Sapolsky, Robert - Handouts for Human Behavioral Psychology

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 1

Hello! This is all of my section handouts I’ve made this year compiled into one document, giving a fairly detailed (though I can’t promise it’s comprehensive) review of class material. It’s 68 pages so if you’re satisfied with your current approach to studying, pay no attention to this and carry on; don’t let it distract or worry you. But for my money, IF YOU REALLY WANT TO DO WELL ON EXAMS, this is what I recommend doing: Look at this study guide as an example. Create your own version of this. How? o Gather a comprehensive understanding of a given topic (extended notes, lecture handout, class notes, recordings), then go through and generate questions and answers that cover each piece of information you encounter. (So instead of just reading “dopamine is implicated in schizophrenia” and assuming you’ll remember that, write down “what neurotransmitters are implicated in schizophrenia?” then answer it. Then “what is the evidence that there’s too much dopamine action in schizophrenia” then answer it. Etc.) o Make them so clear you could share it with a stranger. Your mind will love to convince you that it understands and will remember something when it actually doesn’t and won’t. Don’t trust it! Test it. o Write this all down. (or type this all up?). At this point you’ll probably remember a LOT of what you’ve studied just by engaging the content in this way. To remember everything, go through the study guide you just created and quiz yourself on it. Don’t just read it, retrieve it. (see the papers I posted on the power of retrieval learning earlier this year). Better yet, do it with a knowledgeable study partner. Your gaps in memory will hopefully be non-overlapping. Plus it’s more fun. Obviously focus on the more important things (like the stuff on the lecture handouts, or the stuff we spend half a lecture talking about instead of the stuff that comes up in one brief sentence). Make a realistic plan for when you will do the reviewing and the testing, and stick to it with diligence and discipline. Figure out where your biggest gains are and maximize the utility of your study time, save the minutia for your final go at it. And if you don’t have the time/patience to create your own, using this in the same way (not reading the answers, GENERATING the answers and then seeing if you’re right) will also be helpful. Go through and delete the answers, and see how you fare. When you’re confident you know something solidly, cross it off and don’t rehash it any more. Spend your time on the things you don’t know yet. And DON’T pass up things that you don’t yet know solidly without extra cues and prompting. Be rigorous. Be sure to try out the practice final from last year to see what kind of shape you’re in. Also eat lots of fruits, veggies, and fiber. Get lots of sleep. Get some exercise. They will all do wonders not only for how you feel, but for how you think. Good luck!

Background from section My sections are aimed at those who already know the basic background like the basics of natural selection, how neurons work, central dogma, etc. I was a HumBio major. These filled-in section handouts will be posted after section. NOT a comprehensive handout of testable material, but it covers what I think are the most challenging/interesting/ important topics. Sometimes we'll delve into readings if there's time, but not always. Be sure to do those on your own because there will be a proportion of the test that you won't be able to answer unless you've done your readings.

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Contents Background from section ........................................................................................................................................................ 1 Introduction and Evolution/Sociobiology ............................................................................................................................... 3 Behavioral Genetics .............................................................................................................................................................. 13 Recognizing Relatives ............................................................................................................................................................ 18 Ethology ................................................................................................................................................................................ 21 Advanced Neuro/Endo .......................................................................................................................................................... 25 Limbic System ....................................................................................................................................................................... 29 Reductionism and Chaos....................................................................................................................................................... 31 Sexual Behavior (lecture 1 of 2) ............................................................................................................................................ 36 Sexual Behavior (lecture 2 of 2) ............................................................................................................................................ 41 Aggression I ........................................................................................................................................................................... 45 Depression ............................................................................................................................................................................ 58 Schizophrenia ........................................................................................................................................................................ 61 The Biology of Religion.......................................................................................................................................................... 65 Final Lecture .......................................................................................................................................................................... 68

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Introduction and Evolution/Sociobiology Things that you really need to know (at the end of every extended notes): -Basic tenets of Darwinian evolution -The three building blocks of sociobiology -Understanding kin selection on a mathematical level, to a certain extent. -The application of game theory to reciprocal altruism. -The problem of how reciprocal altruism starts. -How to explain a number of realms of behavior with sociobiological principles. -An array of critiques of the field. Our overall goal is to understand how a sociobiologist would make sense of animal behavior.

Pros and cons of categorical thinking 1. Helps you remember and recognize an example of a group. 2. You tend to see members of a group as more similar than they actually are and members of different groups as more different than they actually are (color perception example). 3. Myopic focus on individual categories (buckets) by leading thinkers of the past has led to disastrous outcomes

Evolution (change over time) caused by a number of things. We focus on the big one: natural selection. Requires what three conditions? 1. Heritability (DNA) 2. Variability (mutation) 3. Differential fitness (success in leaving progeny) Then what happens? 1. Versions that confer more fitness will become more prevalent over time

Sociobiology is the study of the evolution of behavior. What are the three core explanatory pieces you should be able to apply to a wide range of behavior? 1. Individual selection. "A chicken is an egg's way of making another egg." -Samuel Butler 2. Kin selection/inclusive fitness. "I will lay down my life for 2 brothers or 8 cousins" -JBS Haldane 3. Reciprocal altruism.

