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Physiology 2: Sem 3 > NEURO: Neurohormones > Flashcards

NEURO: Neurohormones Flashcards

1
Q

Describe neurohormones.

A

A hormone produced and released by neuroendocrine/neurosecretory nerve cells into the blood

  • circulated in the blood and diffuse out of capillaries to act on complementary receptors
  • could potentially have a widespread effect around the body
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2
Q

Describe the two main control systems of the body (compare and contrast).

A

The body has two main control systems: the endocrine system and the nervous system.

ENDOCRINE SYSTEM:

  • mediators travel within blood vessels
  • utilises chemical mediators (hormones)
  • slow communication
  • effects can be long-lasting

NERVOUS SYSTEM:

  • signalling along the nerve fibres
  • transmission of electrical impulses
  • fast communication
  • effects are generally short-acting
  • effect is not widespread
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3
Q

Describe the different types of hormones.

A

PROTEIN & PEPTIDE HORMONES:

  • vary considerably in size
  • can be synthesised as a large precursor and processed prior to secretion (eg. GH, somatostatin, insulin)
  • can be post-translationally modified (eg. glycosylation)
  • can have multiple subunits synthesised independently and assembled (eg. FSH, LH, TSH)

AMINO ACID DERIVATIVES:

  • mostly tyrosine-derived
  • a neurotransmitter that can also act as a hormone
  • eg. epinephrine, norepinephrine, dopamine

STEROID HORMONES:

  • lipids derived from cholesterol
  • includes cortisol, aldosterone, testosterone, progesterone, oestradiol
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4
Q

Hypophyseal Portal System

A

Neurones project and release neurohormones directly into the portal system in the hypothalamus, and they are transported along with the portal system to the anterior pituitary, where they act on receptors to release other neurohormones into the blood circulation.

These neurohormones are circulated around the body and activate complementary receptors, having a widespread effect all around the body.

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5
Q

The function of magnocellular neurones

A

project from the hypothalamus to the posterior pituitary, releasing neurohormones (peptides- oxytocin & vasopressin) into the capillary network in the posterior pituitary to be circulated around the body and activate complementary receptors

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6
Q

How are neurohormones released into the blood?

A

Most, if not all, bodily activities show periodic rhythms or cyclic changes. Many of the hormones show periodicity.

CIRCADIAN RHYTHMS: based on a 24-hour cycle (eg. secretion of cortisol, GH, PRL)

PULSATILE (ULTRADIAN) RHYTHMS: periodicity of fewer than 24 hours (usually every 1/2 to 2 hours) (eg. secretion of gonadotrophin in adults)

INFRADIAN RHYTHMS: periodicity of longer than 24 hours (eg. menstrual cycle)

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7
Q

List some of the principal endocrine organs in the body.

A
  • hypothalamus
  • pituitary gland
  • thyroid gland
  • parathyroid glands
  • adrenal gland
  • pancreas
  • ovary (females)
  • testes (males)
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8
Q

What are the key nuclei of neurosecretory cells in the brain?

A

Medial preoptic nucleus
Arcuate nucleus
Paraventricular nucleus

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9
Q

How are hormone signals sent to both parts of the pituitary?

A

Neurosecretory cells in the hypothalamus produce “releasing” and “release-inhibiting hormones” into the primary capillary plexus which are transported to the secondary capillary plexus to act on anterior pituitary receptors and induce the release of other hormones.

With the posterior pituitary, we have neurones called magnocellular neurons, which project from the hypothalamus directly into your posterior pituitary. The hormones are released into the PP, where they travel through the capillary network and get released straight into the blood circulation.

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10
Q

Specialised cells in the anterior pituitary responding to hypothalamic hormones

A

ANTERIOR PITUITARY:
· Corticotroph cells that control ACTH secretion in response to CRH
· Thyrotroph cells that regulate TSH secretion in response to TRH
· Gonadotroph cells that secrete LH and FSH in response to GnRH
· Somatotroph cells that control GH secretion in response to GHRH
· Lactotroph cells that control the secretion of prolactin in response to TRH, somatostatin and dopamine-

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11
Q

Hormones released by the anterior pituitary and their respective functions

A

FSH and LH
>Act on gonads
Growth Hormone (GH)
>Activates receptors in muscle and bone
Prolactin
>Stimulates mammary glands for milk production
ACTH
>Stimulates cortisol production in the adrenal cortex
Thyroid Stimulating Hormone
>Binds TSH receptors in thyroid to produce thyroxine

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12
Q

Hormones released by the posterior pituitary and their respective functions

A

Oxytocin (posterior pituitary)
>Stimulates mammary glands for milk production
>Induces smooth muscle contractions

Vasopressin (ADH) (posterior pituitary)
>Acts on kidney tubules to retain water

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13
Q

As a recap, describe the role of ACTH in the release of cortisol.

