Week 4

Question 1

What causes menopause?

Answer 1

Follicles/eggs have run out!

Question 2

Do GnRH and LH-FSH continue to follow their cycles after menopause?

Answer 2

NO because the phenomena that caused the cycling of the HT-PT hormones (with estrogen) has been terminated.

Question 3

Why do women have increased testosterone after menopause?

Answer 3

No estrogen to inhibit FSH/LH release, so FSH/LH are secreted at higher levels, which causes the adrenal cortex to secrete androgens.

Question 4

Estrogen and progestogen mainly provide negative feedback to two different brain structures, which to which?

Answer 4

Estrogen inhibits the anterior pituitary (reduces secretion of LH with alpha-receptors), whereas progestogen inhibits the hypothalamus (reduces GnRH which reduces both FSH & LH).

Question 5

What do very low dose progestogen-only oral contraceptives do?

Answer 5

DON’T inhibit ovulation, just thickens mucus.

Question 6

Which is linked more strongly to adverse health outcomes, early onset menopause or late onset?

Answer 6

Early onset.

Question 7

What were some problems with the Women’s Health Initiative HRT study?

Answer 7

• Women were administered equine & synthetic, constant dose hormones
• The experimental group at baseline had a higher risk of breast cancer

Question 8

What is a confidence interval and why is it important to look at?

Answer 8

There is 95% confidence (if p=0.05) that the true result is within this interval. Important because it shows how generalizable your data is.

Question 9

What is a hazard ratio?

Answer 9

How many times more likely to get the bad outcome.

Question 10

How is estrogen “neuroprotective” (two different pathways)? What brain area does this seem important for?

Answer 10

1. It may facilitate NMDA receptor activation by glutamate, inducing new excitatory synapses to develop in the hippocampus.
2. It also might suppress GABA function on CA1 (of the HC) neurons, disinhibiting them.
   Therefore overall it seems to encourage synapse formation and NMDA receptor upregulation.

Question 11

What is it about being female that seems to increase verbal ability? How do we know?

Answer 11

Higher estrogen levels seem to be the important thing. We know this because women in the follicular phase have better verbal ability than women who are menstruating.

Question 12

What have rat studies using T-mazes taught us about estrogen and learning?

Answer 12

Rats with higher levels of estrogen were more likely to use the “place” strategy of learning where a target is (objective) rather than the “response” strategy (relative to oneself). The place strategy is generally thought of as a more evolved/better quality learning strategy.

Question 13

Why would administering estrogen later in menopause not be good for cognitive faculties?

Answer 13

Because after things have already started to become dysfunctional, if you disinhibit neurons and increase glutamate binding to them, it can have an excitotoxic effect - the glutamate and excess activity will cause apoptosis.

Question 14

If activation of the HC is more related to the “place” learning strategy, what brain area is more related to the “response” strategy?

Answer 14

Caudate Nucleus

Question 15

What is the problem with Voxel Based Morphometry?

Answer 15

Because of the process of morphing all the brains of each group into ONE “average” brain, and THEN measuring the voxel composition, the technique totally misses any individual variation in shape or placement of the structures being studied. The brain areas in a group could be large but irregularly shaped and they would average out to a smaller area, thus making the average size in that group seem smaller than it should.

Question 16

Why does it take ~5 years for symptoms to start to show after onset of hippocampal degeneration?

Answer 16

Think of the “cognitive reserve” concept as a kind of buffer. The individual doesn’t actually need all that tissue to function normally, and it takes a while of the amount of tissue to decrease to the point where it starts to make a difference in functioning.

Question 17

What structure is used to transport peripheral information about energetic needs to the brain?

Answer 17

The Nucleus of the Solitary Tract

Question 18

Why would you start to feel good after ~2 days of famine?

Answer 18

Ghrelin secretion seems to be less acute. You aren’t wasting fluctuating energy on digestion. You are receiving the EXACT correct amount of energy because the body is breaking down and releasing only what it needs.