Five pieces of evidence for evolution? 1. Observable over past 100 years in short-lived species like staph bacteria & penicillin resistance 2. Fossil record shows tons of intermediate forms 3. Genetic evidence: we share huge percentages of our genomes with our closest evolutionary ancestors, and less the further you go back in time to most recent common ancestor 4. Geographic distribution of species: relatives are bunched together in space 5. Unintelligent design: vestigal structures like leg bones in dolphins, pyramidal system for finger movement

In our class: natural selection and sexual selection are different (sometimes opposing) forces. How do they apply to individual selection? 1. Natural: adaptedness to surviving in the environment 2. Sexual: adaptedness at attracting a mate How do they apply to kin selection (inclusive fitness)? 1. Natural: Engage in behaviors that allow related individuals to survive and reproduce 2. Sexual: Work to make related individuals seem attractive to potential mates How do they apply to cooperation/altruism?

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 4 1. Natural: non-related hunters cooperating to get game they couldn't get alone. 2. Sexual: cooperatively making a non-relative more attractive to mates

How do you calculate degrees of relatedness? 1. 50% gene-variant similarity with parent or full sibling. 25% with grandparent. 25% with (biological) aunt/uncle. 12.5% with great grandparent, etc. 2. Each "line" in the family tree that you traverse typically halves the number of genes you share with the next individual.

Cooperation 1. Kin selection/inclusive fitness 1. Cooperate with relatives, encourage their reproduction. 2. Reciprocal altruism, formalized through game theory with the prisoner's dilemma: 1. When to cooperate vs. defect

What typically characterizes species that demonstrate reciprocal altruism? 1. "Species that are social, long-lived enough and in sufficiently stable groups so that individuals interact with each other more than once (how else can the reciprocity occur?), smart enough to recognize individuals and, critically, smart enough to try to cheat at the reciprocity when it’s possible to get away with it (i.e., to not reciprocate an altruistic act), and smart enough to spot someone trying to cheat against them." -extended notes What is Axelrod's famous winning strategy? What does even better under some conditions?

1. Tit for tat. Will lose battles but win wars. Will lose to cheaters, but pairs of TfT will win more than cheaters ever will. 2. Better with forgiving tit for tat (less prone to signal errors) 3. Pavlov can exploit forgiving tit for tat What are five examples of TfT or interesting elaborations?

1. 2. 3. 4. 5.

Vampire bats (TfT) Stickleback fish (TfT) Gender switching fish who defect if the other defected (TfT) Cowardly lions who are good hunters (different domains of contribution) Huge naked mole rats plugging up holes (different domains of contribution)

Related to kin selection: the greenbeard effect. What is it? 1. Not about recognizing kin, necessarily, but instead just one gene that allows for 1. Recognition of the gene in other individuals 2. Cooperation with other individuals that have that gene Related to cooperation: rock-paper-scissors equilibrium 1. Actually restraint from competition. Not true altruism. How does cooperation/altruism start?

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1. Founder population cooperates on a basis of kin selection. Then when re-integrated into large population, they keep "winning the war" and cooperation crystalizes outward or non-cooperation is driven extinct.

Pair Bonding and Tournament Species How do we explain imprinted genes?

1. Father's imprinted genes cause a more "selfish" infant that grows a lot, suckles lots of nutrients, etc. at the expense of the female's future reproductive success. Tournament species males are interested in mating with many females until they get kicked out. 1. What happens when these go unchecked? Choriocarcinoma. 2. Mother's imprinted genes do the opposite. Slow down growth and nutrient uptake. She's equally interested in the success of future progeny as much as this one. 1. What happens when these go unchecked? Egg won't implant 3. Exemplify inter-sexual competition via parent-offspring conflict. Higher in tournament species. How do we explain competitive infanticide? 1. Definitely not for the good of the species! 2. When the average tenure of the head male is shorter than the average interbirth interval in females. 3. Males operating under individual selection: wipe out other infants so mothers can be impregnated (tie to oxytocin - nursing - fertility suppression - endocrinology foreshadowing), plus less competition for his future offspring. 4. Females coping via individual selection principles: smell of new male causes spontaneous miscarriage because it doesn't make sense to have an offspring that will be killed. Save on pregnancy costs and get pregnant with the new male. Female still has 50% genetic interest in her offspring whether it's old male or new. 5. Females coping via kin selection: defending their children up to a point (when would they lay down their life?), also faking pseudo-estrus to fool the new head male into not forcing them to spontaneously miscarry from harassment.

What are some further behavioral examples explained well by sociobiology? 1. Kidnapping by male baboons (and not kidnapping when high-ranking male just joined the troupe) 2. Relatedness in dominance hierarchies. Females inherit their rank 3. Sex ratios.

1. Males are more "expensive" but high ranking tournament species females will gamble on a son instead of a daughter. What's the proximate mechanism here? Higher-ranking females have better nutrition so sons will be more likely to be carried to term. 2. Sex ratios will stabilize over time near 50-50. 4. Paying attention to alarm calls as a function of relatedness 5. Male-male cooperation 6. Instances of polyandry (multiple males leading a harem). Usually adelphic (by related males). Includes humans (see traditional Tibetan marriage patterns). 7. Why would you mate with relatives?

