Summary An introduction to behavioral endocrinology

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ISBN-10 0878936203 ISBN-13 9780878936205
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Summary 1:

  • An introduction to behavioral endocrinology
  • Randy J Nelson
  • 9780878936205 or 0878936203
  • 4th ed.

Summary - An introduction to behavioral endocrinology

  • 1 The Study of Behavioral Endocrinology

  • What is Berthold's experiment and what is it's role in the "birth of endocrinology"?

    Berthold studied the physical and behavioural differences among roosters, hens, capons and immature chickens. He had 3 experimental groups of 2 cockerels. In the first group, the testes were removed and the cockerells developed as capons. The birds never fought, failed to crow and had no interest in mating.

    In the second group, the testes were removed and one was placed back in the abdominal cavity. The birds developed normal rooster behaviour.

    In the tird group,  the testes were removed and one of the testis from the other bird was placed in the abdominal cavity. Also these birds developed normal rooster behaviour.

    Conclusions: (1) testes are transplantable organs; (2) transplanted testicles can function and produce sperm; (3) there are no specific nerves directing testicular function.

    Berthold took the first step in the study of behavioral endocrinology by demonstrating that the well-known  effects of the testes were due to their production of a substance that circulated in the blood.

  • What is the difference between males castrated at birth and those castrated after puberty?

    Males castrated when very young do not develop any hair growth, sexual behaviour and their voice does not change. Males castrated after puberty has hit have developed hair growth and sexual behaviour and their voice already has changed. They experience a diminished hair growth and sexual behaviour whilst their voice will stay low.

  • What are the four interacting levels of analysis?

    causation

    development

    evolution

    adaptive function

  • Berthold's experiment: nineteenth-century, first formal endocrinology study.  Berthold demonstrated experimentally that a product of the testes was necessary for a cockerel (immature male chicken) to develop into a normal adult rooster. 

  • The level of immediate causation (directe oorzaak) encompasses the underlying physiological, or proximate, mechanisms responsible for a given behavior. These mechanisms are mediated by the nervous and endocrine systems.

  • Hormones

    • Hormones are organic chemical messengers produced and released by specialized glands called endocrine glands.
    • Released in the bloodstream where thet may act on target organs/tissue/cells with specific receptors.
    • Hormones are similar to neurotransmitters and cytokines, but can operate over a greater distance and temporal range.
    • BOX 1.3: Differences in neural and hormonal communication. Neural are all-or-nothing events that have a rapid onset and offset, takes place in milliseconds -> mediates rapid changes. Hormonal messages takes seconds, minutes or even hours, mediates long-term porcesses. Difference in releasing, neural needs mediator calcium. More voluntary control in neural signals.
    • Behaviour is seen as the "output". Since musscles are the most common effectors, behaviour is considered to be coordinated movement. But lack of movement can be behaviour too.
    • Also important behaviour: excretion of scent and chemicals, changes in skin coloration and so on, also affected by hormones
  • Hormones must interact with specific receptors to evoke a response. Techniques are development to influence or measure hormone secretion and binding. Also used to research the physiological and behavioral effects after hormones bind to their respective receptors.

  • Hormones do not cause behavioural change per se. Rather, hormones change the probability that a specific behaviour will occur within the appropriate behavioural or social context.

  • Questions of development concern the full range of the organism's lifetime from conception to death.

  • What are Tinbergens four questions of analysis?

    • Immediate causation (Mechanisms/methods); What is the trigger?
    • Development; What is the genetic and developmental mechanism? 
    • Evolution; How is it evolved?
    • Adaptive function; What is the adaptive advantage?
  • Evolutionary approaches involve many generations of animals and address the ways that specific behaviors change during the course of natural selection. Behavioral biologists study the evolutionary bases of behavior in order to learn why behavior varies between closely related species as well as to understand the specific behavioral changes that occur during the evolution of new species. 

  • What is proximate causation and what is ultimate causation?

