Motivation Flashcards
Define motivation
- A driving force
- Physical need (If your bladder is full then you go toilet)
- Wanting something
- Liking something
What is the role of the hypothalamus?
- Responsible for Motivation
- Maintains homeostasis by regulating 3 interrelated functions
- Endocrine secretions
- Autonomic nervous system
- Emotions and drive/behaviour (motivated behaviour)
What happens once you’ve eaten a meal?
- 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
What happens if the glucose, fatty acids and ketones are in excess?
- Any excess of these molecules gets stored as glycogen or triglycerides in the adipose tissues (Annabolism)
- Takes place during the prandial state
What would happen to these molecules in a fasting state?
- Glycogen is broken down into glucose for neurons
- Triglycerides are broken down into fatty acids
- Called catabolism
- Takes place during postabsorptive state
Describe the Intake and expenditure relationship in a normal/obese/starving individual
- Intake = expenditure = fat
- Intake > expenditure = Obesity
- Intake < Expenditure = Starvation
Describe the long term regulation of body weight
- 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
Define parabiosis
Sharing of blood circulation between animals
What are the effects of parabiosis on body weight in ob/ob mice?
- 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
What is the hypothesis generated from this experiment?
The Hypothesis was generated that this ob/ob protein is responsible for the regulation of feeding behaviour due to its activity on the mice
How was this hypothesis experimented on?
- 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
What was the results of this parabiosis experiment
- 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
What did Jeffrey Friedman later discover?
- 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
What happens to leptin in general?
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
Where is the hypothalamus found?
Found under the thalamus
- Located adjacent to the 3rd ventricle of the brain
What is the role of the ventral medial hypothalamus?
- Plays a role in controlling the cessation of eating
- Damage to the VMH results in prolonged and dramatic weight gain
What does lesions of the VMH lead to in mice?
- Led to ventromedial hypothalamic syndrome
- Characterised by over eating and obesity
What does lesions of the lateral hypothalamus lead to?
Led to the lateral hypothalamic syndrome
- Characterised by diminished appetite for food; anorexia
What is the correlation between both of these syndromes?
Both related to leptin signalling
Discuss the hypothalamic response to elevated leptin levels (PART 1)
- 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
Discuss the hypothalamic response to elevated leptin levels (PART 2)
- 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
Discuss the hypothalamic response to elevated leptin levels (PART 3)
- 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
Discuss the hypothalamic response to elevated leptin levels (PART 4)
- 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
What does the stimulation of ãMSH & CART lead to?
- Activate brain stem neurons and preganglionic neurons of the sympathetic activity
- This leads to increase metabolism and increased temperature
What type of response does ÃMSH and CART lead to?
An anorectic response by inhibiting feeding behaviours
How do we know that these neurons act as anorectic factors?
Injection of CART/ÃMSH in the brain mimics high concentrations of leptin
Where are the ãMSH and CART released from?
The Activation of the arcuate neurons release aMSH and CART peptides
What happens to decreased leptin levels? (PART 1)
- 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
What happens to decreased leptin levels? (PART 2)
- 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)
What type of peptides are NPY & AgRP?
- Orexigenic factors (stimulates appetite)
- Injection of NPY/AgRP mimics low concentration of leptin
What receptors does the ÃMSH and AgRP peptides act on?
MC4 receptors in the lateral hypothalamic area
What happens if there is competition for this MC4 receptor?
- 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
What happens during increased levels of Leptin in terms of AgRP?
AgRP levels are decreased causing more aMSH to bind to the receptor inhibiting feeding behaviour
What happens during decreased levels of Leptin in terms of aMSH?
aMSH levels are decreased causing more AgRP to bind to the receptor stimulating feeding behaviour
What other neurons in the hypothalamus can modulate feeding behaviour?
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
What is Orexin also involved in besides food stimulation?
Also involved in sleep regulation and addiction behaviours
Where is MCH and Orexin stimulated?
In the lateral hypothermic area
What is the role of the hypothalamus in the control of body weight and food intake?
- Motivated behaviour
- Accurately regulated by leptin produced by adipose tissue and hypothalamic peptides
- Hypothalamus plays an important role in regulating feeding behaviour (long term)
What does the disruption in the regulation of the hypothalamus lead to?
- Hyperphagia
- Anorexia
- Bulimia nervosa
What does motivation to eat also depend on?
- How long it has been since the last meal
- How much one has already eaten
- What type of food has already been eaten
Define satiety
The feeling of fullness and the suppression of hunger for a period of time after a meal
What can satiety influence?
Why does the feeling of satiety occur?
- 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
Describe the model for short term regulation of feeding graph
- 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
What happens to the body when it smells food?
Goes through 3 phases:
- Cephalic phase
- Gastric phase
- Substrate phase
What happens in the cephalic phase?
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
What happens in the gastric phase?
Much more intense secretions of digestive juices, enteric activation and sympathetic activation when chewing and swallowing
What happens in the sub rate (intestinal) phase?
- 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