1. Share more genes with them so more of your genes make it into the next generation. Great! 2. But if they're too closely related than recessive disease-causing alleles are likely to be inherited and cause disease. Not so great! 3. Where does the "optimal" mating occur, according to the Helgason "Kinship and Fertility" reading? 3rd

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or 4th cousin matings produce the most fertile offspring. 8. How do chimps vs. baboons differ in which gender leaves the troupe? What consequences does that have?

1. Baboons: males leave the troupe. Females stay and are more related. i. Males kill each other more 2. Chimps: females leave the troupe. Males stay and are more related. i. Males band together and often kill neighboring males. This is protowarfare and genocide.

Group selection. Is it valid? What version is invalid? 1. Not for the good of the species. 2. Yes multi-level selection. a. Founder populations evolve cooperation based on kin selection, and can then outcompete other groups they are re-integrated with. b. Situation of ABB. c. Parochial altruism is the phenomenon of cooperating with an in-group against an out-group, regardless of kinship. Like WWII.

What are some common patterns of human behavior across cultures and time? 1. 2. 3. 4.

Males more violent than females Hierarchical systems Emphasis on kinship Polygamy (most cultures contain polygamy; most individuals within those cultures practice (serial) monogamy)

What are four criticisms of sociobiology? 1. Sociobiology says behaviors are heritable. a. Criticism: What is your proximate mechanism? Where's the gene? What protein does it code for?

That's the real basis of evolution. 2. Sociobiology says every social behavior is an adaptation. a. Criticism: This is the adaptationist fallacy that everything is adaptive. You're making up just-so

stories! What about spandrels? 3. Sociobiology says that evolutionary change happens continuously in small incremental steps - gradualism. Evolution, not revolution. a. Criticism: What about punctuated equilibrium? Fossil record shows periods of stasis and periods of

rapid change. Tiny adaptations don't make a difference. 4. And political criticisms. "Oh the conclusions you draw scientifically just happen to justify the hierarchies and inequities our society faces and which you (Southern, white scientists) benefit from."

Example Exam Questions - Filling in prisoner’s dilemma payoffs - Giving example of real-life prisoner’s dilemma situation - Predicting traits (including imprinted genes) for tournament vs. pair bonding species

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How would a sociobiologist justify the existence of parent-offspring conflict over breastfeeding? Name a non-human primate in which female exogamy occurs and what this might have to do with war-like behavior.

We’ll be covering the two molecular genetics lectures this time. And the two behavioral genetics lectures next time. And then ethology and recognizing relatives after that. My sections won’t spend much time reviewing the introductory neuroscience, introductory neurology, and intro to sex lectures which will be done by the TAs next week.

Things to Know 1. 2. 3.

How sociobiologists think of the evolution of a trait, and how molecular biologists do so. Basics of DNA, RNA, protein sequence, structure and function. Classical mutations (point, deletion, insertion), how they are the engines of microevolutionary change and sociobiological ideas about gradualism. 4. How microevolutionary change can relate to behavior. 5. The basic idea of punctuated equilibrium, and the critiques of it. 6. Why it is that a gene doesn’t decide when it activates and directs the construction of a protein, and the role of the environment in this process instead. 7. The basic facts about exons, alternative splicing, promoters, transcriptional networks, transposons. 8. The macroevolutionary consequences of changes in any of these realms. 9. Molecular support for the idea of stasis. 10. Challenges to the central dogma view of genetics and genetic determinism.

Review 1. Proteins are made of amino acids. The sequence of amino acids determine the shape (and therefore the function) of the protein. Amino acids are coded for by DNA. DNA is a gigantically long molecule with four different bases, "letters." Three bases next to each other are called a codon. One codon is read to create one amino acid. 2. Proteins serve tons of roles in the body; almost everything interesting is a protein (enzymes, neurotransmitters, transcription factors, receptors, other signals).

For our purposes, what is the central dogma of life?

1. Information flows from a unique DNA sequence (a gene) to an RNA sequence to an amino acid sequence. 2. By extension, one gene specifies one protein which has one shape and therefore one function And what is the main challenge to the central dogma in this course?

1. That one stretch of DNA can actually lead to many different proteins (through alternative splicing) 2. (also retrotranscription in viruses from RNA --> DNA) 3. (also one protein can take on multiple conformations and serve different functions)

What are the molecular bases for the three tenets of evolution by natural selection? 1. Traits are heritable: you get your genes from your parents, and them from their parents, and so on. 2. Variation: different alleles (versions of genes) code for slightly different proteins that serve the same function. 3. Differential fitness: those different versions might do their protein job slightly better or worse, depending on the environment in which they're working

What are the three types of mutations in classical genetics? 1. A point mutation when a single nucleotide is copied differently (incorrectly) between a mother cell and a daughter cell.

