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BMS381 Developmental Neurobiology > L12 - Energy Balance > Flashcards

L12 - Energy Balance Flashcards

1
Q

What were the early studies performed to implicated hypothalamus in energy balance

A

Ealy lessioning stidues

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2
Q

Lesions to the VMN –>

A

Hyperphagia

Over eating and obestity

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3
Q

Lesions to the LH –>

A

Aphagia leading to starvation

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4
Q

What were the conclusions of the lesioning experiments

How does this compare to the modern view

A

Lead to a theory that the hypothalamus contains a feeding centre and a satiety centre

Modern view is that of a mor eintegrated system - complex set of neurons in various nuclei are invovled

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5
Q

Hypothalamus is sensnisitve to ______ signals

What are these

A

Adiposy signals

Leptin and Insulin

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6
Q

What secretes leptin and insulin

A

Fat cells and pancrease

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7
Q

Where does leptin and insulin act at the hypothalmus

A

Arcuate nucelus

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8
Q

How does leptin reach the arcuate nucelus

A

Through TANYCYTES

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9
Q

Secribe the model of hypothalamuc control of hepatic glucose production

A

Leptin sensing neurones in ARC recieve input regarading energy sotres - in response input pathways that increase hepatic vagal tone which increases hepatic insulin sensitivity

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10
Q

The ARC neurones elicit local responses by connecting to

What is the effect of this

How do they do this

A

PVN VMN LH

Feedback to body via hormonal and nerual outputs to control food intake and energy expenditure

Regulating behaivour, autoomic activty nd metabolical rate

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11
Q

How many classes of LepR+ neurones

A

Two

NPY and Pomc neurones

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12
Q

LepR+ means what

A

Have leptin receptor

So are able to respond to leptin

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13
Q

Leptin ______ NPY nuerones

A

Inhibits

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14
Q

Describe NPY function

A

NPY is a neuropeptide (Y) whose action leads coordination of a vast array of activities to stimulate food intake and reduce energy expenditure

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15
Q

Leptin __________ Pomc neurones

A

Stimulates

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16
Q

Describe pomc function

A

POmc neurohormone.

Reduce food intake and increase energy expendityre

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17
Q

When are leptin levels high

A

When dont need any more food

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18
Q

Two adiposity signals _____________ produced in periphery and travel via ______________ to influence neurones in the ___________

A

Leptin and insulin
ME and tanycytes
Arcuate nucelus

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19
Q

NPY arcuated neurones ______________ and are ________________ inhibited by ______________

A

Synthesise and release
Neuropeptide Y
Inhibited by adipositry signals

20
Q

Pomc arcute neurones sythnesise and release _______________________

A

a-melanocyte-stimulating-hormone (a-MSH)

21
Q

NPY (NPY/AgRP) neurones inhibit the _______ and stimulate the _________

A

INIHIBT PVN

STIMULATE LHA

22
Q

Pomc (a-MSH/CART) stimulates the _________ and inhibits the _____________

A

PVN

LHA (inhibit)

23
Q

PVN has net _________

Causes the release of —— (2)

The net effect is …

A

Catabolic action

Release oxytocin and CRH

Decreases food intake and increases energy expenditure

24
Q

LHA has net __________

Causes the release of ………. (2)

The net effect is …… (2)

A

Anabolic action

Releases orexinA and melanin-concentrating hormone (MCH)

Stimulate food intake and decrease energy expenditure

25
Q

The paper used in the lecture aimed to …

A

Understand the genetic program the establishes the neuronal melanocortingergic phenotype and maintains and fully functional neuronal POMC phenotype

26
Q

title of paper used in lecture

A

Islet 1 specifies the identity of hypothalamic melanocortin neurones and is critical for normal food intake and adiposity in adulthood

27
Q

Transcription factor Islet1 __________________

A

Predicts and prefigures expression of pomc (ACTH)

28
Q

How was it concluded that islet1 predicts and prefigures expression of pomc (ACTH)

A

IHC

Combination of IHC and transgenic reporter line (pomc-EGFP) in the adult

29
Q

Islet two binds

A

To critical homeodomain binding motifs present in the neuronal Pomc enhancers nPE1 and nPE2

30
Q

How did they study the binding of Isl1

A

Mutate sequences with nPE1 and nPE2 show isl1 no longer recognises mutated DNA and no longer binds

31
Q

So ___- and _____ needed for activity of ___________

A

nPE1 and nPE2

Pomc transcription

32
Q

What are the two binding motifs in pomc GENE

A

nPE1

nPE2

33
Q

Mutations of nPE1 and nPE2 completely _________________

How was this studied

A

Prevents the ability of these enahners to drive reported gene expression to hypothalamic pomc neurons in transgenic animals

Reporter line - pomc driving expression of EGFP

34
Q

How would you determine if Isl1 required for pomc neurons

A

Isl1 required for formation of many other other structures ealrier
SO need to use a conditonal KO

35
Q

How was the conditional KO made

A

Mouse 1 - CreERT
Mouse 2 - Isl1/LoxP mouse

Add tamoxifen at any stage in life to recombine out Exon2 and coditonaly KO ISl1

36
Q

What was seeen in the conditional KO for Isl1

A

Pomc neurones fail to differentiate

37
Q

Why would you need to analyse expression of both Isl1 and ACTH by immunohistochemistry

A

To make sure that KO of exon 2 resulted in the absence of Isl1 protein

38
Q

What is the phenotypic effect of KO Isl1

A

No Pomc
Leads to early onset obesity
…
Pomc a neurohormone – reduce food intake

39
Q

What is the model fo rthe development of the hypothalamus

Describe it

A

Sequential anisotropic growth model of hypothalamic development

Anterior and mammary regions grow seqentially and in opposite direction from centrally retained FGF10+ pHyp cels

40
Q

Islet1 progenitors differentiate from

A

Anterior progenitors

41
Q

Isl1+ progenitors give rise to pomc neurones derive from

A

FGF10+ ‘stem’ pool

42
Q

FGF10+ cells are retained in _______ as ________

A

Adulthood

Radial glial cells called tanycytes

43
Q

What is special about some of the FGF10+ tanycytes

A

Some retain their stem cell actiivity and can give rise to Arc neurones throughout life

44
Q

Potentially throughout life Arc neurones are generated from

A

Hypothalamic stem cells

45
Q

What is the imolication of the stem cell theory with the idea that glucose requirements can chancge considerably throguhiut life

A

Pomc and NPY neurones can be generated from hypithalamic stem cells throughout life to anticipate of respond to changes

ALLOSTASIS

46
Q

What is the working hypothesis regarding hypothalamic stem cells

A

Stem cells are stimulated by metabolites/horomones provided by components of the hypothalamic niche and can respond by giving rise to new neurones

BMS381 Developmental Neurobiology (16 decks)

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