Summary An introduction to behavioral endocrinology

ISBN-10 0878936203 ISBN-13 9780878936205
804 Flashcards & Notes
43 Students
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This is the summary of the book "An introduction to behavioral endocrinology". The author(s) of the book is/are Randy J Nelson. The ISBN of the book is 9780878936205 or 0878936203. This summary is written by students who study efficient with the Study Tool of Study Smart With Chris.

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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.

  • 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
  • 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


  • 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.

  • 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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Example questions in this summary

What is Berthold's experiment and what is it's role in the "birth of endocrinology"?
What are Tinbergens four questions of analysis?
What is proximate causation and what is ultimate causation?
What classes of evidence determines hormone-behaviour interactions?
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