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 8 a. Can be a neutral mutation thanks to the redundancy of the codons. That is, multiple sets of 3 DNA bases will code for the same amino acid. So if the point mutation changes from one codon into a different but reduntant codon, it's a neutral/silent mutation. 2. An insertion mutation leading to a frameshift. 3. A deletion mutation leading to a frameshift. Deletions can also be of entire genes.

*What do we mean by microevolutionary vs. macroevolutionary change? 1. Micro: a change in a single protein that affects a single protein and the downstream effects of having a differently shaped protein. 2. Macro: a change in something (promoter, transcription factor, splicing enzyme, transposase, etc) that produces far-reaching changes in the way many proteins are made or when they are expressed.

Four examples of a microevolutionary change having a big impact on behavior?

1. Phenylketonuria (PKU) 2. And two examples related to testosterone? a. If your T receptors are mutated and don't function, you are genetically XY male but have female appearance because your body doesn't respond to the presence of T. This is testicular feminization syndrome. b. Enzyme that makes T is mutated in early life, but doesn't hold back T production at puberty in populations in New Guinea and Dominican republic. Guevedoces: what are thought to be "girls" (but are actually XY) develop male secondary sexual characteristics around puberty when T kicks in. 3. And an example related to anxiety? a. The benzodiazepine receptors come in different versions based on subtle mutations. b. The better the receptor binds BDZs, the less anxious the individual will be. If they're very poor BDZ binders, the individual will have an anxiety disorder. How can micro mutations tell you about evolutionary ancestry trees? 1. We share "the gene" for many proteins with distantly related species (a significant percentage of our genes are shared with bananas, for example). 2. But as species evolve and diverge, differences accumulate in our genes so that the proteins of very distantly related species have many differences between them while the same proteins in very closely-related species have very few differences between them.

How do you know if a protein has undergone positive selection or negative selection? 1. Take a protein product that is shared between species, like a serotonin receptor shared between dogs and humans. 2. Look at the DNA sequence that codes for that protein. Just by random chance we expect, say, 1/3 of the mutations (differences) between those two DNA stretches to actually code for a different AA (amino acids), resulting in a slightly different protein. 3. However, if 3/4 of the mutations coded for different AAs, this gene has undergone positive selection and the differences that have accumulated were the result of selective forces over time selecting for a new and better version of that gene. 4. If say 1/8 of the mutations coded for different AAs (that is, more of the mutations were neutral than you'd expect by chance), then that gene has undergone negative selection/stabilizing selection, meaning that it is very conserved among species because slight changes have been selected against. If that's still confusing, here's another explanation from last year: You start off with a gene in an organism at time T1.

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 9 After a long evolutionary time period during which the gene has undergone numerous mutations, you come back and re-examine the gene, which is no longer identical to its original form. You're comparing the newer version of the gene at time T2 to the original gene at time T1 and looking at the mutations that have happened. Based on the type of mutations (silent/neutral or consequential) that you see, you can know whether this gene has faced selective pressures or not, and if so, what type of selective pressure. o If nothing interesting has happened and those genes have not undergone any particular selection pressures, you'd expect 1/3 of the mutations to be consequential (due to the mathematics of the DNA-amino acid link). o But if significantly more than 1/3 (like 90%) of the mutations are consequential, the gene has undergone positive selection because having so many more consequential mutations (ones that actually make a difference in the protein formed) than would be expected by chance means that, in order for this gene to have evolved this way and exist in its present form, that large number of consequential mutations must have been selected for. o And if significantly fewer than 1/3 (like 5%) of the mutations are consequential, the gene has undergone stabilizing/negative selection (pressures to keep the gene exactly how it functioned originally). This is because when consequential mutations happened along the line from T1 to T2, those changes were selected against and the original genetic sequence is highly conserved.

What is the 95% of DNA that doesn't code for proteins? Promoters, repressors, and "junk DNA" which we don't know much about The longer the genome in a species, the greater percentage of genes tat code for TFs

How do you know when to express certain genes?

1. Can be answered at many levels. a. When the transcription factor (TF) binds to the promoter b. When the intra-cellular environment signals transcription via TFs c. When the inter-cellular environment signals transcription, e.g. via testosterone d. When the inter-organismal environment signals transcription, e.g. a mother smelling her newborn. Overall, this is the concept of if-then clauses. 1. Example: if you smell your newborn baby, then express genes related to nursing.

What's 1 molecular mechanism and 1 example of epigenetic regulation? 1. Chromatin packing patterns can be set for life. 2. Examples include a. Metabolic programming during the Dutch Hunger Winter b. Stress reactivity in rats as a function of licking and grooming from the mother

What do transposons do and where do we see them play out in nature?

1. Transposons are mobile bits of DNA clipped by transposases and inserted into random parts of the genome 2. Originally found by Barbara McClintock in corn. Often found in plants as a stress response to come up with a novel solution under dire circumstances that plants can't run away from.

