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BMS1052 > HYPOTHALAMUS 1 &2 > Flashcards

HYPOTHALAMUS 1 &2 Flashcards

1
Q

What does the hypothalamus do?

A
  • Secretes hormones into the blood
  • Has current state, sensory detector which then compares to set point goal
  • If too high, or too low then correction mechanism e.g. dilate blood vessels.
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2
Q

Where is the hypothalamus situated and what is it comprised of?

A
  • Sits on either side of the third cerebral ventricle (wall of ventrical)
  • Comprised of thin sheet of tissue in human (3-4mm either side of ventricle)
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3
Q

What types of neurons are in the paraventicular nucleus?

A
  • Magnocellular neurons (larger) (lateral from median eminence)
  • Parvocellular neurons (smaller), (medial to median eminence)
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4
Q

Where does the median eminence sit?

A
  • Base of the third ventricle
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5
Q

What is special about the portal blood vessels in the median eminence?

A
  • They are FINESTRATED (tiny pores in them) that allows substances to get in and out of blood vessels (this is unusual acception because blood-brain barrier usually so tight)
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6
Q

What is the hypothalamus connected to the pituitary by?

A
  • Infundibulum (stalk comprised of nerve fibres)
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7
Q

What is the pituitary gland divided into?

A
  • Anterior ( pars distalis)

- Posterior (pars nervosa)

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8
Q

What is the general function of the anterior pituitary gland?

A
  • “master gland”
  • Sends messages to the thyroid, adrenal and mammary gland
  • BUT controlled by hypothalamus
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9
Q

What do parvocellular neurosecretory cells produce in the paraventricular nucleus of the hypothalamus?

A
  • Neurohormones (releasing factrors)
  • These are released into the vicinity of portal vessels (in median eminence)
  • Then transported to the anterior pituitary
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10
Q

Which cells are in control of the anterior pituitary lobe?

A
  • Parvocellular neurosecretory cells
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11
Q

What do neuro-hormones transported to the anterior pituitary cause?

A
  • Release of hormones from specialised secretory cells
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12
Q

What are the releasing factors released from paraventricular nucleus neurons?

A
  • GnRH- Gonadotropin releasing hormone
  • TRH- thyrotropin releasing hormone
  • CRH- corticotropin releasing hormone (peptide)
  • GnRH- Growth Hormone Releasing Hormone
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13
Q

What do portal vessels do?

A

‘Port’ releasing hormones (GnRH etc) down through the small circulation into ANTERIOR PITUITARY
- Vessels are finestrated so releasing facors can EXIT circulation in vicinity of cells in anterior pituitary

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14
Q

Which types of cells are responsive to GnRH?

A
  • FSH (follicle stimulating hormone) prodcing cells

- LH (leutenising hormone) releasing cells

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15
Q

Which types of cells are responsive to CRH?

A

ACTH (AdrenoCorticoTropic Hormone) producing cells

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16
Q

Which types of cells are responsive to TRH?

A

TSH ( thyroid stimulating hormone) producing cells

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17
Q

Which types of cells are responsive to GHRH?

A
  • GH (growth hormone) producing cells
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18
Q

What hormones are part of gonadotrophs and what is their target?

A
  • FSH and LH, exits the anterior pituitary to work on gonads/reproduction
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19
Q

What hormones are part of Thyrotrophs and what is their target/function?

A
  • TSH- after being released from anterior pituitary into blood stream, acts on the thyroid
  • Function in development and energy expenditure
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20
Q

What hormones are part of corticotrophs and what is their target/function?

A
  • Adrenocotricotropic Hormone (ACTH)

- Works on the adrenal gland and mediates stress

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21
Q

What hormones are part of somatotrophs and what is their target/function?

A
  • Growth Hormone

- Widespread anabolic actions

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22
Q

Are there different cells producing SPECIFIC hormones in anterior pituitary that act on DIFFERENT targets in pituitary?

A

-YES!!!!!!!!

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23
Q

Where is stress detected and what does it lead to the release of ?

A
  • Physiological, emotional or psychological stress is detected in the BRAIN
  • Release of CORTICOTROPIN RELEASING HORMONE (CRH)
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24
Q

Where is CRH released from?

A
  • Nerve fibres originating from neurons in PARAVENTRICULAR nucleus of hypothalamus
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25
Q

What is CRH transported via?

A
  • Portal system down the pituitary stalk
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26
Q

Where is CRH transported to?

