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PSYC381 > Midterm > Flashcards

Midterm Flashcards

1
Q

what was the medieval view of BNE?

A

behaviour stemmed from 4 bodily factors (humours)
- phlegm: sluggishness
- blood: hot-blooded
- yellow bile: aggressive nervousness
- black bile

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2
Q

what was Berthold’s experiment? what was it based off of?

A

1st BE experiment based on pangenesis:
- bits and pieces of various organs secreted into the blood
- bits and pieces assembled into tiny humans in the gonads

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3
Q

what important ideas did the idea of pangenesis predispose Berthold to?

A
  • various bodily sites release agents into the blood
  • agents travel through blood to particular targets
  • testes (gonads) are important part of the process
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4
Q

what happened to Group 1 of Berthold’s experiment?

A

castrated (removed both testes) -> developed as capons
- never fought with other males, failed to crow, avoiding females, failed to exhibit mating behaviour, different physical appearance

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5
Q

what happened to Group 2 of Berthold’s experiment?

A

castrated + reimplanted 1 testis from each bird into abdominal cavity -> normal male development
- normal appearance and behaviour (crows, engaged in battle w/ others, usual reactions to hens)

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6
Q

what happened to Group 3 of Berthold’s experiment?

A

castrated + reimplanted 1 testis from each bird into the other’s abdominal cavity -> normal male development

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7
Q

what were the conclusions of Berthold’s experiment?

A
  • testes are transplantable organs
  • transplanted testes can function and produce sperm
  • b/c testes functioned normally after all nerves severed, no specific nerves directing testicular function
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8
Q

what was the important of Berthold’s experiment? what did it cause him to propose?

A

demonstrated that a substance produced by the testes could travel through the bloodstream and eventually effect behaviour
- a product of the testes was necessary for a cockerel to develop into a normal adult rooster
- proposed a secretory blood-borne product of transplanted testes was responsible for normal development of groups 2+3

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9
Q

compare and contrast hormonal signaling and neurotransmission

A

both are chemical in nature
- where does it occur/where are they synthesized
- distance
- graded vs all-or-none
- duration
- mediates what
- voluntary?

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10
Q

what is an example of hormones affecting behaviour?

A

if testes of adult male zebra finches are removed, then the birds reduce singing
- castrated finches can resume singing if the testes are reimplanted or if the birds are provided with testosterone or estradiol (type of estrogen)

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11
Q

what accounts for the reduced singing in adult male zebra finches? when is singing behaviour most frequent?

A

some testosterone from testes converted into estrogens -> lack of estrogens account for reduced singing
- singing behaviour is most frequent when blood estrogen concentrations are high

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12
Q

how can behaviour of adult male zebra finches influence hormones?

A

when seeing a territorial intruder, it may elevate blood testosterone concentrations in the resident male and thereby stimulate singing or fighting behaviour

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13
Q

how can behaviour of mice influence hormones?

A

male mice that lose a fight show reduced circulating testosterone concentrations for several days or weeks afterwards
- similar results in humans

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14
Q

how can behaviour of humans influence hormones?

A

the experience of watching a World Cup soccer final elevated testosterone and cortisol in males when compared with a control day

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15
Q

what is the precursor to all steroids?

A

pregnenalone

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16
Q

what is ectocrine mediation?

A

substances such as pheromones are released into the environment by individuals to communicate with others

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17
Q

what are allomones?

A

pheromone-like compound secreted to the external environment but the target is a different species
ex) bolas spider releases sex pheromone that attracts female moths as prey

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18
Q

what is the hypothalamus? what is unique about it?

A

main structure through which the brain exerts control over the endocrine system
- BBB diminished here, so it is sensitive to numerous blood-borne substances

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19
Q

what are the preoptic area (POA) and ventromedial hypothalamus (VMH) responsible for?

A

sexual behaviour
- sensitive to gonadal hormones

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20
Q

what is the supraoptic nucleus (SON) responsible for?

