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PHRM > L10 - Neuroendocrine > Flashcards

L10 - Neuroendocrine Flashcards

1
Q

!Describe a neuroendocrine cell

A

Specialised neurons embedded in capillaries (blood stream), where hormones (NT/NP) are released. It circulates and affects target tissues

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2
Q

T/F: Neuroendocrine peptides can be both hormones and NP

A

T
The distinction between NP and peptide hormone has to do with the cell types that release and respond to the molecule; NP are secreted from neuronal cells and signal to neighboring cells (primarily neurons). In contrast, peptide hormones are secreted from neuroendocrine cells and travel through the blood to distant tissues where they evoke a response.

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3
Q

Why do neuroendocrine peptides have limited usefulness as drugs? (4)

A
  • Hard to make/purify
  • Poor oral absorption
  • Degraded rapidly by peptidases
  • Non-peptide agonists/antagonists
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4
Q

Hypothalamus direct effect?

A

Releases hormones directly into blood via posterior pituitary – oxytocin and vasopressin

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5
Q

Hypothalamus indirect effect?

A

Releases hormones into portal hypophyseal circulation that act on anterior pituitary

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6
Q

Location of Hypothalamus and pituitary

A
  • Base of brain, right next to the third ventricle

- Pituitary is below the hypothalamus

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7
Q

Oxytocin- function

A
  • Baby crying -> oxytocin release -> milk letdown in mother

- Smooth muscle uterus contraction

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8
Q

Vasopressin - function

A

Released in response to reduction in blood volume or increase in plasma osmolarity, circulates to kidney

  • increases water re absorption
  • vasoconstriction
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9
Q

Hypothalamic indirect pathway

A

Neurons in Arcuate Nucleus projects to median eminence (an area leaky to BBB) then releases hypothalamic releasing factors/hormones into the hypohphyseal portal veins. These hormones circulate and binds to endocrine receptors in the anterior pituitary. This causes release of pituitary hormone in the blood which binds to a target organ. Another hormone is released – having more effects on the body.

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10
Q

Hypothalamic and anterior pituitary hormones are trophic – what does this mean?

A

Overproduction = hypertrophy of organs and hyperplasia
Underproduction = atrophy of organs
*Negative feedback regulates synthesis and release

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11
Q

Corticotropin Releasing Factor (CRF) releases which hormone?

A
  • Adrenocorticotropic hornone
  • alpha-mealanocyte stimulating hormone
  • Beta-endorphin
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12
Q

Thyrotropin Releasing Hormone releases which hormone?

A
  • Thyroid stimulating hormone

- Prolactin

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13
Q

What propetide synthesis increases with CRF?

A

POMC

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14
Q

HPA axis – ACTH synthesis and function

A

1) Activated by environmental/psychological stress
2) PVN axons project to hypophyseal portal veins to release CRF
3) Prohormone Convertase 1 (PC1) cleaves ACTH from POMC (CRF and Vasopressin promote synthesis of POMC)
4) CRF circulates and binds to anterior pituitary
5) Anterior pituitary releases ACTH that binds to melanocortin-2-receptors on adrenal cortex
6) This stimulates releases of GC – e.g. Cortisol
7) ACTH has negative feedback, inhibiting PVN and Ant. Pituitary

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15
Q

Cortisol is released in response to? Function?

A
  • Released in response to stress and low blood-glucose concentration
  • Increases blood sugar through gluconeogenesis
  • Suppress the immune system (inflammation)
  • Increases alertness and cognition
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16
Q

CRF1 Receptors

A
  • GPCR
  • Widely expressed, dominant receptor in brain and pituitary
  • Endogenous agonist = CRF
17
Q

CRF2 Receptors

A
  • GPCR
  • 3 Splice variants CRF2alpha/2beta/2gamma
  • Endogenous agonist = Urocortin
18
Q

CRF antagonists proposed as what kind of medication?

A

Anti-depressants and anxiolytics

19
Q

ACTH can be cleaved to form? Why aren’t these formed in the corticotrophs?

A

Alpha-MSH and CLIP (unknown function currently). Corticotrophs don’t contain PC2 – but these can still be produced elsewhere in the pituitary

20
Q

!Cushing syndrome – causes? Effect?