A

39 amino acid peptide derived from a large precursor glycoprotein called proopiomelanocortin (POMC)

stimulates the production of glucocorticoid (cortisol) and sex hormones from the zona fasciculate of the adrenal cortex

Hypothalamic neurones release corticotrophin-releasing hormone (CRH) to stimulate pituitary corticotrophs to release ACTH into the circulation.

Cortisol provides negative feedback to the hypothalamus and pituitary, reducing the amount of CRH and ACTH released.

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14
Q

Steps of Cortisol Synthesis

A

1) Stress activates the hypothalamic-pituitary axis (HPA) by activating the hypothalamus to release CRH
2) CRH activates corticotroph receptors in the anterior pituitary to release ACTH.
3) ACTH is released into the blood circulation and acts on ACTH receptors in the adrenal cortex to release cortisol.
4) Cortisol is then released into the blood circulation. Cortisol is important because it mobilises energy.

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15
Q

How do cortisol levels decrease?

A

via a negative feedback mechanism
-high cortisol detected by cortisol receptors in hypothalamus and pituitary, inhibiting the release of CRH from hypothalamus or ACTH from pituitary

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16
Q

What does chronic stress cause?

A

hyper-stimulation of the HPA axis, meaning an increase in cortisol production, leading to high basal cortisol levels which eventually cause:

  • depression
  • anxiety-related disorders
17
Q

The rhythm of Cortisol Secretion

A

Circadian rhythm
-cortisol highest in the morning and declines during the day, reflecting the pattern of ACTH secretion from the anterior pituitary

*pattern of cortisol secretion probably reflects the body’s response to low blood glucose after overnight fasting

18
Q

As a recap, describe the regulation of TSH and thyroid secretion by negative feedback.

A

Thyrotropic releasing hormone (TRH) from the hypothalamus stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH).
TSH acts on the thyroid to increase T3/T4 secretion, T3 is the most potent thyroid hormone, and targets the tissues containing a deiodinase enzyme (DI) to convert T4 to T3.

The pituitary also expresses deiodinase to convert T4 to T3 to facilitate negative feedback.

19
Q

As a recap, what happens when you have too much or too little thyroxine?

A

If you have too much thyroxine, it can lead to hyperthyroidism, tachycardia, anxiety, etc.

If you have too little thyroxine, it can lead to weight gain, low energy, cognitive impairment, depression etc.

20
Q

How do thyroxine levels decrease?

A

via negative feedback mechanism:
-high thyroxine detected by thyroxine receptors on the hypothalamus and pituitary, inhibiting the release of TRH from the hypothalamus and TSH from the pituitary

21
Q

As a recap, describe prolactin and its regulation.

A

It is released by the lactotrophs in the anterior pituitary.
It stimulates mammary gland development during puberty. It also maintains lactation (synergised by glucocorticoids, inhibited by oestrogen and progesterone - we get a decrease in both after parturition).

Its regulation is under the dominant-negative control of dopamine. It’s increased during pregnancy and lactation.

-stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus

22
Q

Describe the synthesis and transport of the neurohormones of the posterior pituitary.

A

The neurohormones of the posterior pituitary are vasopressin and oxytocin.

They are synthesised in the supraoptic and paraventricular nuclei in the hypothalamus.
They’re transported to the terminals of the nerve fibres located in the posterior pituitary.

Structurally, they’re quite similar (only a 2 amino acid difference in a 9 amino acid structure), yet they have very different functions.

23
Q

As a recap, describe vasopressin.

A

It is also known as the anti-diuretic hormone (ADH). Its release is stimulated by changes in the activity of the osmoreceptor complex in the hypothalamus.