    • Proximate causation are the "How questions", = Mechanisms and development
    • Ultimate causation are the "Why questions", = Evolution and function
  • Examples hormones affecting behaviour

    • hormones change the probability that a particular behaviour will be emitted in the appropriate situation.
    • Zebra finches: Only the male sings. Without testes reduced singing, but when testes is reimplanted, or bird provided with T/E -> resume normal singing. T converted to E -> accounts for reduced singing. E could affect birdsongs by influencing the sensory capabilities (females or competators better heard), central nervous system (neural architecture or speed of neural processing could change) or effector organs (affect muscles syrinx).

    Examples of behaviour affecting hormones

    • Sight of a territorial intruder may elevate blood testosterone -> stimulate singing/figthing behaviour.
    • Male mice and rhesus monkeys that loose a fight show reduced circulating T.
    • Also found in humans, winners elevated T, loser decreased T. But not only in competing self, sports team wins/loose gives same result.
    • Lighthouse keeper -> isolated life, beard grew thicker in anticipation upon and having sex with fiancee. Correlated with testosterone levels, high T = increase beard grow. (anecdotal evidence)
    • Intercourse in couples -> levels of T were the same on evening with and without intercourse = sexual behaviour increases T more than high T causes sexual activitys
    • Sexual behaviour in women -> Testosterone elevated prior to intercourse compared to other activities.
  • Questions of adaptive function are synonymous with questions of adaptive significance; they are concerned with the role that behavior plays in the adaptation of animals to their environment and with the selective forces that currently maintain behavior. 

  • Proximate causation: How questions
    Ultimate causation: Why questions

  • What classes of evidence determines hormone-behaviour interactions?

    1. A hormonally dependent behaviour should disappear when the source of the hormone is removed or the actions of the hormones are blocked.
    2. After the behaviour stops, resortation of the missing hormonal source or its hormone should reinstate the absent behaviour.
    3. Hormone concentrations and the behaviour in question should be covariant -> the behaviour should be observed only when hormone concentrations are relatively high and never or rarely observed when concentrations are low.
  • Hormones  can have effect on sensory systems, central nervous systems and effectors. Those 3 things can have effect on behavior. 

  • Behavior can effect hormones: winners of a game have higher lvl's of testosteron, and losers lower. 

  • 1. Hormonally dependent behaviour should disappear when source of hormone is removed/hormone actions are blocked.
    2. Restoration for hormone (source) should reïnstate absent behavior.
    3. Hormone + behavior should be covariant: high levels means a certain behavior, and low levels means no or little behavior. 

  • The types of chemical communication are:
    Intracrine mediation --> Regulation intracell events
    Autocrine mediation --> feedback to influence the same cells that secreted them
    Paracrine mediation --> Affecting adjecent cells
    Endocrine mediation --> Via bloodstream
    Ectocrine mediation --> Pheromones

  • What is behavioral endocrinology?

    The scientific study of the interaction between hormones and behaviour

  • Biological half-life of a hormone; the time it takes to remove half of the hormone from the blood. 

  • Peptide hormones: Protein hormones that are only a few amino acids in length.
    TRH (Thyrotropin)
    GHRH (Growth hormone-releasing hormone)
    GnRH (Gonadotropin releasing hormone)
    MRH (Melanotropin-releasing hormone)
    CRH (Corticotropin-releasing hormone)

    Maybe Kisspeptin

    Inhibiting peptide hormones: 
    GHIH (Growth hormone-inhibiting hormone/ somatostatin)
    GnIH (possibly gonadotropin inhibiting hormone)

  • Dopamine (DA) also serves as a neurohormone in the hypothalamus to inhibit the release of prolactin and melanotropin from the anterior pituitary; in these contexts it is known as PIH (prolactin inhibitory hormone) and MIH (melanotropin inhibitory hormone(
    Hypocretin/orexin is found in cells located in the hypothalamus that project widely to the brain and spinal cord. *involved in sleep, metabolic balance and maybe activation of Sympathetic nervous system.

