Week 3 Flashcards

1
Q

How is a dominant follicle selected in the human menstrual cycle?

A

FSH causes follicles to start growing. Their granulose cells will start producing estrogen. Estrogen provides negative feedback to the HT-PT (binding to alpha receptors) which decreases its GnRH and FSH production. The maturing follicles now compete for the decreasing FSH, but there’s not enough, so only one follicle (the biggest, most receptors, etc.) ends up getting enough to finish maturing. The others atrophy. This is called the follicular phase.

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2
Q

What causes the LH surge and ovulation?

A

At one point, the mature dominant follicle is producing so much estrogen that it finally binds to enough BETA receptors (low affinity) in the HT, which secretes GnRH then causes the release of large amounts of LH. The LH surge causes the follicle to burst, releasing the egg.

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3
Q

What is the importance of the corpus luteum?

A

It secretes progesterone and a little estrogen. Progesterone makes the endometrial lining thicken, estrogen changes the cervical mucus. These are to facilitate implantation and support of a fertilized egg. Now that there is less estrogen, it is only binding to alpha receptors which inhibit GnRH and FSH&LH.

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4
Q

If fertilization doesn’t occur, what happens?

A

The corpus luteum eventually atrophies, so now there is no more estrogen and progesterone. The endometrial lining sheds, and there is a lack of negative feedback on the HT-PT. SO they start producing GnRH and FSH-LH, and the FSH makes new follicles start to develop.

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5
Q

What does Dr. P say is a probable cause for the experience of PMS symptoms by many women when they believe they are in the right time frame for PMS?

A

Conditioning and expectations.

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6
Q

What is a probable cause for variations in PMS symptoms between women?

A

Not necessarily differences in hormone levels, more important is women’s sensitivity to hormones (thru # of receptors or distribution).

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7
Q

Why are women born with so many oocytes?

A

Because so many of them atrophy due to random crap like effects from the environment, dysfunction, etc. Also a bunch of them atrophy each month during selection of a dominant follicle.

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8
Q

What is the role of hCG (human chorionic gonadotropin)

A

It maintains the corpus luteum so that progesterone continues to be secreted until the placenta can take over secreting it, which maintains the endometrial lining and prevents shedding.

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9
Q

What are 3 ways of artificially preventing ovulation?

A
  1. A GnRH antagonist
  2. Blocking estrogen-BETA receptors (preventing LH surge)
  3. Providing constant medium levels of estrogen to bind to the estrogen-ALPHA receptors and provide negative feedback (no FSH means no follicles even mature)
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10
Q

What is the current scientific opinion on the causes of gender dysphoria?

A

Exact causes haven’t been able to be established, probably means its due to an interaction of many things (biological predispositions, environmental factors)

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11
Q

Contrast the extreme treatment for gender dysphoria to the light treatment.

A

Extreme treatment: Gender reassignment (surgery, hormones)
Light treatment: Therapy to come to terms with and live in harmony with one’s discrepancy between gender identity and sex

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12
Q

Although effect sizes are quite small, why do the observed gender discrepancies in behaviors make sense?

A

Behavior proficiencies seem to match evolutionary gender roles. Ex. Women took care of the children and provided their education, also organized the households and social relations so it makes sense that they have better verbal ability. Men hunted and provided material resources so it makes sense that they are more aggressive and have better spatial ability.

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13
Q

How do dopamine and testosterone affect sexual behavior?

A

Dopamine seems to be related to sexual activity - animals who have high levels of dopamine (reward center activity) seem to engage in more sexual behavior even without testosterone. Maybe female presence triggers their reward seeking more.
Testosterone seems to facilitate sexual behavior but when actual testosterone levels are controlled, there is still individual variation (must be more going on).

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14
Q

Sexual behavior has an effect on both neurogenesis and corticosterone. What is this effect?

A

Sexual behavior increases corticosterone levels (this is interesting because it shows that pleasurable activity also activates HPA). At the same time, there is increased neurogenesis in the dentate gyrus (HC). Corticosterone levels eventually stop increasing after mating (habituation), but neurogenesis continues. This shows that neurogenesis mustn’t be related to the corticosterone, it must be something else inducing it.

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15
Q

Why does it make sense that female behaviors change (in 3 specific categories) in the late follicular phase?

A

Behaviors change in a way that increases attractivity, proceptivity, and receptivity. This leads to increased chance of mating, at a time when the female is most fertile. This makes sense because it increases the chances of conception.

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16
Q

What claims were made in the breast asymmetry/ovulation study? Why are they sketchy?

A

It was claimed that breast asymmetry varies thru the cycle, but then upon ovulation the breast asymmetry is massively reduced, and that this serves as an indication of fertility.
This is sketchy because 1. is it even noticeable? probably not. 2. the asymmetry could easily be a result of other factors like water retention etc.

17
Q

Explain the results of the TSST study that manipulated panel sex. Why are these results super important?

A

They showed that fertile subjects (males and follicular females) virtually only had HPA responses to a panel of the opposite sex. Infertile women (in the luteal phase) basically didn’t have much of a response at all, and definitely no difference between panel sexes.
This is very important because it suggests something about what EXACTLY the TSST is triggering - it’s not only about general social humiliation, there’s something to do with potential sexual mates. It also means that the menstrual phase of women subjects needs to be controlled for.

18
Q

What’s the difference between attractive and proceptive behavior according to Beach?

A

Attractive behavior doesn’t have to be in presence of a male stimuli. Proceptive behavior is specifically addressed towards a male stimuli. (Ex. increasing ornamentation vs. increasing physical contact with a male). There is crossover in these categories because some behaviors can be performed in both conditions.

19
Q

When are receptive behaviors performed by females?

A

During actual copulation. (lordosis etc.)

20
Q

What study did Dr. P’s lab do that really supported the idea that there is something about sexuality involved in TSST responses?

A

They did the study manipulating panel sex and studied homosexual participants, and they had the OPPOSITE reaction! (i.e. they had a larger HPA response to the panel of the same sex)