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3. Also seen in neuronal wiring of mammalian brains. Significance: the organ having MOST to do with behavior is LEAST deterministically goverend by one set of genes. A lot of noise in the system and less of a role for a deterministic view of genes. 4. Also seen in parasites like the trypanosome worm which uses transposons to reshuffle its surface signal proteins to evade immune defenses. 5. Also seen in the immune system of mammals. What's the basic idea of Punctuated Equilibrium (PE) and what's the evidence for it? How do gradualists respond to those claims? 1. PE is a model that explains evolution. The idea is that there are long periods of stasis (the equilibrium part) in which nothing exciting really changes and then periods of saltation (the punctuated part). 2. Paleontological evidence: we see in the fossil record what looks like saltatory change and periods of equilibrium

a. Gradualist ("creeps", as opposed to PE "jerks") say the fossil record is incomplete and maybe it's gradualist if we had more data. b. Gradualists also say that "sudden" change for PE folks is plenty of time for sociobiologists to examine evolution of behavior in what they'd call a gradual manner. c. Gradualists also say that PE folks are only looking at morphology or the way things are shaped. You get very different behaviors based on neurons and brains, and you can't directly examine those with paleontological evidence. d. Gradualists in the old days also demanded to see molecular mechanisms for these changes. See below for response. What's the molecular mechanism of PE changes?

1. Mutations in the regulatory regions of genes. We call these mutations macroevolutionary. a. These include: promoters, repressors, TFs, splicesomes, and transposases. Transposon action itself (even when not mutated) can change entire if-then sequences. 2. And multiple genes can be regulated by one TF or one promoter 3. And any given single gene probably responds to multiple TFs and promoters. So we have networks of genes and when you disrupt the controllers of those networks, their regulators, you can produce radically new if-then clauses. So a new environmental situation can trigger an existing pattern, OR the same environmental situation can trigger a new pattern if you have just small mutations in any of these regulatory sequences. What about the mechanisms for the stasis part in PE? The price of complexity of everything we've seen means that these small changes that have big amplfied effects are often going to have very deleterious effects, and will not be selected for. So we'll see a lot of stability in these systems. We'll see the saltations at periods where there's an evolutionary bottleneck, like there was with cheetahs.

How can you get multiple proteins from one gene? Alternative splicing. Can rearrange the exons and selectively keep some of them for translation into protein.

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 11 That's how we can have 20,000 genes but also have 100,000 different proteins. 3. This means any given exon may end up in many proteins. Mutate that one exon and you can amplify that mutation to affect many proteins (overlapping genes).

How did the prairie vole example show these principles?

1. A mutation in the promoter for vasopressin receptors changed where the repressors were. 2. In monogamous voles the vasopressin receptors are expressed on dopamine neurons. 3. In polygamous voles the vasopressin receptors are NOT expressed on those dopamine neurons. So when these voles mate and vasopressin is released, the polygamous ones aren't reinforced to be monogamous in the same way the monogamous ones are. 4. This emphasizes that it's not the protein (the vasopressin receptor) itself that's changed, but rather the context in which that gene is expressed. Three (simplistic) examples of novel if-then clauses that you could explain with the above mechanisms. 1. If it's dry out, then retain water --> if it's dry out, then mate. (seasonal mating). 2. If you smell a relative, then nurse them --> if you smell a relative, don't mate with them. (incest avoidance). 3. (or you change the if part): if you are secreting glucocorticoids, then suppress immunity --> if you are secreting progesterone, then suppress immunity. (maternal immunosuppression during pregnancy).

How does the existence of duplicated genes/copy number variants give us more explanatory wiggle room when we're looking at genetics and behavior? 1. So you can have duplications of an entire gene. a. One can get knocked out or mutated into oblivion and you're still okay b. You can also use these duplicates to double the amount of protein you produce given the same promoter activation. c. So one can mutate a bit and the other can serve as a backup. 2. Examples: a. You see a lot of copy number variants in the genomes of those with schizophrenia b. Steroid hormone receptors

Who wins in the end? The gradualist creeps or the PE jerks? 1. Both! Yay. 2. Gradualism: a. Molecular evidence: small point mutations CAN produce slight changes in protein function that can be selected for. b. SOME fossil records show evidence for gradualism 3. PE's evidence is all laid out above. Also: a. We've seen punctuated events in our lifetime. Four examples i. Siberian foxes that look like dogs ii. Chicago rat skins show rapid change since 1850 iii. Human populations exposed to western diets undergo almost a bottleneck of diabetes iv. Bacteria evolving antibiotic resistance 4. And they can both happen simultaneously in different realms.

Example exam questions

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Behavioral Genetics Things to know for behavioral genetics: How behavior geneticists, sociobiologists and molecular biologists differ in their intellectual approach to detecting a genetic influence on behavior. How behavioral geneticists think about behaviors running in families as a function of relatedness, and the criticisms of this. The various approaches dissociating sharing biology with an individual and sharing environment with an individual (i.e., twin studies and adoption studies), and the various pitfalls of these approaches. Approaches in which one studies behaviors that occur in the absence of environmental influences. To understand the strongest critique of that approach, namely prenatal environmental effects. The ways in which genetics that don't follow classic Mendelian rules become relevant. How the behavioral genetics and molecular genetics approach can be combined to find markers for actual genes. What heritability means. Some sense of where chance comes into this.

