quiz Flashcards

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1
Q

Why would deletion of kisspeptin cause obesity?

A

Kiss1 ARH nucleus activates POMC and inhibits NPY, causing a decrease in satiety signals

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2
Q

What is response to kiss1 neurons to estradiol and testosterone in the ARC and AVPV?

A

Kisspeptin is expressed more with an increase in E2 and testosterone, both the ARC and AVPV interact with gonads

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3
Q

Based on the results what element of reproduction does kisspeptin seem to regulate in teleost fish and how does it differ from the reproductive role of kisspeptin in mammals?

A

Motivation for sexual behaviour, whereas in mammals it is important for spawning **

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4
Q

Describe in 1-2 sentences how NKB and dynorphin A regulate KNDy neuronal activity in a singular neuron.

A

Kisspeptin neurons coexpress neurotransmitters (NKB and dynorphin A)
Kisspeptin neurons are named KNDy neurons because they produce 3 relevant hormones (kisspeptin, neurokin B, dynorphin A)
NKB: serves as the initial stimulator to communicate with nearby KNDy neurons and release kisspeptin
Dynorphin A: acts as a KNDy inhibitor to decrease kisspeptin secretion from KNDy neuronal

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5
Q

Do rodents or humans require KNDy for the LH surge to occur?

A

Humans require KNDy, not rodents

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6
Q

Name 2 results that occur when CRISPR knocks down ERS1 in RP3V GABA-kisspeptin neurons?

A

Variable reproductive effects with most mice showing disruptions in estrous cycle and LH secretion

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7
Q

State the main difference in the findings regarding multiple hormone production in pituitary cells in teleost vs mammals.

A

Teleosts:
spatially organized but no clusters of multi-hormonal cells were found
gonadotropes produce both FSH and LH
few species have 3 hormone encoding genes, multi hormonal cells that are greater than 2 have not be detected, bi-hormonal cells

Mammals:
there are 3 different mechanisms that give rise to multi-hormonal cells

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8
Q

Give a specific situation where multi-hormone production would be important and why?

A

Cancer cells can easily change the ability of the cell to produce certain hormones, multi-hormone production help adapt to different conditions, especially during puberty, stress and regeneration

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9
Q

What is the main hormone that drives follicular development in avians? Briefly describe one thing that it does.

A

FSH drives follicular development in avians, causes growth of follicle into preovulatory hierarchal follicle

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10
Q

Name one thing that can disrupt the LH surge in hens.

A

Photoperiods affect the LH surge

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11
Q

What is a practical application of understanding the reproductive system of species?

A

To help to make species that are dying grow again and to make harvesting as efficient as possible

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12
Q

What are the main regulators of AMH expression in the ovary? Do they stimulate or inhibit AMH expression?

A

BMPS (increase), FSH (increase), LH (no effect), E2 (unresponsive) are main regulators of AMH (anti mullerian hormone)

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13
Q

What is a potential receptor for AMH in zebrafish?

A

Bmpr2

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14
Q

What are the roles of sertoli and leydig cells in genital differentiation?

A

Sertoli cells
Secrete glycoproteins AMH (anti-mullerian hormone), causes regression of mullein ducts
Leydig cells
Secretes androgens/testoserone
Differentiation of the wolffian duct
Leydig cell differentiation and androgen production is stimulated by placental human chorionic gonadotropin

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15
Q

Describe the classical and non-classical pathways of estrogen receptor signalling.

A

Classical
ERα and ERβ act as nuclear receptors, influencing gene expression by binding to estrogen response elements (ERE) on target genes after hormone binding.

Non classical
E2 binds to GPCER
cause a phosphorylation cascade that will activate internalized ER
CREB and ER will bind to response elements and cause transcription
predominantly localized in the endoplasmic reticulum, which triggers rapid cellular responses via second messengers.

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16
Q

Name the major endocrine disrupting chemical that was presented in class. What does it inhibit?

A

Bisphenol A and it inhibits the differentiation of sertoli and leydig cells

17
Q

How does bisphenol-A influence male fertility and which mechanisms are activated following BPA exposure?

A

BPA exposure causes hormonal disruption, increased cell apoptosis, and alters mitochondrial dynamics and activity, ultimately leading to decreased male fertility
BPA binds and inactivates ERs (alpha) reducing cell viability and testosterone production
BPA induced apoptosis causes increased expression of apopotitc protein p53
BPA causes ROS overproduction causing oxidative stress
BPA causes decrease LH and testosterone epithelium while up regulating FSH
BPA causes increased epithelium abnormalities affects sperm production and function

18
Q

What is placenta? Placentation?

A

A temporary structure formed in the uterus during pregnancy that is critical for oxygen, food and hormonal interactions and exchange between mothers (uterus) and fetus
Process begins when the blastocyst is implanted into the uterine wall

19
Q

What receptors does BPA act on?

A

BPA binds to estrogen receptor gene (ESR1/2), estrogen receptor and GPR30 which causes fusion, invasion and migration of trophoblasts, as well as apoptosis

20
Q

How does BPA alter the maternal microbiome and how may this cause FGR?

A

BPA causes a decrease in bifidobacterium and increasing verillonella microbiota in the gut, this dysbiosis may be related to inflammation and placental insufficiency, posing a potential explanation for fetal growth restriction