  • Anterior pituitary hormones:
    LH (Luteinizing hormone)                      ---> Secreted by basophils
    FSH (Follicle-stimulating hormone)  ---> Secreted by basophils
    TSH (thyroid-stimulation hormone) ---> Secreted by basophils
    Also known as glycoproteins (composed of alfa and beta-subunits) 
    LH & FSH also known as gonadotropins because in response to GnRH they stimulate steroidogenesis in the gonads as well as the development and maturation of gametes. In response to TRH from hypohtalamus, TSH is released from the anterior pituitary and stimulates the thyroid gland to release thyroid hormones.

  • Anterior pituitary hormones:
    GH (Growth hormone) ---> released from anterior pituitary in response to GHRH from the hypothalamus 
    PRL (Prolactin) ---> Release of PRL is stimulated by TRH from the hypothalamus.  

     

  • ACTH (Adrenocorticotropic hormone) ---> Made in the corticotrope cells. ACTH Is released in response to CRH from the hypothalamus and stimulates the adrenal cortex to secrete corticoids. Comes from:
    POMC (pro-opiomelanocortin). Maakt oa:
    lipotropins (mobilize fat)
    MSH (melanoctye-stimulating hormone (MSH) --> A pigmentation regulator
    B-endorphin
    met-enkephalin

     

  • Posterior pituitary hormones:
    Oxytocin ---> influences reproduces reproductive function in mammals. Important during birth, causing uterine contractions when the uterus is responsive. Also important in suckling reflex.
    Vasopressin (antidiuretic hormone, ADH) --> nonapeptide, found in many mammels. retains water in tetrapod vertebrates. Alcohol is a potential inhibitor.

  • Thyroid hormones:

    Thyroxine (T4) ---> releases its homones in response to TSH stimulation from the anterior pituitary.
    Triiodothyronine (T3) ---> both diffuse readily across cell membranes, but need help of carrier protein to travel through the blood.
    Thyroid hormonescan increase the rate of glucose oxidation. Also metabolic functions. Also important in growth and differentiation.
    PTH (Parathyroid hormone) --> stimulates ca2+ from the bone and absorps ca2+ from the gut.
    CT (calcitonin) ---> released from the C cells of the thyroid, opposite of PTH.Lowers the serum ca2+ levels.

     

  • Gastrointestinal hormones:
    More than 24 are identified, 2 major:
    Secretin --> small peptide, secreted by stimulus in the small intestine (Food passing through). Secretin stimulates the acinar cells of the pancreas to produce water and bicarbonate which aid in digestion. Secretin also stimulates the liver bile flow and pepsin secretion, as well as the inhibition of gastrointestinal tract movement. Also influences insulin release, fat cell lipolysis andrenal function.

    CCK (Cholecystokinin) --->  also called pancreozymin, causes the gallbladder to contract and release bile. There are several additional hormones; bombesin, substance P, motilin, galanin, neurotensin,peptiide YY and neuropeptide Y. Many of those have been identified in the brain. 

  • Stomach Hormones:
    Ghrelin ---> Stimulates GHRH release from the anterior pituitary.

     

    Adipokine hormones:
    Leptin --> Secreted from fat cells, acts on receptorsin the CNS and other sites to induce energy expenditure and inhibit food intake. Leptin concentrations increase after a meal, in concert with insulin release.
    Adiponectin ---> peptide released by fat cells.. Expression of adiponectin mRNA is decreased in obese mice and humans.

  • Pancreatic hormones:
    Insulin ---> only known hormone in the animal kingdom that can lower blood sugar. It promotes energy storage in the form of glycogen.
    Glucagon --->Glucagon travels through the liver, where it stimulates glycogenolysis. Opposite of insulin. Increases blood levels of glucose
    Somatostatin --> is an inhibitory hormone released from the delta-cells of the pancreas. Inhibits the release of insulin and glucagons locally. Somatostatin is also released from the hypothalamus to regulate the release of growth hormone from the anterior pituitary.