It controls plasma osmolality by regulating water excretion and drinking behaviour.

It stimulates vascular smooth muscle contraction in the distal tubules of the kidney to reduce loss of water and raise blood pressure.

24
Q

Steps of Vasopressin Secretion

A

Under these conditions (dehydration and low blood pressure):

1) Kidney releases an important enzyme known as renin
2) Renin cleavages an important molecule found in the liver called angiotensinogen into angiotensin I
3) Angiotensin I is converted to angiotensin II
4) Angiotensin II constricts blood vessels to increase blood pressure
5) Angiotensin II acts on the Subfornical organ in the brain, which signals for the release of vasopressin from the pituitary
6) Once vasopressin is released from the pituitary it induces thirst and also acts on kidneys to retain water in the distal tubules, increasing blood pressure.
7) Vasopressin also increases blood pressure by causing vasoconstriction

25
Q

As a recap, describe oxytocin.

A

Normally, it’s undetectable, but its levels are elevated during parturition, lactation and mating.
It is released in response to peripheral stimuli of the cervical stretch receptors and suckling at the breast. It may also be involved in responses to stroking, caressing, grooming, etc.

It regulates the contraction of smooth muscles (e.g. uterus during labour, myoepithelial cells lining the mammary duct, contraction of reproductive tract during sperm ejaculation).

26
Q

Oxytocin Release During Labour

A

During labour:

1) Baby is pushing against the uterus, and the uterus stretches, stimulating neurones
2) Neurones send a signal to magnocellular neurones to start releasing oxytocin
3) Oxytocin is released into the blood circulation and will act on oxytocin receptors in the uterus to cause uterine smooth muscle contractions
4) Baby is pushed forwards, causing more stretching, and causing more oxytocin release via a positive feedback mechanism
5) This stops when the baby is delivered as there is no more stretching of the uterus

27
Q

Social effects of oxytocin (peptide of love)

A

There are also oxytocinergic projections from hypothalamus to other brain regions e.g. olfactory region, amygdala, nucleus accumbens and septum etc. which have no peripheral effects and only social effects

found in animals that monogamy is due to high oxytocin receptors located in reward centres, confirming that oxytocin is extremely important for paired bonding behaviour and is seen as a pro-social hormone

28
Q

List some CNS effects of oxytocin.

A
  • antidepressant
  • anitpsychotic
  • social cognition
  • induces trust
  • anti-OCD
  • treatment of autism
  • anxiolytic (reduces anxiety)
  • hypnotic
29
Q

Oxytocin as a psychoactive drug

A

because it is important as a pro-social hormone, it has potential to be used as a psychoactive drug in behavioural treatments

30
Q

Describe the two-way interaction between the kidneys and the hypothalamus.

A

The kidneys secrete renin (in response to low BP, etc.).
The renin converts angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II.

Angiotensin II is detected by the subfornical organ in the brain. The subfornical organ projects to vasopressin cells and neurons in the lateral hypothalamus. The vasopressin then goes to affect the kidneys and cause them to retain more water.

31
Q

Insulin & Growth Hormone Receptor

A

> Bind to cell surface receptors leads to dimerization of the receptors, subsequently recruiting tyrosine kinases (e.g. JAK2 or MAPK) which phosphorylate target protein (e.g. STAT) to induce biological responses.

Mutations in the growth hormone receptor gene can result in defective hormone binding or reduced efficiency of receptor dimerization, causing growth hormone resistance (Laron syndrome).

32
Q

TSH and ACTH Receptor

A

G-protein coupled receptor/adenylate cyclase pathway (Gi & Gs):
-stimulation of adenylate cyclases increases intracellular cAMP, that activates PKA which phosphorylate target proteins (e.g. CREB) to initiate specific gene expressions and biological responses

Activating mutations of TSH receptor cause thyroid adenomas (constitutive ON)
Inactivating mutations of TSH receptor cause resistance to TSH

33
Q

Oxytocin and GnRH receptor

A

G-protein coupled receptor (Gq)

  • PhospholipaseC converted to PIP2
  • PIP2 converted to IP3 and DAG
  • IP3 stimulates Ca2+ release from intracellular stores (ER)
  • DAG activates PKC, which stimulates phosphorylation of protein and alters enzyme activities to initiate a biological response

*loss-of-function mutations in GnRH causes sex hormone deficiency and delayed puberty (hypogonadotropic hypogonadism)

Loss-of-function mutations in GnRHR can lead to sex hormone deficiencies and delayed puberty (hypogonadotrophic hypogonadism).

