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Biol 405: Comparative Endocrinology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Berthold’s experiment

A

First evidence of hormones; reimplanted and transplanted testes developed vascular connections and generated sperm
Conclusions
1. Testes are transplantable organs
2. Transplanted testes can function and produce sperm
3. Because testes functioned normally after all nerves severed, no specific nerves direct testicular function —-> a “secretory blood-borne product’ of the transplanted tested was responsible for development of the roosters”

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2
Q

where are hormones made?

A

golgi apparatus of endocrine cells

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3
Q

approximately how far do hormones travel?

A

1mm to 2 m

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4
Q

hormones can only influence ______________

A

target cells that have receptors for that specific hormone

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5
Q

enough receptors must be present -__________________-

A

for a hormone to produce any effects

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6
Q

how do neurotransmitters work?

A

Influx of calcium ions in presynaptic neuron causes vesicles with NT to fuse with membrane and release NT into cleft to travel 20-30 nm to bind to receptors on postsynaptic neuron

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7
Q

Effector

A

output organs; any type of output can be considered a behavior

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8
Q

what are some examples of behavior that can be affected by hormones?

A

lack of movement, excretion of scents, changes in skin coloration, flashing lights of fireflies, production of electrical signals

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9
Q

evidence to determine hormone-behavior interactions

A
  1. Necessity- hormonal dependent behavior should disappear when the source of the hormone is removed or the actions of hormone are blocked
  2. Sufficiency- after the behavior stops, restoration of the missing hormonal source should reinstate the absent behavior
  3. [Hormone] and behavior should be covariant: behavior should mostly be observed when [hormone] are high and rarely observed when low
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10
Q

Recording electrical activity of neurons

A
  1. Single unit recording- very small electrodes placed near individual neurons to record changes in their electrical activity (ex: after/during exposure to hormones
  2. Activate neurons using electrical current to determine what happens when certain neurons are activated (non specific technique- stimulates all neurons near stimulation electrode)
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11
Q

optogenetics

A
  • can manipulate to see activity of specific nerves
  • use light to activate neurons in hormone circuits that have optogenetic constructs
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12
Q

when does calcium sensor fluoresce increase?

A

when a neuron is active (fires action potential)–> increased levels in calcium

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13
Q

intracrine vs autocrine mediation

A

intracrine: regulate intracellular events
autocrine: feed back to influence same cells that secreted them

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14
Q

paracrine vs endocrine vs ectocrine mediation

A

paracrine- cells secrete chemicals that affect adjacent cells
endocrine- cells secrete chemicals into bloodstream, where they travel to distant target cells
ectocrine- released into environment by individual to communicate with others (ex: pheromones)

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15
Q

what type of molecule does not require carrier proteins?

A

blood soluble

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16
Q

biological half-life

A
  • time required to remove half of a protein hormone from the blood via degradation (by peptidases) or excretion
  • Larger proteins typically have longer half-lives
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17
Q

Leptin case study

A
  1. Ob gene codes for leptin
  2. extremely small percentage of obese humans have leptin mutations; effects of leptin treatment on obesity are mixed
  3. Daily injection of leptin in a child with leptin gene mutation reduced his obesity
  4. Leptin injections reduce appetite and food intake of children with leptin gene mutation but immune system begins to produce antibodies against leptin, so higher doses are needed
  5. Leptin treatments are unsuccessful in reversing human obesity except in patients with leptin gene mutation
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18
Q

same peptide hormones can have ……..,……….., and ………..

A

autocrine, paracrine, and endocrine functions

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19
Q

Hormones vary in their amino acid sequence across

A

vertebrates

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20
Q

protein hormones from one group of animals may not …………….of another group of animas

A

activate the receptor

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21
Q

In mammals, foreign hormones only differ slightly but ………..

A

but can induce an immune response in humans

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22
Q

what is hypothalamus made up of and what do those things do?

A

nuclei (multiple neurons) that carry out integrative functions (reproduction, metabolism, biological rhythms)

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23
Q

what does hypothalamus secrete?

A

releasing and inhibiting hormones

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24
Q

hypothalamus: releasing hormones?