What are the major approaches used by the behavioral geneticists? What are the criticisms of these approaches? Remember they're all about teasing apart genetic and various environmental influences. Universality, shared among family, and shared as a function of relatedness. a. Saying traits more shared with closer relatives must be due to the more shared genetics.

b. Criticism: Genetics and environment tend to correlate well within families as a function of relatedness c. Criticism: you're not actually controlling for environment because your pre-natal maternal environment is crucial (Dutch Hunger Winter, epigenetics, etc.) MZ vs. DZ twins. a. Criticism: even among MZ twins you have i. Splitting before day 4 two separate placentas (dichorionic) and two amniotic sacs ii. Splitting between day 4-7 one placenta (monochorionic) but two amniotic sacs iii. Splitting after day 7 one placenta and one amniotic sac b. Criticism: MZ twins are also treated more similarly than DZ twins Adoption studies. Saying that traits more shared with closer relatives must be due to more shared genetics because the environment is random and not shared. a. Cross-fostering in animals b. With MZ twins separated at birth c. Compare MZ and DZ twins separated at birth

i. ii. iii.

Criticism: adoptees are placed non-randomly Criticism: you're going to have pretty small sample size with these very unique cases Criticism: again, environment starts at conception, not at birth

Behavior in the absence of environmental influence a. Social smiling in congenitally blind babies and babbling in congenitally deaf babies b. Lab rats 100 generations away from ever seeing a cat are still averse to cat pheromones

What 3 important things happen in the pre-natal environment? o Circulating hormones (from mother and from rat siblings strung up on the same circulatory chain) o Glucocorticoids and other stress hormones. High exposure to these brings, as an adult, smaller brain, lower capacity for learning, more tendency towards anxiety/hypertension/diabetes. Sheesh!

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o

o

Leads to epigenetic effects of inability to shut down stress response thanks to smaller hippocampus o Maternal and sibling estrogen influences also influence subsequent development (earlier puberty, etc). Nutrition and metabolic programming o Prime example of epigenetics (non-mendelian inheritance of traits, even multigenerationally, that has nothing to do with genes - are not heritable traits). o We also see pelvic arch size evolutionary battles with Massai malnutrition Learning (mother's voice)

Some would say maternal and paternal genetic contributions are equal, and that mom also gives the prenatal environment. How would you then explain any differences you saw in behavior as shared more with mom? Due to the influence of the prenatal environment. That's how we can control for it. But what complicates that assertion? In what ways is mom more than just 50% genes + prenatal environment?

Paternal uncertainty Mitochondrial DNA Imprinted genes TF inequality and Lamarkian inheritance And say we do discover a strong genetic component for something like extroversion. What might the genes actually be influencing? 3 examples: Something indirectly related to extroversion, like attractiveness. These are indirect genetic effects. Another example: high heritability for political affiliation may have to do with the genetics of ambiguity tolerance Aggression in rats also seems highly heritable. Not actually genes for aggression! About pain tolerance thresholds.

How do behavioral geneticists hone in on actual genes? Find genetic differences, then look for differences in behavior. To find genetic differences in order of awesomeness: o phenotypic marker linkage < o protein marker linkage/protein size < o RFLPs more dopamine. o D1/D2 dopamine receptor situation Receptor location

D2 receptors are on the post-synaptic neuron per usual D1 receptors are pre-synaptic autoreceptors, the bookkeepers. Receptor function

D2 stimulation facilitates formation of a new pair bond D1 stimulation does the opposite: makes voles uninterested in forming pair bonds Plasticity

D2 receptors up-regulated in the dopamine circuit when voles are first mating. Forms the pair bond. After pair bonding, D1 receptors are up-regulated, so they aren't inclined to form new pair-bonds What region is associated with long-term relationships and feelings of comfort, familiarity, needing? o The anterior cingulate What's the role of the frontal cortex in sexual behavior? What NT does it tend to use? o Tends to use serotonin, but receives lots of dopamine projections. o Makes "the hard choice." Could be inhibiting sexual impulses in inappropriate contexts. Or could be fueling sexual impulses in cases where it's scary/difficult to do so.

What are the endocrine RESPONSES to sex? How do hormones differ between genders in RESPONSE to sex? Females: o Progesterone increase (reinforces pleasure, prepares for pregnancy) o Androgens increase (mediates sexual motivation) o Oxytocin increase (attachment, trust, mediate release of dopamine for pair bonds) Males o Testosterone increase AFTER sex o Vasopressin increase – we see high levels of vasopressin receptors in meso-limbic dopamine system of pair-bonding species, which cause dopamine release (increasing monogamous behavior) Ex. Change VP receptors in voles can cause poly to be mono Ex. Men with mono version more likely to marry and not divorce Remember: this is the vasopressin receptor promoter that has the variation, not the receptor itself. So it's about expression patterns. Take-home point (THP): express vasopressin receptors in the mesolimbic regions of the brain and the animal will be more likely to be monogamous.

What's the neurobiology of sexual orientation in males? The INAH-3 (interstitial nucleus of the anterior hypothalamus) comes in different sizes. o Men have a 2x larger INAH-3 on average with huge variability and overlap compared to women.

