with area V1. From V1, there are two pathways leading to other visual areas in the cortex: a) Ventral stream-- visual pathway that leads to areas in the temporal cortex that are specialized for identifying and recognizing objects, including object shape (V4). b) Dorsal stream-- Visual pathway that leads to the parietal cortex, with a "side route" that leads to the medial temporal (MT) and medial superior temporal (MST) cortex. This pathway detects "where" and "how", including motion detection. It lets the individual determine how to find and grasp objects. II-6d Discuss the visual impairments of people born with cataracts in either one eye or both eyes.

Both eyes- The person will have near-normal vision after cataract surgery, but will have mild prosopagnosia and may have problems with subtle visual discrimination tasks. Cataracts in left eye-- Moderate prosopagnosia after cataract surgery Hunger: 10/16/07- CH.9: Wakefulness & Sleep Biological Clock Circadian rhythms-- daily patterns of sleep and wakefulness Circannual rhythms-- yearly patterns such as those migratory animals Suprachiasmatic nucleus (SCN) in hypothalamus- Neurons in the SCN fire at specific times of day; this area controls activity in the pineal gland, which release the hormone, melatonin, that increases sleepiness. The free-running rhythm of the SCN is more than 24 hours. There are cues, called "zeitgebers" (time-giver), are used by the SCN to set its rhythms. One zeitgeber is light; others are temperature, meals, exercise. Disruptions of the biological clock:

1. jet lag-- Disruption of the circadian rhythm due to changing time zones; it's harder going EAST than WEST, because you have to go to bed earlier than you're used to.
2. Shift work-- When you're sleeping in the morning or afternoon, when your body temperature and metabolism are peaking, you will not sleep soundly or for more than a brief duration. Stages of Sleep NREM stages: Stage 1-- Body relaxes, muscle tone diminishes, heart rate slows, breathing becomes deeper; brain wave activity becomes slower, more irregular; increase alpha activity compared to waking beta 14-30Hz alpha 8-13 Hz theta 4-7 Hz delta 0.5-4 Hz Stage 2- Brain wave activity that is characterized by sleep spindles (which are bursts of relatively fast, 12-14 Hz activity), and K complexes (which are bursts of high-amplitude activity).

Stage 3-- An increase in slow wave activity (i.e., theta and delta), with 20% delta. Stage 4-- Primarily theta and delta activity; defined by having at least 50% delta activity. REM Sleep: Paradoxical sleep REM seems like deep sleep in some ways and very light sleep in other ways. Increased activity: Brain-wave activity is relatively high (closest of any sleep stage to waking), increase in eye moevements, increases in heart rate, bp, and respiration rate (although irregular), increased genital arousal. Decreased activity: Nearly complete loss of muscle tone (the skeletal muscles become relaxed to the point of paralysis). 80-90% of REM awakenings produce a dream report. These dreams are characterized by a PLOT (narrative storyline) and mental imagery (usually visual). REM sleep deprivation-- Mental fatigue; REM rebound-- When you're allowed to have REM sleep, you have more than the normal amount to compensate for what you lost. Brain areas associated with sleep and wakefulness:

1. The SCN in the hypothalamus
2. Reticular formation-- axons from this area extend into the hypothalamus, thalamus, and basal forebrain; regulates arousal levels.
3. Locus coeruleus-- found in the pons; it's inactive most of the time but has bursts of activity that increase wakefulness and that strengthen the storage of recent memories; The LC is silent during sleep.
4. Basal forebrain-- This area is located just in front of and above the hypothalamus; axons from the BF extend into the thalamus and cortex; it releases acetylcholine, which is an excitatory neurotransmitter and that thends to increas arousal; but it also releases GABA, which is inhibitory and essential for sleep. Parts of the BF stimulate sleepiness, and other parts stimulate arousal. Adenosine (amino acid) inhibits the BF cells responsible for arousal; caffeine blocks adenosine receptors. Physiology of REM Sleep PGO Wave-- Pons-->Lateral Geniculate Nucleus-->Occipital Cortex

Every eye movement in REM is accompanied by a PGO spike. Activity in the pons triggers the onset of REM sleep. Sleep Disorders Insomnia- Sleep onset and sleep maintenance. Sleep apnea- Inability to breathe during sleep; often associated with individuals who are obese. Narcolepsy-- Considered a "parasomnia" which is a condition in which sleeping intrudes on waking life. There are four characteristics of narcolepsy:

