Canal Flashcards

1
Q

What part of the brain develops slower during puberty and what is its function

A

the prefrontal cortex, rational thinking

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2
Q

What sex steroids are active in the HPG axis

A

hypothalamus - GnRH
Pituitary - LH
gonads - FSH

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3
Q

Steps in menstruation

A
  • FSH stimulates egg maturation and oestrogen release
  • Oestrogen stops FSH production and stimulates LH release
  • LH causes mature egg release
  • Progesterone maintains uterus lining
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4
Q

What is the result of the menopause

A
  • increased risk of CV disease
  • loss of bone mass, higher risk of fractures
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5
Q

history of kisspeptin

A

‘96 - Kiss1 gene discovered
‘99 - GPR 54 gene identified
‘01 - Kisspeptin protein is a high-affinity ligand for GPR54 (kiss1R)
‘03 - mutations in KISS1R means defecit in reproductive function

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6
Q

What is function of kisspeptin

A

Kisspeptin signalling, via Kiss1R, essential for proper pubertal development and reproductive function

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7
Q

what does a GPR54 mutation lead to

A

sexual immaturity, failure or gonadal function and hypogonadotropism

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8
Q

Difference between preoptic and arcuate ksispeptin

A
  • low levels of kisspeptin in preoptic, high in arcuate because effect of oestrogen is lost
  • Arcuate has neurokynin B and dynorphin, Preoptic has galanine and tyrosine
  • Arcuate receives from metabolic, Preoptic from gonads
  • preoptic +, arcuate -
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9
Q

What happens to GnRH inputs during perinatal

A

receive inputs from:
- developing neural GABA-glutatmate innervations and glia
- Arcuate kiss neurons

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10
Q

Postnatal GnRH neural network

A
  • sexual differences in AVPV kiss1 neurons, more in females
  • differences happen in development and then stay this way
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11
Q

organisational hypothesis

A
  • increase in testosterone results in masculinisation of kiss1 expression, leads to deletion of kiss/AVPV neurons
  • Decrease in oestrogen necessary for feminisation of Kiss1 neurons in AVPV
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12
Q

what could explain slump in GnRH expression in juveniles

A

suppression of stimulatory ARC kiss neuronal input

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13
Q

What triggers puberty

A
  • before puberty, kisspeptin decreases, less GnRH, less sex steroids
  • just before, brakes come off! high kisspeptin and GnRH leads to egg/sperm
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14
Q

What enables pubertal period in females

A

late development of kisspeptin neurons from preoptic to GnRH cell bodies enables generation of GnRH surge in pubertal period
Surge is vital

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15
Q

Leptin

A
  • signal of energy abundance
  • secreted in body fat stores
  • stimulates activation of GnRH
  • kiss2 neurons in Arc express leptin receptors
  • leptin treatment partially rescues defective Kiss1 levels
  • reason for premature puberty in obese
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16
Q

HPG axis senescence

A
  • in puberty, increase in gonadal hormones = sexual maturation
  • also permanent sensitisation neural circuits, leads to social reproductive behaviours and incentive seeking behaviours
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17
Q

What is imprinting? how does it happen?

A

parental origin-specific differential gene expression
- in eutherian mammals, marsupials and flowering plants
- happens through epigenetic instructions laid down in parental germ cells

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18
Q

what does 2x copies of the maternal genome result in? what does it mean?

A

decrease in placenta size, means that maternal genome contributes to development of foetus

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19
Q

what does 2x copies of paternal genome result in? what does it mean?

A

extra-embryonic tissue, means some cells are selectively switched off in testis, others in ovaries

20
Q

Why does imprinting occur?

A

imprinted genes thought to influence transfer of nutrients to foetus and newborn from the mother - Selfish gene

21
Q

Parental conflict of kinship hypothesis

A

1991:
- in polygynous mammals, mothers bear offspring for multiple fathers
- paternally-derived genomes compete with other males, selection facours those that extract most maternal resources
- its why imprinted paternal genomes are in the placenta

22
Q

co-adaptaion hypothesis

A

2006:
- imprinted genes act co-adaptively to optimise foetal development and maternal provisioning and nurturing
- only a subset of genes fit, mainly paternal in both placenta and hypoT

23
Q

What is Peg3

A

‘paternal expressed gene 3’
- maternal copy is imprinted to be silenced
- expressed in maternal hypoT, palcenta and foetal hypoT
- example of co-adaptation

24
Q

How is Peg3 expressed?

A

only if inherited paternally

25
What is Peg3's function?
it effects maternal care: - milk release in adults - suckling in newborns - causes crouching over pups and nest building in females - allows males to find fertile mates
26
what does Peg3 KO do?
causes impair in growth and puberty
27
Why is Peg3 an example of co-adaptation
because converging actions of Peg3 in mother and foetus illustrate its functional co-adaptation for hypoT and placenta
28
Turner syndrome
- 1/2000 female babies - XO happens when conceived - 70% have female X, 30% male
29
physical characteristics of Turner's
- short - ovarian female --> no sex steroids - no secondary sex characteristics - potentially autism
30
treatments for turner's
- no cure - hormone replacement therapy - growth hormone therapy - heart/kidney checkups
31
cognitive features of turner's
- likely X-linked - ovarian failure = impaired neuro development - executive function effected, impairments in attention, working memory, cognitive flexibility, abstract reasoning - moderate social impairment
32
Impact of Skuse's study
- some genes involved in behavioural and social cognitive skills are imprinted - resulted in search for genes in X chromosomes - data suggest there are non-primary factors contributing to the difference between sexes - caused research into autism
33
autism spectrum disorder
- prevalence increasing - strong familial link - strong sex bias - threshold higher for females --> males have higher chance
34
how did Skuse's study relate to autism?
- Skuse proposed female protection lies within the X chromosome in an imprinted X-linked gene - expressed only on paternal X-chromosome, which would only be inherited by a girl, hence why threshold is higher
35
How does the HPA axis regulate stress?
- PVN of hypothalamus: CRH and AVP - Pituitary gland: ACTH - Adrenal gland: glucocorticoids and catecholamines - Negative feedback to brain: GR and MR
36
What behaviours in mothers are measured to assess future stress of offspring?
licking and grooming (LG) arched back nursing (ABN)
37
What do offspring of high LG/ABN mothers show?
- reduced plasma ACTH and corticosterone responses to stress - increase hippocampal GR expression --> low adulthood stress
38
Why do poor mothers produce more stressed offspring
low GR levels, weak feedback on CRH, elevated glucocorticoid secretion
39
what mechanisms underlie long-term effects of maternal care
Epigenetic mechanisms: - DNA methylation - histone modification - small non-coding RNAs
40
How does DNA methylation work?
- high levels of DNA methylation result in repressive chromatin - low levels results in permissive chromatin
41
histone modifications
- histone H3K9 acetylation and H4K4 methylation both present at actively transcribed regions of genome - basically pups from low LG mothers have high DNA methylation, low histone modification
42
human stress data
- childhood trauma alters HPA stress response, decreased GR response, increased risk of antisocial behaviour
43
holocaust victims
- low urinary cortisol - increased risk of anxiety/depression
44
Is PTSD maternally or paternally linked
maternally
45
mismatch hypothesis
high levels of stress in childhood means you can deal with it later in life
46
cumulative hypothesis
opposite of mismatch
47
MAOa in stress
boys with low MAOa activity have increased risk of adolescent and adult antisocial behaviour