A
  • Anterior pituitary via the portal system (pituitary stalk)
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27
Q

Once at the anterior pituitary, what does CRH act on and what is released from this?

A
  • CRH acts on CORTICOTROPHS

- Causing release of Adrenocroticotropic Hormone (ACTH)-AKA corticotropin

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28
Q

What does ACTH act on?

A
  • Acts on the cortex of adrenal gland which causes release of CORTISOL
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29
Q

What does cortisol do?

A
  • Circulates in bloodstream and mobilises energy stores and supresses the immune system
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30
Q

Where is GnRH produced?

A
  • Neurons in preoptic area of hypothalamus
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31
Q

What is GnRH activity like and what factors is it under feedback control by?

A
  • Pulsatile (rhythmic) activity
  • Feedback control of some hormones
  • Also light stimuli (day length)–> some animals sync mating with day length
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32
Q

Where is GnRH released into and what does it act on?

A
  • Released into portal system

- Acts on gonadotrophs in anterior pituitary (LH release, FSH release)

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33
Q

What do FSH and LH do in males?

A
  • Produce testosterone and sperm
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34
Q

What do FSH and LH do in females?

A
  • Cause oestrogen release (cyclic release of LH and FSH- mestrual cycle)
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35
Q

What does the POSTERIOR pituitary have to do with?

A
  • Control of vasopressin and oxytocin release
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36
Q

What is another name for vasopressin?

A

-Anti-diuretic hormone

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37
Q

When is vasopressin released in Magnocellular neurons?

A
  • In response to hemorrhage or dehydration
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38
Q

What happens when you are dehydrated?

A
  • Increase in tonicity (osmality-conc.) of blood

- So plasma sodiums increase and this acts on OSMORECEPTORS (just in front of the hypothalamus)

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39
Q

Where do the sensors send neural connections?

A
  • To MAGNOCELLULAR neurons in the paraventricular nucleus that contain VASOPRESSIN
40
Q

What happens when you have a haemorrhage?

A
  • Same mechanism as dehydration
  • BUT cardiac volume receptors activated
  • Angiotensin II released
41
Q

What does angiotensin II do in relation to hemorrhage?

A
  • Acts on sensors in the brain that feeds into MAGNOCELLULAR neurons to produce VASOPRESSIN which leads to a feeling of thirst to help increase blood volume
42
Q

What are the similarities and differences in the losing blood and dehydration pathways?

A
  • DIFFERENT STARTING POINTS (osmoreceptors and angiotensin II) but the SAME END POINTS (magnocellular neurons to release vasopressin)
43
Q

How is the posterior pituitary mechanism different to the anterior pituitary?

A
  • After VASOPRESSIN, magnocellular neurons are activated
  • Vasopressin is taken down axons (without stopping in median eminence)
  • Goes straight to posterior ptuitary where it is dumped DIRECTLY INTO THE CIRCULATION (different to anterior)
  • Then goes out into bloodstream and it goes to kidneys to reduce urine output
44
Q

What is the difference between oxytocin and vasopressin?

A
  • Oxytocin is STILL produced in the paraventricular nucleus, STILL MAGNOCELLULAR but produced in DIFFERENT NERVE FIBRES and has DIFFERENT FUNCTIONS to vasopressin
45
Q

What happens when a baby is suckling?

A
  • Causes activation of sensory receptors in breast
  • Sends info via the spinal cord up into hypothalamus where it acts on OXYTOCIN containing neurons in PARAVENTRICULAR nucleus
  • Then goes down axons, gets released into blood vessels and taken out into peripheri
  • Acts on breast to let down milk and also acts on uterus to cause contractions (especially when oxytocin receptors build up before childbirth)
46
Q

Are there also emotional impacts on the same oxytocin neurons?

A
  • YES!
  • They don’t come from the simple reflex
  • Happens for lactating mums recognising baby crying that isn’t theirs
47
Q

What happens if an animal lacks vasopressin gene?

A
  • Urinates all day
48
Q

Are vasopressin and oxytonin produced by magnocellular neurons in posterior pituitary of ?

A
  • In the MAGNOCELLULAR neurons of paraventricular nucleus
49
Q

Are vasopressin and oxytocin also produced in parvocellular neurons? 0

A
  • YES! But are very different in these cells -acts as TRANSMITTER in brain to cause certain effects
50
Q

What do ocytocin and vasopressin have to do with in the parovocellular neurons of posterior pituitary and what is an example of this?