  • Gonadal peptide hormones:
    MIH (Müllerian inhibitory hormone) --> inhibits the development of the Müllerian duct sstem, the embryonic duct system that gives rise to thefemale accessory sex organs.

    Inhibin ---> Secreted by sertoli cells in the testes and granulosa cells in the ovaries. Inhibin feeds back to block the secretion of FSH from the anterior pituitary.
    Activin --> stimulates FSH-secretion.
    relaxin ---> produces b the corpora lutea during pregnancy. It functions to soften estrogen-primed pelvic ligaments to allow them to stretch sufficientl to permit passage of the large mammalian fetushead.

  • Placenta hormones:
    CG (chorionic gonadotropin(s)) ---> LH-like functions + maintain progesteron production during pregnancy.
    CS = PL (placental lactogen) ---> acts like PRL + GH

  • Cholesterol is the precursor of steroid hormones

  • Steroid hormones:
    Pregnenolone, progesterone, corticosterone/cortisol (glucocorticoids), aldosterone (mineralcorticoid), testosteron/androstenedionedihdrotestosterone (DHT) (androgens), 17beta-estradiol (estrogens, neurosteroids.

  • Aromatization: testosterone -> estrogens b cleaving the carbon at position 19 from androgen precursors. Aromatic compound remeans. DHT can NOT be aromatized.

  • Cholesterol is the precursor of steroid hormones

  • Monoamine hormones:
    Hormones derived from a single amino acid.

    Catecholamines: epinephrine,norepinephrine, dopamine
    General effect: - Increased heart rate + cardiac output
                                - Vasoconstriction deep + superficialarteries and vein
                                 - dilation skeletal + liver blood vessels
                                - Increased glycolysis

                                - Increased blood glucagon concentration + decreased blood insulin concentration.

  • Monoamine hormones:
    Indole ring, present in both hormones
    Serotonin ---> more GH release, TSH, ACTH. Inhibits LH realease.
    Melatonin: affects reproductive functions and sleep. pineal gland.

     

  • Prostaglandins are lipid-based.

  • Receptor types:

    - Steroid receptors; located inside the cell; hormone (apolar) binds, the complex moves to nucleus, there it regulates gene transcription.

    - Peptide receptors; in cell membrane;3 domains

    Transcription factors bind to beginning of DNA sequence.

     

  • Receptor regulation:

    up-regulation (homo specific priming) : High concentration of hormone stimulates production of more receptors. (prolactin)
    down-regulation: High concentration reduces number of receptors (Insulin)|
    hetero-specific priming : one hormone induces production of receptors of another hormone. Estrogens -> progestin receptors.

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Summary 2:

  • An introduction to behavioral endocrinology
  • Randy J Nelson
  • 9780878936175 or 0878936173
  • 3rd ed.

Summary - An introduction to behavioral endocrinology

  • 1 The study of behavioral endicrinology

  • What are proximate factors?

    Immediate causation and development

  • What are ultimate factors?

    Evolution and adaptive function

  • Immediate causation: mechanisms are typically mediated bij the nervous and endocrine systems.
    Development: is usually a result from the interaction between genes and environmental factors
    Evolution: many generations, natural selection
    Adaptive function: the role that behaviour plays in the adaptiation of animals to environment and with the selective forces that currently maintain behaviour. 

  • Berthold's experiment.
    The two birds in group 1 were castrated, and when observerd several months later, were smaller than normal roosters and failed to engage in rooster-typical behaviour.
    The two birds in group 2 were also castrated, but the testes was reimplanted in the abdominal cavity. These birds lookad and behaved like normal roosters when adults.
    The two birds n group 3 were also castrated, and one testis from each bird was transplanted into the abdomen of the other. Several months later, these birds also looked and behaved like normal roosters.
    Berhold found that the reimplanted and transplanted testes in group 2 and 3 developed vasculaer connections and generated sperm. 