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 39 o

One finding from Simon LeVay shows that gay men's INAH-3 is about halfway between the size of straight men and women. Has confounds because the gay men had died of AIDS. Finger-length ratios and otoacoustic emission also show a gender difference with gay men, on average, between straight men and women.

And the nbio of sexual orientation in females? o

"The literature here is smaller than for male sexual orientation. Some studies suggested elevated levels of androgenic hormones in lesbians versus straight women, some suggestions of elevated prenatal exposure to androgens. A few studies suggest that the 4th to 2nd finger ratio in lesbians differs from that of straight woman, in the direction more of the male average. Ditto for otoacoustic emission. There’s also some studies suggesting “male-like” cognitive profiles in terms of visuospatial tasks, verbal fluency. Of note, though, these are all very small effects, highly variable. A few studies have suggested that these patterns are more pronounced in lesbians who are self-described “butches” (i.e., women who take more stereotypically masculine roles during sex)." -from Extended Notes

And the nbio of transsexuality? o o

o

Note on defining gender/sex: can be done by chromosomes, gonads, hormones, external genitalia, secondary sexual characteristics, and/or psychosocial identity. The BNST (bed nucleus of the stria terminalis) comes in different sizes. o Large sex difference in the size of a part of the BNST with a lot of predictive power o In transgender people (who feel their anatomical sex doesn't match their identity), the BNST tends to be the size of the sex they feel they should be rather than the one they are. o Conclusion: maybe less of a "psychological pathology" as it's been thought of; more a case of being stuck in the body of the wrong gender. "Around 60% of men who have had their penises removed (because of penile cancer) have phantom penis sensations, whereas male-to-female transgendered individuals do not." -Extended notes

The Releasing Stimuli for Sex What examples of visual releasing stimuli do we have? o o

Rhesus monkeys pay for sexual imagery of female rhesus monkeys (esp the perineum of a female in estrus). Also pay to see a dominant male - might be "gathering information." Both sexes in humans have the amygdala, hypothalamus, and mesolimbic dopamine systems activated when viewing a picture of somebody they find sexually attractive.

Tactile stimuli? o o o

Lordosis! Also skin can be more sensitive if and only if you have certain levels of gonadal hormones. Touch evokes activation of dopamine systems

Olfactory stimuli? o o o

Pheromones! They're breakdown products of sex hormones. What can you know by smelling them? o Gender, age, fertility, reproductive state What do you need to detect them? o Intact gonads What are the intrasexual effects of pheromones?

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 40

Gustatory stimuli? o

Some ungulates do flehmening where they lick each other's genitals to gain the pheromonoal information.

Auditory stimuli o o

A stag's roar can induce ovulation in females. Pandas and human females have slightly higher pitched voices around ovulation

OTHER stimuli? o o o

Thought: like fantasy in humans (and Sapolsky would say in his baboon observation) Rage/fear/stress: inhibit sexual behavior and physiology Variety and the Coolidge effect. A new partner can re-invigorate sexual motivation. More often

found in males than in females.

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 41

Sexual Behavior (lecture 2 of 2) How Hormones in Adulthood Affect Sexual Behavior First: note what we mean by "sexual behavior." Proceptive, receptive, attractive behavior. Erections, pelvic thrusts, lordosis, likelihood of orgasm, interest in sex, etc.

Second: note what we mean by organizational vs. activational effects Organizational: perinatal environmental hormones. Setting up the framework and the structuring for the whole life. Activational: acute hormonal effects in adulthood. Immediate triggers.

Where in the menstrual cycle does sexual behavior peak in most female animals? In humans? Most animals: peaks at ovulation. Sometimes only occurs at ovulation. Humans: same thing, but also get a peak at menstruation, hypothesized to be due to "relief" at not having gotten pregnant. What effects are female hormones having? Estrogen works in brain to increase progesterone and oxytocin receptors in the limbic system. Skin more sensitive to touch Androgens also present (at 5% the level of males), involved in sexual motivation.

What does Testosterone (T) have to do with male sexual behavior? How do we know? Castration (no T) reduces sexual behavior, but it doesn't go down to 0. Replacing T at 10%, 100%, or even 200% the original levels causes sexual behavior to come back at the same level. Only with 1000% T way above normal physiological levels do we get an increase in sexual behavior. When castrated, animals exhibit amounts of sexual behavior proportional to their pre-castration levels showing that sexual behavior is also determined by the environment and experience, not just T. It doesn't initiate neuronal action, testosterone potentiates the effects of other excitatory stimuli.

How do we go about having seasonal matings? Why would we? How: use melatonin. A hormone whose release is inhibited by light exposure. When day lengths are increasing, you're approaching summer; when decreasing (one day compared to the next), you're approaching winter. Why: want to give birth during fertile spring/summer times when offspring can survive best. Who: depends on gestation period. If 2 month gestation period then melatonin stimulates reproduction (you have a lot of melatonin in the winter, just before spring birth). If 6 month gestation period then melatonin inhibits reproduction.