A
  • Love, monotony
    e. g. In prarie voles, monotomous, mutual grooming, looks after babies equally
  • Oxytocin and vasopressin released
51
Q

Are oxytocin and vasopressin released in the montane vole?

A
  • NO!
  • These voles have different distribution of receptors
  • One night stand mating and don’t look after babies at all really..
52
Q

What is the important factor during sexual activity important for forming a MONOGAMOUS pair bond with partner?

A
  • OXYTOCIN released into brain (from parvocellular, oxytocin containing neurons) from female during sexual activity
  • VASOPRESSIN seems to have a similar effect on males
53
Q

What is another thing that oxytocin can activate?

A
  • reward pathways in the brain (release dopamine)
54
Q

What can activation of reward pathways (in ventral pallidum) consolidate after mating?

A
  • Partner preference
55
Q

What is the human implication for magnocellular release of oxytocin?

A
  • Female reproduction
  • Released in large amounts during labour and suckling - Facilitator for childbirth and breastfeeding
  • Stimulant used to induce labour and speed up contractions
56
Q

What is the human implication for parvocellular release of oxytocin?

A
  • Potential role in orgasm. social recognition, bonding, maternal behaviour
  • Potential increased trust in people
  • Oxytocin higher in people who claimed to be falling in love
57
Q

What does oxytocin trigger the release of in reward pathways?

A
  • Dopamine and serotonin in, heightens feelings of intimacy and trust (even in strangers)
58
Q

Where is integration of endocrine and autonomic functions centred in?

A
  • Paraventricular nucleus of hypo

- Heart blood vessel, kidney, brown fat, adrenals are also mediated by the sympathetic nervous system **

59
Q

What is known as the ‘feeding centre’ ?

A

The lateral hypothalamus

60
Q

What is known as the ‘satiety centre’?

A
  • The ventromedial hypothalamus
61
Q

What is the lipostatic theory? (1960s)

A
  • Action between peripheri and brain in setting body weight
  • Brain monitors amount of body fat and acts to ‘defent’ THAT set amount of body fat (energy stores) from changes
  • Likely to be a link or messenger between body fat and brain
  • Messenger is a product of gene expressed in fat (OB gene)
62
Q

What does OB gene product do?

A
  • Circulates in blood and tells brain the extent of fat in the body
63
Q

What is the name for the factor circulating in the blood letting the brain know the extent of fat in the body?

A
  • Leptin (greek–> lepto=thin)
  • Increased metabolic weight
  • Decrese in glucose and insulin
64
Q

What was leptin a good fix for?

A
  • People that lacked the OB gene to produce leptin (didn’t benefit those that had a fine gene-so can’t cure obesity epidemic)
65
Q

Leptin will inhibit…

A

..neurons that promote feeding

66
Q

Leptin will excite…

A

..neurons that inhibit feeding

67
Q

What is the circuitry mediating LONG TERM energy balance?

A
  • Satiety centre in medial basal hypothalamus (1960s knowledge)
  • BUT not just satiety centre- that is the overall response that can be produced
  • Within it there are a number of competing drives (to eat or not to eat)
68
Q

Where is the arcuate nucleus?

A
  • Near the 3rd cerebral ventricle at the base of hypothalamus (near midline)
69
Q

Which types of neurons are in the arcuate nucleus?

A

Neuron that contains: Neuropeptide Y (NPY) + Agouti Related Peptide (AgRP)
- These produce an “orexigenic” effect (promotes feeding)

  • Second neuron (different set of neurotransmitters)
  • Contains Proopiomelanocortin (POMC) + Cocaine Amphetamine Regulated Transcript (CART)
  • “Anorexigenic effect” (prevents feeding)
70
Q

What does an oxigenic effect mean?

A
  • Promotes feeding
71
Q

What effect do NPY and AgRP have in the arcuate nucleus?

A
  • “orexigenic” effect (promotes feeding)
72
Q

What effect do POMC and CART have in the arcuate nucleus?

A
  • “anorexigenic” effects (prevents feeding)
73
Q

What is the motivation/predisposition to feed based on?

A
  • “dance” between the two types of neurons in the arcuate nucleus (relative activity of two neurons)
74
Q

What occurs in starvation?

