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SGUL - Physiology 2 > Motivation > Flashcards

Motivation Flashcards

1
Q

Define motivation

A
  • A driving force
  • Physical need (If your bladder is full then you go toilet)
  • Wanting something
  • Liking something
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2
Q

What is the role of the hypothalamus?

A
  • Responsible for Motivation
  • Maintains homeostasis by regulating 3 interrelated functions
  • Endocrine secretions
  • Autonomic nervous system
  • Emotions and drive/behaviour (motivated behaviour)
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3
Q

What happens once you’ve eaten a meal?

A
  • Once you’ve eaten your meal, nutrients gets absorbed via the intestines into your blood circulation
  • Glucose, fatty acids and ketones go onto feeding all cells and neurons
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4
Q

What happens if the glucose, fatty acids and ketones are in excess?

A
  • Any excess of these molecules gets stored as glycogen or triglycerides in the adipose tissues (Annabolism)
  • Takes place during the prandial state
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5
Q

What would happen to these molecules in a fasting state?

A
  • Glycogen is broken down into glucose for neurons
  • Triglycerides are broken down into fatty acids
  • Called catabolism
  • Takes place during postabsorptive state
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6
Q

Describe the Intake and expenditure relationship in a normal/obese/starving individual

A
  • Intake = expenditure = fat
  • Intake > expenditure = Obesity
  • Intake < Expenditure = Starvation
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7
Q

Describe the long term regulation of body weight

A
  • When there is a period of starvation, the body weight begins to drop
  • When there is a period of force feeding, the body weight begins to increase
  • When the Force feeding stops, the Body weight levels goes back to its homeostatic levels
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8
Q

Define parabiosis

A

Sharing of blood circulation between animals

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9
Q

What are the effects of parabiosis on body weight in ob/ob mice?

A
  • Blood borne signals are shared and can effect the hypothalamus
  • E.g 1. A Genetically obese mouse ob/ob: it’s fat cells do not produce leptin (Leptin inhibits food intake)
  • Was Connected to a normal mouse (Which produces leptin)
  • Lead to a reduction of obesity in the ob/ob mouse
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10
Q

What is the hypothesis generated from this experiment?

A

The Hypothesis was generated that this ob/ob protein is responsible for the regulation of feeding behaviour due to its activity on the mice

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11
Q

How was this hypothesis experimented on?

A
  • They fused a normal mouse with an ob/ob mouse
  • They done this so they both have a common blood circulation
  • They observed the behaviour of these mice over time
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12
Q

What was the results of this parabiosis experiment

A
  • The ob/ob mouse started reducing its feeding behaviour and started losing weight
  • From really obese, it eventually had the normal weight as it’s normal counterpart
  • This proved the hypothesis to be correct that the ob/ob protein causes obesity
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13
Q

What did Jeffrey Friedman later discover?

A
  • He managed to separate the ob/ob protein into Leptin and Saline
  • He proved that leptin was responsible for the regulation of feeding behaviour
  • Done so by taking the obese mice, injected one group with saline and the other with leptin
  • The Saline group remained obese
  • The leptin group reduced their weight to normal levels
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14
Q

What happens to leptin in general?

A

Following an energy rich meal
- adipose tissues get replenished with fat
- As a result, fatty tissues produce leptin into blood when satisfied
- Leptin travels to the brain acting on leptin receptors found in the hypothalamus
- which suppresses feeding behaviour

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15
Q

Where is the hypothalamus found?

A

Found under the thalamus
- Located adjacent to the 3rd ventricle of the brain

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16
Q

What is the role of the ventral medial hypothalamus?

A
  • Plays a role in controlling the cessation of eating
  • Damage to the VMH results in prolonged and dramatic weight gain
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17
Q

What does lesions of the VMH lead to in mice?

A
  • Led to ventromedial hypothalamic syndrome
  • Characterised by over eating and obesity
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18
Q

What does lesions of the lateral hypothalamus lead to?

A

Led to the lateral hypothalamic syndrome
- Characterised by diminished appetite for food; anorexia

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19
Q

What is the correlation between both of these syndromes?

A

Both related to leptin signalling

20
Q

Discuss the hypothalamic response to elevated leptin levels (PART 1)

A
  • A rise in leptin levels in the blood is detected by neurons in the acuate nucleus contains peptides ãMSH & CART
  • These neurons project axons to lower brain stem and spinal cord, the paraventricular nuclei of the hypothalamus & lateral hypothalamic area
21
Q

Discuss the hypothalamic response to elevated leptin levels (PART 2)

A
  • Each of these connections contribute to the coordinated humoral, viscermotor and somatic motor responses to increased leptin levels
  • This induces the inhibition of feeding behaviour by ãMSH
  • ÃMSH is also projected to the paraventricular nucleus
22
Q

Discuss the hypothalamic response to elevated leptin levels (PART 3)

A
  • These neuron’s will induce the release of corticotrophin releasing factors as well as fibrotrophin releasing factors
  • TRH &CRH will be released in the portal system and transported to the anterior pituitary
  • This will induce the release of ACTH and TSH in the blood circulation
23
Q

Discuss the hypothalamic response to elevated leptin levels (PART 4)

A
  • This induces the release of thyroxine and cortisol as adrenal and thyroid glands
  • Elavated levels of Thyroxine and cortisol causes an increase of basal metabolic rate increasing the metabolism
24
Q

What does the stimulation of ãMSH & CART lead to?