A

TRH, GnRH, MRH, CRH, GHRH

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25
Q

hypothalamus: inhibiting hormones

A

somatostatin (GHIH), GnIH, PIH (domaine), MIH (dopamine)

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26
Q

anterior pituitary

A
  • front part of pituitary gland that extends from the base of the brain
  • Secretes tropic hormones (hormones that cause the release of something else) in response to hormonal signals from the hypothalamus, a 2-step process
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27
Q

anterior pituitary hormones

A

GH, prolactin, LH, FSH, TSH, POMC, ACTH, MSH, B-endorphins and met-enkephalin

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28
Q

what does GH do?

A

stimulates somatic (body) growth

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29
Q

what does prolactin do?

A

promotes lactation (reproduction, growth and development, electrolyte balance, synergy with steroid hormones on target tissues)

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30
Q

what do LH and FSH do?

A

stimulate steroidogenesis in the gonads and the development and maturation of gametes

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31
Q

what does TSH do?

A

stimulate thyroid gland to release thyroid hormones

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32
Q

what can POMC turn into?

A

ACTH or MSH

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33
Q

what does ACTH do?

A

stimulates adrenal gland in response to CRH to produce glucocorticoids

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34
Q

what does MSH do?

A

regulates pigmentation in non-mammalian vertebrates; behavioral functions in mammals

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35
Q

what do B-endorphins and met-enkephalin do?

A

endogenous opioids that ameliorate pain sensations

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36
Q

posterior pituitary hormones route

A
  • neurohormones go to the posterior pituitary diffuse into blood capillaries
  • Whatever goes into hypothalamus goes into blood stream
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37
Q

posterior pituitary hormones

A
  1. oxytocin
  2. vasopressin
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38
Q

what is oxytocyn and what does it do?

A
  • neurohormone that influences reproductive function and social behavior in mammals
  • required for suckling reflex; causes cells of the mammary glands to contract, releasing milk
  • positive feedback loop
  • artificial oxytocin used to medically induce labor
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39
Q

what is vasopressin and what does it do?

A
  • antidiuretic hormone
  • acts on kidneys to retain water; increases blood pressure (pressor or hypertensive effects) during serious blood loss to slow blood flow
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40
Q

pancreatic hormones

A
  1. islets of Langerhans
  2. Insulin
  3. Glucagon
  4. Somatostatin
  5. Pancreatic polypeptide
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41
Q

Islets of Langerhans

A
  • endocrine tissue within the pancreas, makes up a, B, o, F cells
  • Dumps stuff into blood
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42
Q

Insulin

A
  • secreted by B cells
  • promotes energy storage in the liver as glycogen, reduces blood levels of glucose
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43
Q

Glucagon

A

secreted by a cells; stimulates the breakdown glycogen in the liver; increases blood levels of glucose

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44
Q

Somatostatin

A

secreted by delta cells; inhibits release of insulin and glucagon in pancreas

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45
Q

Pancreatic polypeptide

A

secreted by F cells; regulates exocrine pancreas enzyme (secretes)

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46
Q

steroid hormones qualities

A
  • fat-soluble: move easily through cell membranes but not through water –> interact with receptors inside the cell
  • form hormone-receptor complex that activates DNA sequences called hormone response elements to increase/ suppress gene transcription
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47
Q

C21 steroids

A
  1. progestins
  2. corticoids (glucocorticoids, mineralcorticoids)
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48
Q

progestins

A
  • “progestational” or pregnancy-maintaining effects
  • Obligate precursors of all other steroid hormones
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49
Q

what are corticoids secreted by>

A

secreted by adrenal cortices

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50
Q

what is released in response to stress (ACTH stimulation)?

A

glucocorticoids

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51
Q

what are the 2 types of glucocorticoids

A
  1. corticosterone: reptiles, birds, mice
  2. cortisol: humans, fish
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52
Q

what do mineralcorticoids do?