Question 19

Ghrelin is secreted by two areas, what are they and what do they do?

Answer 19

1. From the stomach, it travels in the blood stream to the brain to stimulate food intake.
2. From the hypothalamus (arcuate nucleus), travels to the pituitary to stimulate GH secretion.
   MAKES SENSE: The ghrelin intends for you to be eating soon, so it would make sense to also have some growth hormone circulating to be able to use the energy you’re about to receive.

Question 20

What happens to hormone levels in Prader Willi syndrome?

Answer 20

Ghrelin levels are elevated.

Question 21

Which hormone is produced by fat cells?

Answer 21

Leptin

Question 22

What is one simple hormone related theory for obesity?

Answer 22

That there is a dysfunction in the active transport system so leptin is not able to carry its “I’m full” message to the brain.

Question 23

What is the link between ghrelin receptors and cortisol?

Answer 23

Having normal ghrelin receptors is linked to higher cortisol responses to stress. These are linked to having more normal social behavior, even when chronically socially stressed. Having normal ghrelin receptors is also linked to seeking out a high-fat diet when stressed, which might be adaptive because it creates energy stores.

Question 24

Link the ghrelin receptor/cortisol story to depression.

Answer 24

Having normal ghrelin receptors is linked to less social isolation when chronically socially stressed. The normal ghrelin/cortisol activity might be protective against social isolation. Social isolation often occurs in depression, so maybe ghrelin has a role in buffering against depression.

Question 25

Contrast the “emotional eating during stress” theory of obesity to the “selfish brain” theory of stress-induced obesity.

Answer 25

The emotional eating idea is that during stress (unpleasant emotions) people seek out rewarding stimuli to make themselves feel better. High fat diets activate the reward circuits more than low, so this leads to overconsumption and overweight.
In contrast, the selfish-brain theory states that stress hormones are the ones who regulate energy metabolism. When there is stress, they prevent insulin secretion, induce insulin resistance, so that the glucose from the normal diet stays in the blood and the brain gets more. BUT when the stress systems are chronically activated, stress hormone receptors are down-regulated so there is a resistance to these hormones… they’re not able to make the brain “request” glucose normally anymore.
So the “pull” mechanism takes over, simply increasing consumption to make sure there’s lots of glucose in the blood so the brain gets enough whether or not it’s asking for it. THIS leads to overconsumption and overweight.

Question 26

Describe the study that gives good support to the selfish-brain theory.

Answer 26

What would make sense if the theory is correct is that during stress, glucose levels wouldn’t go down again as they normally do after a meal (because the brain is “pulling”, preventing glucose storage in the periphery). The results show that in fact this seems to be correct, glucose levels remain higher longer after stress than no stress. Insulin levels also remain higher longer. Stress also results in a higher-carb diet than no stress.

Question 27

What are the main differences in anorexia and bulimia DSM IV diagnosis criteria?

Answer 27

Anorexia: 
- Actually is underweight, refuses to maintain normal weight
- Amenorrhea (ENDOCRINE ABNORMALITY)
Bulimia: 
- Binging and compensatory behavior
- Lack of control over eating behavior

Question 28

What are some personality differences between anorexia and bulimia patients?

Answer 28

Anorexia:
- Highly perfectionist, controlling
Bulimia:
- Lack of impulse control
- Mood swings
- Comorbidities with anxiety, substance use, depression

Question 29

How do gender and sexual orientation affect the incidence of eating disorders?

Answer 29

Women more than men.
Homosexual men more than straight men.
Homosexual women LESS than straight women.

Question 30

How do sex hormones correlate with eating disorder incidence?

Answer 30

ED’s seem more likely in higher levels of estrogen (commence around puberty and decrease at menopause).
Testosterone exposure during rats’ critical period seems to have organizational effects increasing food intake and body weight.

Question 31

How did the study correlate prenatal androgen exposure in humans to disordered eating?