A

thirst and drinking behaviour

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21
Q

what are the paraventricular nucleus (PVN) and arcuate responsible for?

A

eating, appetite regulation, etc.

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22
Q

what are the ten hypothalamic nuclei?

A
  • paraventricular (PVN)
  • preoptic (POA)
  • anterior
  • supraoptic (SON)
  • suprachiasmatic (SCN) (biological rhythms)
  • arcuate
  • mammillary body (memory)
  • ventromedial
  • posterior
  • dorsomedial
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23
Q

what is a characteristic of the posterior pituitary? why is this important?

A

richly vascular
1) neurosecretory cells secrete oxytocin and vasopressin directly into vessels of posterior pituitary, circulating them throughout the body
2) other hypothalamic cells secrete releasing hormones in the hypophyseal portal system (circulates from median eminence to anterior pituitary)
- stimulates release of corresponding hormones

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24
Q

what is an example of how the posterior pituitary works?

A

neurosecretory cells in PVN and SON
- oxytocin and vasopressin are transported down the axons of magnocellular neurons of the SON and PVN, reaching capillaries of the posterior lobe (via Herring bodies - axon terminals that release hormones into capillaries)

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25
Q

what are some functions of oxytocin?

A
  • milk letdown reflex
  • uterus (increases contractility, induces labour)
  • orgasms (wave of contracility)
  • learning
  • love
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26
Q

what are some functions of vasopressin (ADH)?

A
  • water level (retention of water + regulating BP)
  • affiliation
  • social behaviour
  • monogamy (ex. adding ADH receptors to polygamous voles make them monogamous)
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27
Q

what is an example of how the anterior pituitary works?

A

neurosecretory cells of the hypothalamus secrete releasing hormones into the hypophyseal portal system where they gain access to the anterior lobe of the pituitary
- releasing hormones stimulate secretory cells to release corresponding hormones into circulation

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28
Q

what are some examples of releasing factors?

A
  • gonadotropin releasing/inhibiting hormone (GnRH/GnIH)
  • corticotropin releasing hormone (CRH)
  • thyroid releasing hormone (TRH)
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29
Q

what are some examples of anterior pituitary hormones?

A
  • growth hormone (GH)
  • adrenocorticotropic hormone (ACTH)
  • LH, FSH (gonadotropins)
  • thyroid stimulating hormone (TSH)
  • prolactin
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30
Q

what hormones does the adrenal cortex produce/secrete?

A
  • glucocorticoids (cortisol)
  • mineralocorticoids (aldosterone)
  • androgens (androstenedione - contributes to secondary sex characteristics)
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31
Q

what 2 major cell types are present in the testes?

A
  • Sertoli cells (produce sperm, under control of FSH)
  • Leydig cells (produce testosterone under control of luteinizing hormone (LH))
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32
Q

what specialized structures in the ovaries secrete the 2 major types of ovarian steroids?

A
  • follicles (each contains a maturing ovum, secrete estrogens (most potent = estradiol))
  • corpus luteum (follicles that have ruptured and released ova, secrete progestins (most important = progesterone))
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33
Q

what do estrogens do? what do progestins do?

A
  • estrogens govern female body characteristics (secondary sex characteristics) and sexual behaviour by acting on the brain
  • progestins prepare uterus for implantation of an embryo
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34
Q

what are the 5 types of steroid hormones?

A

all derived from cholesterol, fat soluble, must have carrier proteins in order to circulate
- gonadal: progestins, estrogens, androgens
- adrenal: glucocorticoids, mineralcorticoids

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35
Q

what are examples of progestins, estrogens, and androgens?

A
  • progestine: pregnenolone - precursor to all other steroids
  • estrogens: 17β-estradiol (E2) (female sexual behaviour, masculinization of brain structures and behaviours)
  • androgens: testosterone (masculine sex characteristics, male sexual behaviour, spermatogenesis, aggression)
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36
Q

what are examples of glucocorticoids and mineralocorticoids?