    Based on the results of this experiment, Berhold drew 3 major conclusions:
    1. The testes are transplantable organs
    2. Transplanted testes can function and produce sperm.
    3. Because the teses functioned nromally after all neves were severed, the are no specific nerves directing testicular function. 

  • Name an example of hormones affecting behaviour?

    Singing behaviour in zebra-finches. Testosterone affect bird song. 

  • Name an example of behaviour affection hormones? 

    Testosterone concentration in terms of anticipation, example, anticipation for a football match. 

  • What are the classes of evidence for determining hormone-behavior interactions?

    1. A hormonally dependent behaviorr shoeld dissapeur when the source of the hormone is removed or the actions of the hormone are blocked.
    2. After the behaviorr stops, restoration of the missing hormonal source or its hormone should reinstate the absent behaviour.
    3. Finally, hormone concentrations and the behavior in question should be covariant; that is, the behavior should be observed only when hormone concentrations are relatively high and never or rarely observed when hormone concentrations are low. 

  • 2 The endocrine system

  • Name the ways of endocrine communication

    Intacrine, autocrine, paracrine, endocrine, ectocrine and neuro-endocrine. 

  • What do the PVN and SON produce?

    Vasopressin and oxytocin

  • Where is somatostatin made?

    In the hypothalamus and pancreas

  • What do T3/T4 do?

    In mammals:  increase metabolism, heat production and general permissive actions. In amphibians and reptiles: it has a role in metamorphics and skin shedding. 

  • What is biological half-life?

    The amount of time required to remove half of a hormone or other substance from the blood 

  • Protein/peptide hormones.
    TRH, GnRH, GHRH, CRH, MRH, somatostatin, P, GnIH, hypocretin, kisspeptin, POMC, prolactin, GH, LH, FSH, TSH, ACTH, MSH, oxytocin, vasopressin/ADH, PTH, calcitonin, secretin, cholecystokinin (CCK), ghrelin, leptin, adiponectin, insulin, glucagon, MIH, inhibin, activin, follistatin, relaxin, (h)CG, CS (=placental lactogen). 

  • Where is cholesterol a precursor for?

    All steroid hormones

  • Steroid hormones.
    Pregnelonolone, progesterone, corticosterone/cortisol (glucocorticoids), aldosterone (mineralcorticoid), testosterone/androstenedione/DHT (androgens), estradiol (estrogens), neurosteroids. 

  • What are lipid-based hormones?

    Prostoglandines

  • 3 Sex differences in behavior: sex determination and differentation

  • Why is there sexual reproduction?

    Because asexual reproduction might be costly

  • Name the costs of sexual reproduction

    - Costs of meiosis (sacrifying half the genotype)
    - Costs of recombination (risk of unsuccsessfull genotypes)

    - Costs of producing males
    - Costs of mating, finding mates and fighting for mates

  • Name the benefits of sexual reproduction

    - Genetic hypothesis
    - Ecological hypothesis
    - Red queen hypothesis

  • What is intrasexual selection?

    Male vs. male

  • What is intersexual selection

    Male vs. female

  • What is the female reproductive strategy?

    Invest in rearing offspring (parental care)

  • What is the male reproductive strategy?

    Invest in maximizing the number of offspring

  • There are small sex differences in monogamous species, but big sex difference in polygenous mating. 

  • What is in reptiles and amphibians a determining factor for sex?

    Temperature

  • What is protogynous?

    From female to male

  • What is protoandrous?

    From male to female

  • What are the most important testis cell types?

    - Germ cells
    - Leydig cells
    - Sertoli cells

  • What is spermatogenesis?

    The development of sperm.

  • What are the steps of spermatogenesis?

    Spermatogenium - spermatocytes - spermatids

  • What do Leydig cells do?

    Produce androgens

  • What do Sertoli cells do?

    Produce inhibin and estradiol

  • What does testosterone do in the brain?

    Masculinization and defeminization

  • What is ACTH?