34
Q

Steroid and Thyroid Hormone Receptor

A

Cytoplasmic/Nuclear Receptors

  • diffuse across the plasma membrane of target cells and bind to intracellular receptors in the cytoplasm or the nucleus
  • these receptors function as hormone-regulated transcription factors, controlling gene expression
  • nuclear receptors commonly share a transcriptional activation domain (AF1), a Zn2+ finger DNA binding domain and a ligand (hormone) binding/dimerization domain
35
Q

What can happen as a result of pituitary adenoma?

A
  • Loss of visual field (pressure on optic nerve)
  • Too much growth hormone, causing gigantism and acromegaly
  • Hypogonadism and infertility
  • Hypopituitarism (reduced pituitary function)
  • Too much ACTH secretion, causing excess cortisol secretion (Cushing’s syndrome)
  • Too much PRL (hyperprolactinaemia)
36
Q

What happens when you have hyposecretion of thyroxine from your thyroid glands?

A

Cause:
>Hashimoto’s disease, an autoimmune disease in which the immune system makes antibodies to the thyroid
>Seen more often in women and those with a family history of thyroid disease

Signs and Symptoms
>Induces decreased basal metabolic rate, increasing weight, bradycardia
>In terms of behaviour, induces cretinism, cognitive deficits, lethargy and depression
>In older people, it may follow radioactive iodine treatment, thyroid surgery or pituitary dysfunction

Complications
>goitre, heart failure, depression and slowed mental functioning, myxedema, birth defects
>Babies may be stillborn or premature with lower IQ later in life
>If left untreated can cause mental retardation, slow growth, cold hands and feet, and lack of energy among other things

37
Q

What happens when you have hypersecretion of thyroxine from your thyroid glands?

A

Hypersecretion occurs if there is too much thyroid hormone. This is known as hyperthyroidism or Grave’s Disease.

CAUSE:
Grave’s diseases is also an autoimmune disease. Antibodies attack the thyroid gland and mimic TSH so the gland makes too much thyroid hormone. It often occurs in women (20-50; with a family history of the disease).

SIGNS AND SYMPTOMS:

  • goitre (enlarged thyroid gland)
  • difficulty breathing
  • anxiety, irritability
  • difficulty sleeping, fatigue
  • rapid or irregular heartbeat
  • trembling fingers
  • excess perspiration, heat sensitivity
  • weight loss despite normal food intake

COMPLICATIONS:
heart failure
- osteoporosis
- pregnant women with uncontrolled Grave’s disease are at greater risk of a miscarriage, premature birth and babies with low birth weight
- Grave’s opthalmopathy (occurs if untreated, bulging eyes, relatively rare).

38
Q

What happens when there is a deficiency in adrenal hormones?

A

Adrenal insufficiency (AI) is also known as Addison’s disease. It occurs when the adrenals do not secrete enough steroids.

CAUSE:
The most common cause of primary AI is autoimmune.

SYMPTOMS:

  • fatigue
  • muscle weakness
  • decreased appetite and weight loss
  • nausea and vomiting and diarrhoea
  • muscle and joint pain
  • low BP, dizziness
  • low blood glucose
  • sweating
  • darkened skin on the face, neck, and back of hands
  • irregular menstruation
39
Q

What happens when there is hypersecretion in adrenal hormones?

A

Cause
>Excess cortisol secretion
>Exogenous Cushing’s syndrome occurs in patients taking cortisol-like medications such as prednisone for the treatment of inflammatory disorders e.g. asthma and rheumatoid arthritis or after an organ transplant
>Cushing’s Disease is when a pituitary tumour produces too much ACTH

SIGNS AND SYMPTOMS:

  • weight gain
  • rounded face and extra fat on the upper back and above the clavicles
  • diabetes, hypertension
  • osteoporosis
  • muscle loss and weakness
  • thin, fragile skin that bruises easily
  • purple-red stretch marks
  • facial hair in women
  • irregular menstruation

Physiology 2: Sem 3 (39 decks)

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