A
  • glucocorticoid: cortisol (preparation of action; stress, arousal)
  • mineralocorticoid: aldosterone (maintains sodium balance)
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37
Q

how are estrogens made?

A

testosterone derived from progesterone (which is derived from pregnenolone)
- testosterone can aromatize to 17β-estradiol via aromatase
- testosterone can reduce into dihydrotestosterone (DHT) via 5α-reductase

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38
Q

how do steroid receptors work?

A

once bound with steroid ligand (in cytoplasm or bound to nucleus), hormone-receptor complex binds to DNA and alters gene transcription
- SLOW (hrs to days)

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39
Q

what are peptide (protein) hormones? what are some examples?

A

chain of amino acids released via exocytosis
- gonadotropins (LH, FSH)
- insulin/glucagon

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40
Q

what are amine hormones?

A

modifications of single amino acid molecules
- epinephrine/norepinephrine
- DA

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41
Q

what is simple positive feedback?

A

the endocrine gland produces hormone to the target and produces a product, which further excites the endocrine gland to accelerate hormone release -> accelerates the hormonal response
- feedback drives hormone concentrations away from homeostasis

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42
Q

what is simple negative feedback?

A

the endocrine gland produces hormone to the target and produces a product, which in turn inhibits the endocrine gland to decrease hormone release -> inhibits the hormonal response
- feedback drives hormone concentrations back to homeostasis

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43
Q

what is complex negative feedback? what is an example?

A

involves multiple negative pathways to inhibit a process
ex) in response to certain external/endogenous stimuli, the hypothalamus released GnRH, which stimulates the anterior pituitary to release gonadotropins such as LH -> secreted LH stimulates steroid synthesis (testosterone) and secretion in the testes

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44
Q

what are the negative feedback pathways associated with the complex negative feedback example?

A
  • testosterone acts on target tissues + feedback to inhibit activity in anterior pituitary and hypothalamus
  • increasing levels of gonadotropin (LH) slow down its secretion from the anterior pituitary and GnRH secretion from the hypothalamus
  • as GnRH is secreted, the hypothalamus responds to increasing levels of the hormone by slowing down its secretion
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45
Q

when is male chromosomal sex determined?

A

at fertilization by sperm bearing either a Y chromosome
- causes a thickened ridge of tissue on each protokidney to develop into a testis (otherwise into an ovary)

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46
Q

what determines if a testis is developed?

A

sex determining region of the Y chromosome (SRY) gene -> first step to developing as male
- if mutated, will express as a woman with XY chromosomes (gonads do not produce sex steroids, secondary sex characteristics absent without treatment)
- expresses testis determining factor (TDF)

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47
Q

what does TDF do?

A

promotes SOX9 expression on chromosome 17
- TDF acts locally (b/c in some cases its possible for one gonad to develop into a testis and the other an ovary)

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48
Q

what happens when both the SRY and SOX9 genes are expressed?

A

the germinal ridge on the protokidney forms into a testis (otherwise develops into an ovary)
- embryonic testes produce androgens and peptide hormones that guide male development

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49
Q

how do the male accessory sex organs develop?

A

testosterone and Mullerian inhibitory hormone (MIH) released from testes allows the Wolffian duct system to develop into male accessory sex organs; Mullerian duct system regresses
- later develop seminal vesicles and vas deferens

50
Q

what are genital folds? how do they masculinize?

A

surround the urogenital sinus during embryo development
- develop into scrotal sac

51
Q

what is the genital tubercle? how does it masculinize?

A

in front where the ridges of the genital folds meet
- genital fusion occurs in the presence of DHT (produced from testosterone by 5α-reductase)
- in absence of androgens, develops into clitoris

52
Q

how does the gynandromorphic zebra finch tell us that differentiation in birds is not completely hormonal?

A

feminized on one side, masculinized on the other
- one circulatory system would cause hormones to be dispersed throughout body, not just one side
- due to expression of sex genes on one side vs the other

53
Q

what are the major characteristics of sex differentiation in mammals?