How Early Environment Affects Sexual Behavior What happens to socially isolated primates' sexual behavior? Can still do it, just don't know the right contexts. What social imprinting happens in human children? You learn who the appropriate targets for sexual behavior are. Kibbutz studies show us that's how we "learn" who our siblings are.

What role does early environment play in the development of homosexuality?

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 42 No evidence that it has any role. "neurotic homosexuality" caused by mothers and "absent father" theories haven't held up to scientific scrutiny.

How Perinatal Hormones Affect Sexual Behavior What is a "feminized" brain vs. "masculinized" brain? How accurate is this dichotomy? Feminized: Hypothalamic gonadal hormone signaling is cyclic (ovulation, menstruation, etc) Masculinized: produces male reproductive FAPs like erections and pelvic thrusts Tons of animals fall in-between. An artificial dichotomy.

Through what pathways does T have its effects? Peripheral body effects: converted to DHT and influences sensation. Few areas of the brain: acts just as T, no conversion. Most areas of the brain: is converted to estrogen and binds to estrogen receptors. How do females avoid a masculinized brain? They would have one because of all the estrogen floating around their prenatal environment But estrogen is pulled out of fetal circulation by alpha-feto protein

In what cases are females "masculinized." And what are their outcomes? Two ways: o DES drug exposure generates high androgen levels during pregnancy o Congenital adrenal hyperplasia Outcomes: o Less interest in "female-typical" sexual behavior and roles. More likely to be gay. Confounds: many reconstructive genital surgeries and being a taller, more muscular woman

What is the case of testicular feminized males? How do their bodies and brains develop? Born XY (genetically male) but androgen receptor mutates. T doesn't have bodily effects (as DHT). But in brain T is converted to estrogen and thus produces a masculinized brain. Male secondary sexual characteristics emerge at pubertyGender identity and bodily characteristics usually remain female.

Do gay men have "feminized" brains? Why yes? Why no? Yes: more older brothers increases likelihood of being gay because mother has antibodies that target T. Less T on board, therefore a "demasculinized" brain. Probably no: gay men have a lot more sex (look more "masculinized" than straight men in that respect).

Genetic influences on Sexual Behavior How do you interpret the twin study research on sexual orientation? Full siblings are only 9% concordant for sexual orientation, so the higher percentages in DZ and MZ twins are probably due to environment (esp fetal environment!). And the Hammer studies showing genetic markers? o Not the same marker in different pairs o Not replicated o Poor scientific reputation

Evolutionary Influences on Sexual Behavior Is sex for the purpose of social cohesion and cooperation? Probably not. Probably more about reproduction. Bonobos as exception. Sex differences in promiscuity Sperm cost a lot less than pregnancies so females are choosy and males are promiscuous. Most seen in tournament species. Less seen in pair bonding species. Males often try to control female reproduction across the animal and human kingdom. In what ways?

Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012. 43 o o o o o o

Clitorectomies and chastity belts in nomadic societies Males actively decreasing the attractiveness of females to other males. Sperm compete with sperm from other males. Male domination and linear access models (with exceptions below) Also rape Also subterfuge What female counterstrategies exist? o Concealed ovulation to trick males o Pseudo-estrus to trick males (esp in cases of competitive infanticide) o Female choice. Sneaky sex in the bushes to subvert the linear access model: stolen copulations. They like the nice guys (nice guys FTW!). o Sperm dumping from males they don't prefer

How do we explain the evolution of homosexuality? (this is assuming there are genetic influences: see above for why there's probably very few) Heterozygote vigor argument Traits that are maladaptive in males but adaptive in females Kin selection: helper at the nest hypothesis. Evidence supports this hypothesis. What traits are markers of a good mate? Lots of support for symmetry. o Women judged to be more symetrical when ovulating. o Babies prefer symmetrical faces. o A marker of health. Secondary sexual characteristics like lions' manes, big bushy beards, colorful bird spots, etc. Why would these be good markers for a mate? o

o

o

Handicap principle: I can be wasteful on these traits so I'm very fit. Lots of evidence here. The worse the health and life expectancy in a country, the more women prefer faces of men with pronounced secondary sexual characteristics! Interesting, no? Could be markers of immune competence. Esp with caretinoids in birds. But males will try to cheat and put their last dying gasp of energy into their secondary sexual characteristics so they can mate before they die. Markers of fertility. Females: Like estrus swellings which indicate estrogen levels, earlier puberty, better child survival. Females: Like high breast:waist and low waist:hip ratios indicating fertility. Males: Like jutting jaws, high foreheads, heavy musculature indicating high T.

But how do these markers run into the problem of a self-fulfilling prophesy? o Take a given male bird and the females don't like him that much. But then surround him with fake female birds: make him seem all popular. Then all the other females now like him. A bandwagon effect. Interpretation: other females recognize that this male can attract females, so offspring of this male will be able to attract females and thus have high fitness. Therefore those females will have high fitness. Has individual selection written all over it. What features of human couples show a lot of homogamy? o

Religion, age, race, ethnicity, politics, SES

Shared in 90% of couples

IQ, education, introversion/extroversion

>40%

Height, weight, hair color, eye color, width of nose, length of earlobe, lung volume