1. Gradual or sudden attacks of sleepiness during the day.
2. Occasional cataplexy-- Muscle weakness while awake.
3. Sleep paralysis-- The inability to move while falling asleep or waking up.
4. Hypnogogic hallucinations-- Dreamlike experiences that cannot be distinguished from waking reality. Periodic limb disorder- Involuntary muscle movements during NREM; most common in older adults who have possibly had a microstroke or other brain trauma. REM behavior disorder- Movement during REM Night terrors- Waking up from NREM with intense anxiety; most common in children NREM "sleep mentation" is different from dreams; when people are awakened from Stage 3 or 4 sleep, they report vague, abstract experiences, but nothing that resembles a REM dream in terms of plot or imagery. Why do we sleep?
5. Conserve energy- Why can't we conserve energy by just lying still for several hours? Why do we have to undergo the changes in consciousness associated with sleep?
6. Restorative function-- Sleep increases the repair and synthesis of proteins in the brain; synapses get reorganized during sleep.
7. Strengthening of memories- When people learn information during the day, certain brain areas are activated, and those same areas get re-activated that night during sleep. The extent to which the individual learns the information is directly correlated with the amount of activation during sleep. None of these theories accounts for REM sleep.

Why do we have to undergo this strange paradoxical stage of sleep?

1. Maurice (1998)-- REM shakes the eyeballs so that the corneas can get the oxygen they need.
2. Activation-synthesis (Hobson & McCarley)-- Random activation in the pons and other brain areas, and the mind tries to make sense of that activation. For example, activation of the vestibular system, which provides information about orientation in 3D, may give the impression of flying. Firing of the motor cortex might result in a chase dream. One criticism is that this theory has put too much emphasis on the pons, and there is evidence of dreaming in people who have "pontine" damage. There is no established correlation between activity in specific areas and the content of dreams. Lucid dreaming research indicates that dreams are not solely the result of random brain activity.
3. Clinico-anatomical theory-- Dreaming is thinking that occurs in the absence of information from the sensory organs or from the primary motor cortex. 10/9/07- Prosopagnosia-- Damage to the boundary between the occipital and temporal cortex. "Cognitive Neuropsychology" by Elizabeth Warrington CH.8: Movement Three types of muscles: Striated-- skeletal muscles that control movement of the body relative to the environment Smooth-- muscles of the internal organs Cardiac-- muscles of the heart, usually considered smooth muscle fiber but have certain properties in common with striated muscle Striated muscles are antagonistic-- Paired muscles that move a part of the body in opposing directions (flexors vs. extensors, adductors vs. abductors) Proprioceptors-- Receptors that detect the position or movement of a body part. One kind of proprioceptor is a muscle spindle, which attached to a muscle and when the spindle is stretched, it sends a message to a motor neuron, which causes the muscle to contract

A second distinction among muscles is fast-twitch vs. slow-twitch: Fast-twitch muscles produce fast contractions but fatigue easily; they are need for intense, strenuous activity of short duration (anaerobic); slow-twitch produce less vigorous contractions without fatiguing easily. There are three types of reflexes that occur in newborns but not in adults: Grasp reflex- You put an object in an infant's hand and it will grasp tightly. Babinski- You stroke the sole of the foot and the big toe will extend while the other toes fan out. Rooting- You touch the infant's cheek and the head will tirn and the infant will begin sucking movements. The parts of the brain associated with the control of movement: Many cortical areas associated with movement are in the frontal lobes:

1. The motor cortex-- This area does not have any direct connections of the muscles of the body; its axons connect to the brainstem and spinal cord. It is more important for comple movements (talking, writing, hand gestures) than for basic movements (coughing, sneezing, gagging, laughing).
2. Premotor cortex-- This area is most active in preparation for a movement; it receive information about the location of a target in space towards which a movement is directed.
3. Supplementary motor cortex-- This area is responsible for planning and organizing a rapid sequence of events, such as pushing, pulling, or turning an object.
4. Prefrontal cortex-- This area responds to sensory stimuli (noises, lights) that lead to a movement and calculate the probable outcomes of the movement.
5. Posterior parietal cortex-- This area keeps track of the position of the body relative to space. Figure 8.8 The cerebellum is involved in coordination and "ballistic movements" (movements that are performed all at once, in a "single shot") People with damage to the cerebellum have trouble with movements requiring accurate aim and timing: tapping a rhythm, clapping hands, pointing at a moving object,