A
  • males are heterogametic (XY) and females are homogametic (XX) -> females are default sex
  • testosterone required to masculinize
  • presence of SRY gene
  • genes and steroids crucial
  • sex stays constant throughout life
  • dimorphic
54
Q

what are the major characteristics of sex differentiation in birds?

A
  • males are homogametic (ZZ) and females are heterogametic (ZW) -> males are default sex (develop in absent of gonad hormones)
  • estrogens required for masculinizing of birdsong
  • no sex-determining genes (ex. SRY) but presence of W chromosome causes estrogen secretion
55
Q

what are the major characteristics of sex differentiation in reptiles?

A
  • instead of genes and steroids, environment is crucial (temperature-dependent)
  • can be hermaphrodites, allowing sex to change throughout lifetime
  • male polymorphism (some males mimic females to avoid competition with other males, some are territorial)
56
Q

what are the types of hermaphrodites in reptiles?

A
  • simultaneous: possess ovotestes
  • sequential: begin life as one sex, change to another sex in response to environmental changes
57
Q

what is responsible for the masculinizing effects on the brain?

A

testosterone converting into estradiol via aromatase
- androgen receptors are activated by testosterone, which is then converted into estradiol

58
Q

what prevents neural masculinization of females?

A

estrogens (but not androgens) produced by mother become bound to α-fetoprotein, preventing BBB bypass

59
Q

what is evidence of estrogens having organizational function?

A
  • αERKO animals still display normal mount behaviour but reduced intromissions and ejaculations
  • less aggressive than wild type; still have ERβ (motivated to mate due to ERβ but less successful)
  • αβERKO animals fail to display any components of sexual behaviour (most estrogen receptors absent)
60
Q

what is evidence of androgens having activational function?

A
  • androgen receptor knockout animals (ARKO) show reduced male-typical reproductive and aggressive behaviours
  • DHT can restore aggressive behaviours (therefore aggression is not solely coming from ARs), but not reproductive behaviour
  • animals lacking the AR only in the NS will develop genitals normally, but still show impaired sexual/aggressive behaviour
61
Q

how is the medial preoptic area (mPOA) different between sexes in hamsters?

A

7x larger male nucleus in mPOA, termed the sexually dimorphic nucleus of the preoptic area (SDN-POA)

62
Q

what structure is known as the extended amygdala? what are the sex differences?

A

bed nucleus of the stria terminalis (BNST)
- larger in males by 20%

63
Q

what circuit regulates aggression and reproduction?

A
  • anteroventral pariventricular nucleus (AVPV; which regulates ovulation and projects to the arcuate nucleus, larger in females)
  • SDN-POA
  • BNST
64
Q

what are characteristics of the SCN?

A
  • larger in homosexual men
  • contains steroid receptors
  • in rats, lesions do not change male sexual behaviour
65
Q

what hormonal/neurotransmitter correlates are present with aggression?

A
  • low 5-HT
  • high T
  • high cortisol
66
Q

what has been linked to sexual dimorphic behaviour in birds?

A

steroid exposure and size of brain structures
- males usually sing more in most species

67
Q

what are the 2 major neural circuits involved in song in songbirds?

A

efferent motor pathway (actually express the song)
- controls neural output to the syrinx (vocal organ of birds)
anterior forebrain pathway (responds to environment (when/how much to sing, etc.), uses feedback)
- recursive loop: runs from the HVC (high vocal centre) to the RA (archistriatum) via area X, dorsolateral thalamus, anterior neostriatum

68
Q

what are the sex differences present in zebra finches?

A

HVC and RA in male zebra finches are 3-6x larger than females, who do not display a recognizable area X

69
Q

what does castration do to male zebra finches? what does this mean?

A

reduces song, but not song brain areas (HVC, RA)
- activational effects are insufficient to account for song, organizational effects required as well

70
Q

how do we know that organization effects are required for bird song?

A
  • females treated with DHT after hatching showed male-typical song brain areas, but did not sing
  • estradiol treatment post-hatching and adult T/DHT treatment: they sing!
71
Q

what are some sexually dimorphic behaviours that can be attributed to organizational effects of hormones?