Answer 31

They used finger-length ratio as evidence of androgen exposure, and found associations with disordered eating and both extremes of finger-length ratios.

Question 32

What hormonal associations found in the human study may explain gender differences in eating disorder incidence?

Answer 32

Low prenatal T and high adult E –> more ED’s.
Prenatal testosterone might have protective effects against later estrogen.
BUT some women with bulimia actually have the opposite; super high testosterone and low estrogen (maybe the high testosterone is causing binging, and then the women compensate).

Question 33

What calls into question the “hormone influence on ED’s” theory?

Answer 33

The fact that although homosexual men have higher levels of ED than heterosexual, they don’t have significantly different finger ratios.

Question 34

There are many social factors which also have been correlated to ED incidence. Name 3.

Answer 34

1. Childhood sexual abuse
2. Parenting style (low nurture, high control)
3. Thin culture in the media
4. Socialization and gender norms

Question 35

What’s the name of the researcher who did all the prairie/montane vole studying?

Answer 35

(Tom) Insel

Question 36

Which vole is the monogamous one?

Answer 36

The prairie vole

Question 37

What is the (organizational) hormone-related difference between the prairie and montane vole?

Answer 37

Prairie voles have 3 to 7 times MORE oxytocin receptors than montane.

Question 38

Where are the oxytocin receptors concentrated?

Answer 38

Oxytocin receptors are concentrated in the NAcc and PLC (think of the reward system and limbic cortex)

Question 39

How are montane voles even able to keep their offspring alive if they’re so unattached?

Answer 39

Nursing stimulates up-regulation of oxytocin receptors, so that they are temporarily attached to their pups. As soon as the suckling stops (~16 days), they stop caring.

Question 40

Why do montane voles spend less time (than prairie) with females when exposed to a strange female and one he’s mated with before?

Answer 40

Perhaps it’s an “approach-approach dilemma”, he can’t choose because they’re both equally attractive (he’s not attached to the one he mated with before).

Question 41

How do we know that it’s probably oxytocin in the PLC and NAcc that makes prairie voles spend more time with a vole they’ve previously mated with?

Answer 41

When injected with an oxytocin antagonist (OTA) in the NACC and PLC, prairie voles lose their preference for their partner… but when the OTA is injected elsewhere, the partner preference remains.

Question 42

What seems to be the effect of vasopressin?

Answer 42

It influences the bonding. (makes voles behave as though mated when they haven’t // blocking it makes voles behave as though not bonded when they have mated)

Question 43

How does the birth process influence bonding? physiologically and environmentally?

Answer 43

1. The actual vaginocervical stimulation induces release of noradrenaline, which induces release of oxytocin (which decreases aggression, enhances nurturing)
2. The environmental stimuli of being exposed to the baby (olfactory, tactile, visual) stimulates release of oxytocin & vasopressin

Question 44

In the trust game study, in which condition did oxytocin seem to increase trusting behavior (investing more money)?

Answer 44

With HUMANS

Question 45

How do we know oxytocin doesn’t just stimulate pro-social behavior?

Answer 45

Because they administered oxytocin to the trustees, and if it was just pro-social behavior, they would be expected to give more money back to the investor. They DIDN’T, which means that the oxytocin facilitated something specifically related to trusting another person.

Question 46

What were the results of the borderline personality disorder study with oxytocin?

Answer 46

Administration of oxytocin decreased cooperative behavior in subjects with BPD overall.
When studied in more detail, the “high-avoidance” type of BPD (with high anxiety) very strongly correlated to the DECREASE in cooperation with oxytocin.
The “high-anxiety LOW-avoidance” type very strongly correlated to an increase in cooperative behavior with oxytocin.

Question 47

Overall what can we conclude about the effects of oxytocin on behavior in humans?

Answer 47

That it seems to facilitate previous patterns of behavior, either adaptive or maladaptive. It is easier to obtain a “bioavailable response” meaning that it is easier to facilitate a behavior that you were leaning towards in the first place. It won’t create love or attraction where there is none.