A
  • Hyper secretion of ACTH caused by tumour
  • Prolonged exogenous GC (e.g. prednisone or dexamethasone) treat inflammatory or autoimmune diseases
  • Exogenous GC tends to be inhaled orally, hence effects aren’t as severe

-Effects: fat abs, thin arms and legs (muscle wasting), poor wound healing, osteoporosis, tendency hyperglycaemia

21
Q

Growth Hormone (GH) – activates? How are defects treated?

A
  • Activates GH receptors to induce IGF-1 synthesis and releases from the liver – increased protein synthesis and lipolysis
  • Somatropin recomb prep used to treat growth defects
  • High in newborn and declines after puberty
  • Release is pulsatile
22
Q

Somatostatin – what is it? What’s its analogue?

A
  • HRF that inhibits release of GH from ant pituitary
  • Octreotide – long acting analogue of somatostatin
  • Used to treat gigantism in children (Excess GH pre-puberty)
  • Treats acromegaly in adults (an excess prod of GF due to benign pituitary tumour – enlarged facial structures, hands and feet)
  • Octreotide + surgery or radiotherapy to remove tumour
23
Q

Hypothalamus receives 2 signals (regarding weight)

A

1) LT Adiposity signals: Leptin from adipose or Insulin from pancreas (these hormones circulate in our bloodstream proportional to our fat mass)
2) ST Satiety signals: liver, sympathetic input, vagus nerve input, CCK -> ultimately reaches NTS of medulla -> hypothalamus

24
Q

What hormone is released by an empty stomach that will signal the brain? (This signal, unlike the others, doesn’t terminate when a meal is started– only stops when the stomach is stretched)

A

Ghrelin – the hunger hormone produced by GIT

25
Q

CCK stimulates

A

Digestion of fats, carbs, and proteins. It is a prototypical signal binding to CCK-A receptors on vagus nerve that terminates the meal

26
Q

Leptin – ‘leptos’ meaning thin – secreted from? Transported? Receptors activated?

A
  • Secreted from fat cells
  • Plasma levels proportional to BMI and fat
  • Leptin has to be transported actively across BBB
  • Crosses BBB via a saturable process, there is a finite amount of leptin that can cross BBB
  • Receptors located in the hypothalamus (inhibits NPY/AGRP receptor and stimulates POMC)
  • Inhibits food intake via CNS mechanism
27
Q

Why do people (who have leptin), just keep on getting fatter?

A

Crosses BBB via a saturable process, there is a finite amount of leptin that can cross BBB

28
Q

Alpha-MSH inhibits food intake via (receptor) and what does it do?

A

MC4R agonist, Gs, tonic inhibition of food intake as a-MSH constantly released, it also increases in energy expenditure
*ACTH binds to Melano cortin 2 Receptors

29
Q

Agouti-related peptide (AGRP)

A
  • Within CNS AGRP: synthesis limited to ARC and only located in NPY neurones
  • Inverse agonist at MC4R (decreases receptor activity below basal)
  • Inhibits a-MSH from binding to MC4R
  • Increases food intake and inhibits energy expenditure
30
Q

What receptor causes increase in Agouti colour?

A

MC1R – found in hair follicles

31
Q

NPY – member of? Low/high conserved across species? Synthesized in? Co-localized with?

A
  • Member of pancreatic polypeptide family – NPY stimulates appetite, other 2 members inhibit
  • Highly conserved across species
  • Synthesized in the locus coerulus, NTS, ARC nucleus of the hypothalamus
  • Co-localised with AGRP in ARC neurons and in LDCV with NA
32
Q

T/F: NPY stimulates feeding in satiated animals (chronic admin. Causes obesity)

A

T

33
Q

NPY receptors?

A
  • Y1/2/5 receptors
  • Y2 is an autoreceptor
  • Y1/5 is post-synaptic
34
Q

SYNTHESIS: AgRp limited to? POMC limited to? NPY limited to?

A

AGRP - ARC
POMC - ARC and NTS
NPY - ARC, NTS, Locus coerulus

PHRM (24 decks)

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