A
  • Inhibitory break on peptides that promote feeding (NPY and AGrP) is removed
  • So feeding is stimulated (in lateral hypothalmic area) and there is reduced leptin to try and get back to higher body weight
  • Secretion of ACTH and TSH is INHIBITED so decrease metabolic weight
75
Q

What occurs in INCREASED levels of leptin?

A
  • Activate neurons with alpha MSH (product of POMC) and CART to now inhibit feeding!
  • Activate neurons in the paraventricular nucleus that increase metabolic weight
  • Drags back down to lower body weight
76
Q

What does the concept of ‘set point’ of body weight mean?

A
  • If we overeat for a period of time and put on weight THEN STOP, we will move back down to the appropriate (set) body weight.
  • If we under eat for a period of time THEN STOP, we will put back ON body weight until set weight is reached.
77
Q

Why is it so difficult to maintain weight loss in the LONG TERM?

A
  • Because metabolic adaptation occurs

- After week 30, actual energy expenditure is MUCH LOWER than predicted

78
Q

What is feeling of hunger before breakfast caused by?

A
  • hormone Ghrelin (produced in stomach)

- This rises just before you have a meal

79
Q

What happens as you have a meal in terms of Ghrelin hormone?

A
  • Levels of ghrelins start to plumet
80
Q

At the same time when you are having your meal, what signals are being produced?

A
  • Satiety signals (produced in different parts of the gut)
  • turned on and can go into blood
  • LIMIT food intake (‘i’ve had enough to eat)
81
Q

Is Ghrelin the ONLY HUNGER hormone?

A

YES!

82
Q

What are examples of satiety signals (that regulate body weight) ?

A
  • Cholecystekinin (CCK)
  • Insulin
  • Gastric Distension
  • Leptn
  • PYY3-36 (produced from small intestine)
  • Amylin (pancreas)
  • Ghrelin (from stomach)
83
Q

What does Gastric Distension do?

A
  • the more you eat food, the more your stomach swells–> sensory nerve fibres sense stretch and relay info to satiety centres in brain that say “I’ve had enough”
84
Q

How do changes in these hormones AFTER weight loss make it difficult to maintain weight loss?

A
  • Study done: 8 weeks on low calorie diet then return to normal ‘healthy diet’
  • compared hormones 4 hours after meals
    1. Baseline
    2. 10 weeks
    3. 62 weeks (about 1 year)
  • At 62 weeks, Ghrelin levels still elevated (red in graph)
  • Satiety hormones (that make you less hungry) normally go up after a meal BUT after 1 year they were still REDUCED! (PYY, Amlyin, CCK)
  • in people that have lost weight the desire to eat stays up!
85
Q

What is one pathway that sets our ‘set point’ of boy weight?

A
  • Things released from gut that act back on brain to modulate amount of energy expenditure there is
  • But there are complexities with reward associated with food (executive control from cortex)
86
Q

What does executive control from cortex affect?

A
  • Impact on motivation to eat, when and how (more cognintive)
87
Q

What does hedonstic mean in terms of eating?

A
  • Pleasure of eating
88
Q

What does hedonistic eating involve? ***

A
  • Excitation of dopaminergic neurons arising from ventrical tegmental area and projecting to basal forebrain
89
Q

What can reward be divided into in these pathways?

A
  • “liking” and “wanting”
90
Q

What is “liking” about?

A
  • Pleasure

- Hedonic ‘liking’ reactions are stereotypical and preserved across species and exist WITHOUT higher centres

91
Q

What are the key brain regions and neurotransmitters involved in the “liking” pathway?

A
  • Mediated by MU OPIOIDS acting at receptors in the nucleus accumbens
92
Q

What blocks “liking” pathways?

A
  • Mu opioid receptor agonist

- Reduces the liking of things that you previously liked

93
Q

What is the “wanting” pathway about?

A
  • Motivation (not pleasure) (Homeostatic)

- “incentive salience”

94
Q

What are the transmitters involved in the “wanting” pathway ?

A
  • Dopamine
95
Q

What does an increase in the dopamine levels in nucleus accumbens cause?

A
  • Does not change “liking” BUT increases the motivational component of reward (wanting-mediated by dopamine)
96
Q

What occurs in a herroin addict?

A
  • At the start, both the mu opioid (liking) and dopamine (wanting) are there, HOWEVER after a while (chronic over-stimulation)- of pathwat causes homeostatic response so will just be dopamine (but system will be downregulated- addiction)

BMS1052 (14 decks)

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