A
  • girls with CAH
  • vasopressin projection
  • arginine vasotocin (AVT)
  • males initiating play
  • homosexual rams
72
Q

how are girls with congenital adrenal hyperplasia attributed to organizational effects of hormones?

A

girls with CAH prefer male-typical toys
- many of these behaviours influenced by hormones exposure (seen in castration and androgen treatment studies)

73
Q

how is vasopressin projection attributed to organizational effects of hormones?

A

sexually dimorphic in vertebrates
- 2-3x more ADH cells in BNST and mAMY in males
- ADH injected into ventricles inhibits lordosis in female rats

74
Q

how is arginine vasotocin (AVT) attributed to organizational effects of hormones?

A

molecular precursor to ADH in mammals; modulates sexually dimorphic behaviour in bullfrogs
- only males produce it and females move towards mate call

75
Q

how is males initiating play attributed to organizational effects of hormones?

A

males initiate play more than females, have higher rates of pursuit play (regardless of species)
- female young of pregnant monkeys given androgens have masculinized genitalia, male young still engage in more threat and rough-and-tumble play
- Castration did not decrease this play, so it’s not activational effects
- CAH has the same effect
- synthetic progestin MPA injected prenatally feminizes girls but has androgenic effects, increasing high energy and aggressive play

76
Q

how are homosexual rams attributed to organizational effects of hormones?

A

show female pattern of amygdala estrogen binding, lower aromatase levels in the POA, and lower testosterone levels

77
Q

how do hormones contribute to sex differences in pain?

A

men exhibit larger opioid system activation in the anterior thalamus, ventral basal ganglia, and amygdala
- causes lower thresholds for pain (temp/pressure) for women (varies over menstrual cycle) and higher for men
- chest pain differences

78
Q

how do hormones contribute to sex differences in olfaction?

A
  • before puberty, girls are better at detecting certain odors than boys (women are 1000x more sensitive to musk-like odors than men, beginning at puberty and is a function of estrogen levels)
  • menstruating women show reduced sensitivity compared to other cycle phases, and oral contraceptive (progesterone) users are relatively insensitive to male odors that cue attraction/repulsion
79
Q

how do hormones contribute to sex differences in audition?

A
  • women are more sensitive to sound than men, with lower thresholds for sounds at all frequencies (especially high)
  • tolerance for high amplitude sounds is lower in females than males at any age -> organization effects of sex steroids
  • infant girls more easily classically conditioned to auditory reinforces than infant boys
80
Q

how does affect display sex differences?

A
  • sexes have a face preference for the corresponding sex
  • when asking a child to draw, females draw more stereotypical female things (flowers, butterflies, etc.)
  • when eye-tracking is used while subjects view emotional faces, females are consistently faster and look more frequently at eyes
81
Q

how do hormones contribute to sex differences in cognition?

A
  • males perform better at map reading and directional tasks, including solving mazes (due hormonal effects on hpc) -> testosterone treated women perform better
  • female advantage for verbal, perceptual, fine motor skills, calculation
  • male advantage for quantification, spatial/mathematical reasoning
82
Q

how does connectivity vary between the sexes?

A

males have a higher degree of modularity compared to females, who have more integration
- increased intrahemispheric connectivity in males; increase interhemispheric connectivity in females

ex) rhyming tasks involve only the left hemisphere activity for males, while for females both right and left hemispheres contribute

83
Q

how is male sex behaviour in rats different than primates?

A

more directly contingent on androgens
- primates influenced by social learning

84
Q

how does castration affect rodents and primates?

A

leads to a decline in sexual motivation
- the timing of loss is contingent on previous sexual experience; castrating a juvenile vs an adult (has sex had the opportunity to reinforce their reinforcement circuitry?)
- lose number and frequency of intromissions first, then gradually lose ability to ejaculate, then lose interest entirely

85
Q

what are the 3 consummatory components of mating behaviour in rats?