    Adrenocoricotropic hormone, stimulates synthesis and release of glucocorticoids.

  • What is avian sexual differentation?

    Males: ZZ
    Females: WZ
    Opposite of mammals. 

  • What does the presence of the srY gene do?

    In presence of the srY gene, testes develop. In absence, ovaries develop. 

  • What develops in male in the presence of testosteron?

    Wolffian ducts (male reproductive structures)

  • What develops in females in the absence of MIS?

    Müllerian ducts (female reproductive structures)

  • What hormonal effect has the growing of antral follicels?

    Increase of E2. (And LH + FSH)

  • What hormonal effect has the presence of a corpus luteum?

    High P levels (low LH + FSH)

  • What is the Fisher runaway effect?

    Fisherian runaway is an explanation for sexually dimorphic secondary traits that do not play a role in intra-sexual selection. Fisher's explanation is that selection of such traits is a result of sexual preference; that members of the opposite sex find a trait desirable. This preference makes the trait advantageous, which in turn makes having a preference for the trait advantageous.[3] The process is termed "runaway", because over time, it would facilitate the development of greater preference and more pronounced traits, until the costs of producing the trait balance the reproductive benefit of possessing it. An example is the peacock's tail. 

  • What are freemartins?

    A freemartin is a sterile female twin found in cattle, sheep, goats and pigs. The theory behind freemartism is that anrogens produced by the male fetus are able to reach the female due to fusion of some of the placental blood vessels that supply the twins. 

  • What is Turner syndrome?

    A congenital absence of one of the X chromosomes (XO)

  • What is CAIS/PAIS?

    Complete or partial androgen insensitivy syndrome. XY individuals develop secondary sexual charesteristics the feminine way. 

  • What is 5a-reductase deficiency?

    Resulst in incomplete genetical masculinization at birth. Usually these individuals are sexed as girls at birth. 

    Sometimes they change gender in puberty. 

  • Fish.
    Simultaneous hermaphrodites possess ovotestes that produces both eggs and sperm, and they alter between two behavioral roles in providing eggs or sperm during spawning.
    There are two types of sequential hermaphrodites: animals that begin live as one sex, than change in another sex in response to social, environmental or genotypic factors. Protogynous and androgynous. 

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What are the four interacting levels of analysis?

causation

development

evolution

adaptive function

why does the organizational. activational hypothesis fall short in explaining the sexual differentiation of zebra finches?

1. effective masculinizing dosis of estradiol are high, often toxic, and some females are not masculinized even by high dosis. 2. males castratareed as hatchlings sing normally, 3. the song control nuclei have few estrogen receptors during early development. 4. the sex differences in neuron size and number in the HVC present by posthatching day 9, despite the lack of estrogen receptors at that age. 5. treatment of hatchling males with antiestrogens, antiandrogens, or aromatase inhibitors fail to demasculinize the song system or singing behvior. 6. females hatched from eggs injected with fadrozole, and aromatase inhibitor, have testes or ovotestes by still possess female-typical song systems and no singing behavior. 

What does treatment with estrodiol in early life result in?

increases sensitivity to androgens in adulthood

How can you make female finches sing?

post hatching treat them with estrodiol, then  treat them with either testosterone or DHT in adulthood. 

What are the two main sex differences in the brain?

the connectivity pattern of dendrites (MPOA) and the size of the SDN. 

What happens when the SDN-POA is lesioned?

Nothing. 

Why has the POA received special attention?

The preoptic area has a prominent role in the mediation of male mating behaviour. In rats the POA can be 5 to 7 times the size of the POA in females, this region of the POA is called the SDN-POA (sexually dimorphic nucleus)

Does maternal stress affect adult reproductive behaviour of offspring?

Yes, male fetuses produce less androgen.. More like females.. 

What do male and female ARKO mice show (androgen knockout)

Male: reductions in male-typical aggression and reproductive behaviours. 

Female: Normal 

What happens to male a + b knockout mice? (abERKO)

fail to express any sexual behaviours.