A

regulate ion exchange and water metabolism in kidneys (ex: aldosterone)

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53
Q

C19 steroids

A
  • androgens
  • testosterone
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54
Q

androgens

A
  • primary steroid hormone produced by the testes (made from progestins)
  • influence reproductive behavior and aggression
  • affect metabolism and can have bad side effects
55
Q

what is produced by Leydig cells and why?

A

Testosterone and androstenedione produced in response to gonadotropin release in anterior pituitary

56
Q

what does DHT bind more strongly to?

A

stronger: androgen receptors
than: testosterone/androstenedione

57
Q

C18 steroids

A

estrogens

58
Q

estrogens characteristics

A
  • made from testosterone
  • Initiate formulation of corpora lutea in ovaries and influence secondary sex characteristics
  • Affect water and calcium metabolism
  • Affect reproductive behavior and aggression
59
Q

what enzyme converts androgens into estrogens?

A

aromatase

60
Q

what are sex steroid hormones released from?

A

zona reticularis of adrenal cortex in small amounts

61
Q

males produce some ………… and ……… in ………….

A

some estrogen and progestins in testes

62
Q

females produce ………….. in ovaries

A

androgens

63
Q

both steroids produce in …………………. of both males and females

A

adrenal cortex

64
Q

what do androgens do in females?

A
  • bone development
  • increase insulin release
  • overian follicle growth
  • regulation of parturition (giving birth)
65
Q

what does estrogen do in males?

A
  • inhibits fat cell development
  • maintains healthy blood vessels
  • muscle and bone development
66
Q

where are steroid receptors located?

A

inside cells

67
Q

steroids are ……-soluble

A

lipid-soluble

68
Q

what happens once hormone-receptor complex is assembled?

A

moves into nucleus to regulate gene transcription

69
Q

steroid hormone receptors act as …………….. that ……….

A

act as transcription factors that promote or block gene transcription (mRNA production)

70
Q

where are protein and peptide hormone receptors?

A

embedded in cell membrane because proteins can’t diffuse through membrane

71
Q

what are the 3 domains of protein hormone receptors?

A
  1. extracellular domain that binds the hormone (ligand)
  2. transmembrane domain
  3. cytoplasmic domain
72
Q

receptors with intrinsic enzymatic activity have ……………….. that ………………….

A

cytoplasmic domain that phosphorylate intracellular proteins

73
Q

what are common receptors with intrinsic enzymatic activity?

A

tyrosine kinase, guanylate cyclase, tyrosine phosphatase, and serine/threonine kinase

74
Q

what are G-protein coupled receptors?

A
  • receptors coupled to G-proteins that activate second messengers through a signal transduction pathway
  • seconday messengers amplify the initial hormone signal
75
Q

what are the 3 main classes of GPCRs?

A

Gs: activates adenylate cyclase –> increases cAMP
Gi: inhibits adenylate cyclase –> decreases cAMP
Gq: activates phospholipase C –> increases intracellular calium

76
Q

embryos develop a …………….. on the developing kidney: …………….

A

develop a germinal ridge: a bipotential priomordial gonad

77
Q

what happens to the outer part of the germinal ridge if SRY is not present?

A

cortex becomes an ovary

78
Q

what do mice with XX and transgenic SRY develop?

A

develop testeshormonal secretion from the developing gonads (androgens in testes) -> determine male/female development

79
Q

Anlagen

A

primordial substance (2 exist for the development of accessory sex organs)

80
Q

accessory sex organs

A

connect gonads to the external environment

81
Q

Mullerian duct system

A
  • develops into female accessory sex organs: seminal vesicles, uterus, cervix)
  • default state
82
Q

what are the male accessory organs and what do their development require?

A
  • organs: seminal vesicles, vas derens
  • testosterone and MIH to produce testes
  • testosterone triggers development of Wolffian duct
  • MIH triggers regression of Mullerian duct
83
Q

what are the 2 dimensions that accessory sex organs develop accross?

A
  • feminization-defeminization
  • maculinization-demasculinization
84
Q

what are the 2 flaps of skin around the urogenital sinus called?

A

genital folds meet at genital tubercle

85
Q

unlike accessory sex organs, external ones develop along …………… based on …………..

A
  • a single masculine-feminine continuum
  • based on levels of DHT fetus is exposed to
86
Q

what do female gential folds turn into?