A

1) mounting
2) intromission
3) ejaculation
- post-ejaculation interval includes absolute and relative refractory periods

86
Q

what are some genetic knockout studies that have helped us understand male sexual behaviour?

A
  • ERKO mice (α and β)
  • αERKO mice
  • βERKO mice
  • aromatase KO mice
87
Q

what do α and β ERKO mice exhibit?

A

display no sexual activity at all; neither appetitive (inclination/motivation towards sex) nor consummatory (act of sex)

88
Q

what do αERKO mice exhibit? what do βERKO mice exhibit?

A
  • αERKO mice show subtle sexual differences (mainly reduced ejaculation) -> led to the discovery of ERβ isoform of estrogen receptor
  • βERKO mice are completely intact sexually
89
Q

what do aromatase KO mice exhibit?

A

similar to αERKO, have reduced sexual response (estrogens derived from testosterone gone, but some local estrogen production is sufficient)
- suggests that ERα is sufficient for organizational effects

90
Q

why aren’t ARKO mice observed?

A

only 1 type of androgen receptor; knocking it out will change the development of mice (no longer have a penis, etc.)

91
Q

what effects do androgenic steroids have in castrated rats?

A

testosterone and androstenedione can restore sexual behaviour in castrated rats, but not DHT
- suggests aromatization underlies it

92
Q

how do testosterone and DHT work together to display male sexual behaviour?

A

testosterone aromatizes into estradiol, which affects CNS to promote mating behaviour (mediates copulatory behaviour), whereas DHT affects periphery to maintain tactile sensory feedback and regulate penile responses
- DHT maintains/restores penile responses to precastration levels (restores copulation displays, but not copulation itself)

93
Q

using birds as an example, how does DHT exert different effects on male sexual behaviour than other androgenic steroids?

A

most birds have highly ritualized, often complex courtship behaviours -> DHT restores these behaviours after castration, but does not restore copulation
- testosterone must be converted to estradiol in the MPOA before it produces an effect on copulation

94
Q

what are the neural correlates for sexual behaviour in male rats?

A
  • spinal cord
  • medial preoptic area (MPOA)
  • ventromedial hypothalamus (VMHvl)
  • chemosensory system
  • amygdala
95
Q

how is the spinal cord implicated in the sexual behaviour of male rats?

A

erections, intromission, and ejaculation are programmed in the spinal cord (can be fully elicited even after isolation from the brain)
- the brain inhibits these spinal reflexes (constantly telling body not to have an erection)

96
Q

how is the MPOA implicated in the sexual behaviour of male rats?

A

crucial for sensorimotor integration related to sex (electrical stimulation of this area accelerates ejaculation in rats)
- DA is released into the MPOA when sensing a receptive female; further increased during copulation itself
- testosterone (converted to estradiol) increases this release of DA, and the mesolimbic release of DA is inhibited after ejaculation (absolute refractory period)

97
Q

what is the feedback circuit involving the MPOA?

A

MPOA neurons project to the VTA – the mesolimbic DA source

98
Q

what occurs with POA lesions?

A

will eliminate sex behaviour but not motivation (won’t initiate but will still pursue/compete)

99
Q

how is the VMHvl implicated in the sexual behaviour of male rats?

A

contains the aggression locus, which is inhibited during mating
- when stimulated, increases attacks at females

100
Q

how is the chemosensory system implicated in the sexual behaviour of male rats? what is the main organ involved?

A

rats use chemosensory cues of estrus significantly more than humans
- olfactory bulb in rats is ~4% of their CNS; rats possess a vomeronasal organ (VNO) that detects pheromones (absent in humans)

101
Q

how is the VNO implicated in the sexual behaviour of male rats?

A
  • VNO projects to the accessory olfactory bulb, the removal of which eliminates all sexual behaviour in mice
  • VNO V1Rs and V2Rs are necessary for males to identify males vs females
102
Q

how is the amygdala implicated in the sexual behaviour of male rats? what do various lesions to the amygdala cause?