A
  • Activate brain stem neurons and preganglionic neurons of the sympathetic activity
  • This leads to increase metabolism and increased temperature
25
Q

What type of response does ÃMSH and CART lead to?

A

An anorectic response by inhibiting feeding behaviours

26
Q

How do we know that these neurons act as anorectic factors?

A

Injection of CART/ÃMSH in the brain mimics high concentrations of leptin

27
Q

Where are the ãMSH and CART released from?

A

The Activation of the arcuate neurons release aMSH and CART peptides

28
Q

What happens to decreased leptin levels? (PART 1)

A
  • A reduction in leptin blood levels is detected by neurons in the arcuate nucleus containing NPY & AgRP peptides
  • These arcuate neurons inhibit neurons in the paraventricular nuclei that control the release of TSH & ACTH from the pituitary
29
Q

What happens to decreased leptin levels? (PART 2)

A
  • In addition, they activate the neurons in the lateral hypothalamus that stimulate feeding behaviour
  • Some of the activated lateral hypothalamic neurons contain the peptide MCH (melanin concentrating hormone)
30
Q

What type of peptides are NPY & AgRP?

A
  • Orexigenic factors (stimulates appetite)
  • Injection of NPY/AgRP mimics low concentration of leptin
31
Q

What receptors does the ÃMSH and AgRP peptides act on?

A

MC4 receptors in the lateral hypothalamic area

32
Q

What happens if there is competition for this MC4 receptor?

A
  • ÃMSH plays an agonistic role and activates the MC4 receptor which inhibits feeding behaviour
  • AgRP plays an antagonist role by blocking the ãMSH from acting on the MC4 receptor stimulating feeding behaviour
33
Q

What happens during increased levels of Leptin in terms of AgRP?

A

AgRP levels are decreased causing more aMSH to bind to the receptor inhibiting feeding behaviour

34
Q

What happens during decreased levels of Leptin in terms of aMSH?

A

aMSH levels are decreased causing more AgRP to bind to the receptor stimulating feeding behaviour

35
Q

What other neurons in the hypothalamus can modulate feeding behaviour?

A

LH neurons stimulating feeding behaviour contain:
- Melanin concentrating hormone (MCH)
- Widespread connections in the brain
- Prolongs consumption

Orexin
- Also with widespread cortical connections
- Promote meal initiation

36
Q

What is Orexin also involved in besides food stimulation?

A

Also involved in sleep regulation and addiction behaviours

37
Q

Where is MCH and Orexin stimulated?

A

In the lateral hypothermic area

38
Q

What is the role of the hypothalamus in the control of body weight and food intake?

A
  • Motivated behaviour
  • Accurately regulated by leptin produced by adipose tissue and hypothalamic peptides
  • Hypothalamus plays an important role in regulating feeding behaviour (long term)
39
Q

What does the disruption in the regulation of the hypothalamus lead to?

A
  • Hyperphagia
  • Anorexia
  • Bulimia nervosa
40
Q

What does motivation to eat also depend on?

A
  • How long it has been since the last meal
  • How much one has already eaten
  • What type of food has already been eaten
41
Q

Define satiety

A

The feeling of fullness and the suppression of hunger for a period of time after a meal

42
Q

What can satiety influence?
Why does the feeling of satiety occur?

A
  • Can influence how soon and how much you next eat
  • The feelings of satiety occurs due to a number of bodily signals that begin when a food or drink is consumed
  • Continues as it enters the gut and is digested and absorbed
43
Q

Describe the model for short term regulation of feeding graph

A
  • The graph shows a possible means of regulating food consumption by satiety signals
  • Satiety signals rise in response to feeding
  • When satiety signals are high, food consumption is inhibited
  • When satiety signals fall to zero, inhibition is elimated and food consumption ensues
44
Q

What happens to the body when it smells food?

A

Goes through 3 phases:
- Cephalic phase
- Gastric phase
- Substrate phase

45
Q

What happens in the cephalic phase?

A

Cephalic: hunger
- Ghrelin released when the stomach is empty
- Activates NPY/AgRP containing neurons in the arcuate nucleus
- Removal of ghrelin secreting cells of stomach thought to cause loss of appetite

46
Q

What happens in the gastric phase?

A

Much more intense secretions of digestive juices, enteric activation and sympathetic activation when chewing and swallowing

47
Q

What happens in the sub rate (intestinal) phase?

A
  • Food gets transported from the extended stomach to the intestine
  • Gastric distension signals brain via vagus nerve
  • Work synergistically with CCK released in intestines in response to certain foods
  • Insulin also released by Beta cells of the pancreas
  • Induces satiety by acting on arcuate nucleus of the hypothalamus

SGUL - Physiology 2 (37 decks)

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