A

labia minora; genital tubercle –> clitoris

87
Q

what happens if female has high levels of androgens?

A

DHT conversion still occurs –> male genitalia

88
Q

what do male gential folds turn into?

A
  • scrotum; genital tubercle –> penis
  • in the presence of androgens
89
Q

what do males lacking 5a-reductase result in?

A

incomplete genital masculinzation

90
Q

hermaphrodite

A
  • had both ovaries and testes
  • true hermaphrodites are extremely rare
  • will never have female breasts and male genitalia - would have either female or ambigious genitalia
91
Q

intersex

A

humans born with ambigous genitalia and are affected by difference in (disorders of) sex development

92
Q

Turner Syndrome

A
  • individuals with X chromosomes (XO), female external appearance but overian development limited
  • require hormone treatment to induce puberty
  • X chromosome inactivation- halted in some cells in females (“double doses” of some X chromosme genes needed for normal ovarian development)
93
Q

since females are the “default sex”, neither……… nor ……….. are necessary for female development before puberty

A

neither ovaries nor hormones

94
Q

what is the most common reason for anomalous sexual differentiation in females?

A

prenatal exposure to sex steroid
exogenous- treatment of pregnant mother with steroid hormones to maintain the pregnancy (DES, MPA)
endogenous- androgens secreted from ovaries/adrenal gland

95
Q

congenital adrenal hyperplasia

A
  • overproduction of androgens by the adrenal glands due to lack of 21-hydroxylase
  • no sexual development problems in males, but results in moderate to severe masculinzation of genitalia in genetic females
96
Q

5a-reductase deficienty

A
  • results in incomplete genital masculinization
  • genetic males (XY) considered female at birth and reared as females
  • in puberty, testosterone can masculinize the body, leading to masculine secondary sex characteristics (masculature, body hair)
  • genitalia are partially masculinized by androgens during puberty
  • some ppl raised as females may take on a male gender identity at puberty
97
Q

sexual differentitation in birds: chromosomes and hormones

A
  • females are heterogametic: ZW
  • males are homogametic: ZZ
  • males are default sex for some behaviors (mounting, birdsong)
  • male-typical behavior develops in male embryo without any hormonal influence but lost in female ____ if exposed to estrogen
  • in the absence of gonad hormones, masculine sex development occurs
  • estrogen masculinizes males- female sex development only attained by hormone secretion
98
Q

sexual differentiation in birds: gonads

A
  • same thing but there is a left and right duct
  • avian embros have both Mullerian and Wolffian duct primordia
  • Mullerian duct regresses in male bird during development (begin to develop in birds to form the oviduct and shell gland)
  • only left duct fully develops in females
  • if embryotic birds are gonadectomized early in development both left and right millerian ducts persis
  • neither defeminization nor feminization occurs without sex hormones (requires estrogen)
99
Q

defeminization and feminization in birds

A

defeminization: regression of Mullerian duct in males
feminization: development of left mullerian duct in females

100
Q

what behaviors do male and female rodents exhibit?

A

female: lordosis (sexually receptive behavior)
male: mounting

101
Q

rodent behaviors are under control of……….. & example

A
  • gonadal steroids
  • castration stops mounting, testosterone restores
102
Q

does testosterone increase mounting in rodent females?

A

no

103
Q

does estrogen increase lordosis in male rodents?

A

no

104
Q

how are female rodents demasculinzed (but dont show mounting) and male rodents defeminized (but dont show lordosis) in development?

A

can remove behavior but not replace it because it is locked in

105
Q

organizational/activational hypothesis

A
  • sex differences in behavior rise from 2 processes
  • organizational- hormones early in development act to differentiate the nervous system in male/female direction
    reflect alterations in function- not structure - even females with genitalia that are not physically masculinized demonstrate behavioral masculinization and defemenization
  • activational- hormones act on these differentitated circuits later in life to drive behavior in sex-typical manner
106
Q

According to the organizational/activational hypothesis, during development, sex steroid hormones………
During adulthood, these same hormones ……………….