A

olfactory info travels directly here; 2 regions
1) basolateral amygdala: lesions reduce motivation
2) corticomedial amygdala: lesions reduce copulation
- info passed onto the MPOA via stria terminalis and amydalofugal pathway
- non-contact erections lost after amygdala lesions (require direct stimulation to penis)

103
Q

what are the 6 components of female reproduction?

A
  • courtship
  • mating
  • ovulation
  • pregnancy
  • parturition
  • lactation
104
Q

what is estrus? what is anestrus?

A
  • estrus: point in the female reproductive cycle characterized by high fertility and motivation
  • anestrus: other points in reproductive cycle in which fertility and motivation are lower
105
Q

what is the role of the POA in female sexual behaviour?

A
  • estrogen in the MPOA inhibits lordosis in females
  • MPOA contains dense expression of ERs and PRs
  • during proceptive behaviours (initiating copulation), MPO at 40% activation
  • during sex, MPO at 90% activation
106
Q

what are the distinct cytological stages that can be observed over the estrus cycle?

A
  • metestrus: development of a primary follicle from immature oocytes
  • diestrus: oocytes nourished by surrounding follicular cells, which produce estrogen
  • proestrus: several primary follicles divide to create a secondary oocyte
  • vaginal estrus: follicular rupture of secondary oocyte, releasing eggs
107
Q

what are the 2 conditions that would not cause the estrus cycle to restart?

A
  • pregnancy
  • pseudopregnancy (occurs following sufficient copulatory stimuli that does not result in conception) -> corpora lutea maintained for 14 days in rats
108
Q

what hormones are involved in the estrus cycle?

A
  • estrogen
  • luteinizing hormone (LH)
  • progesterone
109
Q

what happens to the remaining follicle cells after vaginal estrus?

A

form the corpus luteum, which produces estrogen and progesterone
- if pregnancy does not occur, corpus luteum degenerates

110
Q

how is estrogen related to the estrus cycle?

A

generic term originally used to refer “estrus-generating substances”, and came to encompass ligands for ERs

111
Q

how is luteinizing hormone (LH) related to the estrus cycle?

A

induces formation of the corpora lutea, thereby initiating a surge of progesterone after ovulation

112
Q

how is progesterone related to the estrus cycle?

A

prepares (and maintains) the uterus for pregnancy
- some species require a synergistic relationship between estrogen and progesterone to initiate behavioural estrus

113
Q

what regulates ovarian states?

A

hypothalamic-pituitary-gonadal (HPG) axis
- hypothalamus uses GnRH to signal anterior pituitary release of LH and follicle-stimulating hormone (FSH), which in turn signal the ovarian release of estrogens

114
Q

what does an ovariectomy do?

A

eliminates mating behaviour, and additionally suppresses the cycle (no more cyclic pattern)

115
Q

what are the ovarian phases?

A
  • follicular phase: prior to ovulation, involved in development and release of egg
  • ovulation: egg released from ovary
  • luteal phase: after ovulation, during which the corpora lutea are active and producing progesterone
116
Q

when does menstruation occur?

A

when estrogen and progesterone are at their lowest values

117
Q

what do type 1 reproductive cycles entail? what are the subtypes?

A

spontaneous ovulation and pseudopregnancy
- 1.1A: 2-5 weeks; copulation limited to periovulatory (follicular) period
- 1.1B: 2-5 weeks; copulation may occur throughout cycle
- 1.2: >5 weeks; copulation limited to periovulatory (follicular) period

118
Q

what type of reproductive cycle do humans have?

A

1.1B

119
Q

what do type 2 reproductive cycles entail? what are the subtypes?

A

induced ovulation (via copulation), but spontaneous pseudopregnancy
- 2.1: 3-5 weeks
- 2.2: >5 weeks

120
Q

what is the type 3 reproductive cycle?

A

spontaneous ovulation, but induced pseudopregnancy (due to sufficient copulatory stimuli)
- <1 week

PSYC381 (2 decks)

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