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
Q

What is Peg3’s function?

A

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
Q

what does Peg3 KO do?

A

causes impair in growth and puberty

27
Q

Why is Peg3 an example of co-adaptation

A

because converging actions of Peg3 in mother and foetus illustrate its functional co-adaptation for hypoT and placenta

28
Q

Turner syndrome

A
  • 1/2000 female babies
  • XO happens when conceived
  • 70% have female X, 30% male
29
Q

physical characteristics of Turner’s

A
  • short
  • ovarian female –> no sex steroids
  • no secondary sex characteristics
  • potentially autism
30
Q

treatments for turner’s

A
  • no cure
  • hormone replacement therapy
  • growth hormone therapy
  • heart/kidney checkups
31
Q

cognitive features of turner’s

A
  • likely X-linked
  • ovarian failure = impaired neuro development
  • executive function effected, impairments in attention, working memory, cognitive flexibility, abstract reasoning
  • moderate social impairment
32
Q

Impact of Skuse’s study

A
  • 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
Q

autism spectrum disorder

A
  • prevalence increasing
  • strong familial link
  • strong sex bias
  • threshold higher for females –> males have higher chance
34
Q

how did Skuse’s study relate to autism?

A
  • 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
Q

How does the HPA axis regulate stress?

A
  • PVN of hypothalamus: CRH and AVP
  • Pituitary gland: ACTH
  • Adrenal gland: glucocorticoids and catecholamines
  • Negative feedback to brain: GR and MR
36
Q

What behaviours in mothers are measured to assess future stress of offspring?

A

licking and grooming (LG)
arched back nursing (ABN)

37
Q

What do offspring of high LG/ABN mothers show?

A
  • reduced plasma ACTH and corticosterone responses to stress
  • increase hippocampal GR expression –> low adulthood stress
38
Q

Why do poor mothers produce more stressed offspring

A

low GR levels, weak feedback on CRH, elevated glucocorticoid secretion

39
Q

what mechanisms underlie long-term effects of maternal care

A

Epigenetic mechanisms:
- DNA methylation
- histone modification
- small non-coding RNAs

40
Q

How does DNA methylation work?

A
  • high levels of DNA methylation result in repressive chromatin
  • low levels results in permissive chromatin
41
Q

histone modifications

A
  • 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
Q

human stress data

A
  • childhood trauma alters HPA stress response, decreased GR response, increased risk of antisocial behaviour
43
Q

holocaust victims

A
  • low urinary cortisol
  • increased risk of anxiety/depression
44
Q

Is PTSD maternally or paternally linked

A

maternally

45
Q

mismatch hypothesis

A

high levels of stress in childhood means you can deal with it later in life

46
Q

cumulative hypothesis

A

opposite of mismatch

47
Q

MAOa in stress

A

boys with low MAOa activity have increased risk of adolescent and adult antisocial behaviour