A
  • organize the components of the nervous system that will be needed for male or female typical behavior in adulthood
  • in adulthood, activate, modulate, or inhibit the function of these existing neural circuits
107
Q

According to the organizational/activational hypothesis, what are critical periods?

A
  • when an animal is maximally susceptible to the organizational effects of hormones
  • required for sex-specific behaviors
108
Q

what are sexually-dimorphic behaviors?
what are some examples of behaviors that are organized/activated?

A
  • behaviors with sex differences
  • mating, aggression, taste preferences, and parental behavior
109
Q

why arent all females masculinized?

A

masculinizing effects of testosterone on behavior depend on its aromatization to estrogen in the brain

110
Q

what were the effects of estrogen injections in newborn rats?

A
  • masculinzied later sexual behavior more effectively than injection of androgens
  • prenatal rats produce a-fetoprotein that binds circulation estrogens, causing them to be removed through the placenta and metabolized by their mother
  • androgens are not bound by a-fetoprotein, so androgens from developing males reach their braines and are aromatized to estrogens to masculinize behavior
  • cant reach the brain & dont all wire their circuit; androgens enter the brain and are aromatized (local production of estrogen in the brain); estrogen masculinites behavior only if it enters the brain
  • in males, testosterone enters the brain and turns into estrogen

KNOW THIS

111
Q

what controls pulsatile realease of LH in males and females?

A

GnRH release from VMH and accurate

112
Q

what controls LH surge in females alone?

A
  • GnRH release from preoptic area
  • requires connections from anteroventral periventricular nucleus (Kisspeptin) and suprahciasmatic nucleus (circadian signal)
113
Q

what causes ovulation?

A

massive LH release

114
Q

what feedback is used in sex steroid secretion in males and females?

A
  • negative feedback
  • increasing [sex steroid], feed back to gonads, anterior pituitary, and hypothalamus to slow secretion of GnRH, LH, and sex steroid
115
Q

why do females “escape” negative feedback of sex steroid secretion?

A

to allow for positive feedback, LH surge, and ovulation

116
Q

in male rats, POA have……………….

A

have more synapses on dendritic shafts and less on dendritic spines

117
Q

in female rats, POA have………………..

A

have more on dendritic spines and less on dendritic shafts

118
Q

what happened to male rats castrated on day 1 of life in terms of POA?

A

have female pattern of synapses

119
Q

what happened to female rates injected with androgens before day 4 of life in terms of POA?

A

have male patterns of synapses

120
Q

what collection of cell bodies in medial preoptic area is larger in males than females?

A

SDN-POA

121
Q

femeales treated early in life with androgens have …………..SDN-POA

A

larger

122
Q

castrated males have ………… SDN-POA

A

smaller

123
Q
  1. SDN-POA lesion in males
  2. SDN-POA lesions in females
  3. larger SDN-POA in males
A
  1. mostly normal mating behavior
  2. normal reproductive cycles
  3. may inhibit (instead of drive) female sexual behavior but inconclusive
124
Q

BNST and POA are higher in ……………. due to

A

higher in males due to sex differences in aromatase activity

125
Q

what type of receptors regulate aromatase activity?

A

androgen receptors

126
Q

no sex difference in aromatase in ……….

A

amygdala

126
Q

what does AVT (analog to vasopressin) modulate?

A
  • sexually dimorphic behavior in bullfrogs
  • males exhibit “calling” behavior to attract mates
127
Q

AVT injection increases calling behavior in

A

males but not females

128
Q

Sex differences in AVT receptor levels in POA

A

female < male

129
Q

which hormones modulate AVT receptor levels in amgdala in both males and females?

A

estrogens

130
Q

which hormones modulate AVT receptor levels in pretrigeminal nucleus of males, but NOT females?

A

both estrogens and androgens

131
Q

how does testosterone affect dog urinary behavior?

A

circuit organized by testosterone but not activated

132
Q

parts of brain involved in birdsong are much bigger in …… due to…..

A

larger in male zebra finches due to larger neuron size (from early development by estrogens and activated by androgens)

Biol 405: Comparative Endocrinology (5 decks)

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