W10 - Neuro: Motivation Flashcards
What is motivation?
*Driving force
*Physical need
*Wanting, liking
What roles do the hypothalamus play?
*Maintain homeostasis by regulating three
interrelated functions
–endocrine secretion
–autonomic nervous system
–emotions and drive/behaviour
*Motivated behaviour, e.g. drinking, eating
How does the body’s energy system work?
a) Anabolism during the prandial state
This is where we eat food and is absorbed into the system and gets stored as glycogen and triglycerides turn into adipose tissue etc.
b) Catabolism during the post-absorptive state is
This occurs after about 8 hours of fasting. The system still requires food, so the previously stored energy sources are broken down.
Together this is called metabolism.
What are The long-term regulations of feeding
behaviour and body fat?
a) Intake = expenditure = normal adiposity
b) Intake > expenditure = obesity
c) Intake < expenditure = Starvation
What are the effects of Parabiosis on body weight in ob/ob mice
*Parabiosis: sharing of blood circulation between animals.
*Blood borne signals are shared and can affect the hypothalamus.
*Example 1:–A genetically obese mouse ob/ob: its fat cells do not produce leptin. (Leptin inhibits food intake)–Connected to a normal mouse (which produces leptin) will lead to a reduction of obesity in the ob/ob mouse.
They did an experiment with normal mice and ob ob mice, where the ob ob mice were obese. They found a way to create 2 mice with a shared circulatory system (like conjoint twins) with one normal mouse and one ob ob mouse. They found that the ob ob mouse started losing weight since the chemical regulating factor was crossing over to its brain.
What is Jeffrey Friedman: Discovery of Leptin?
Leptin means thin in Greek.
He isolated the leptin protein by separating ob ob mice into 2 groups, one with saline and the other with leptin.
How does feedback work?
Fatty tissues produce leptin when satisfied.
Leptin then travels to the brain to tell you to stop eating.
They relay this information to the Arcuate nucleus in the hypothalamus.
What role does the frontal section of the hypothalamus play?
Structures in descending order:
-The third ventricle sends messages to and receives messages from the lateral ventricles.
- Paraventricular nucleus - This is where the magocellular neurones and cell bodies project from to the posterior pituitary to release oxytocin and vasopressin.
- Lateral hypothalamic area
- Ventromedial Hypothalamic nuclei
- Arcuate nucleus
How did they investigate homeostasis, body weight and food intake from the hypothalamus?
Similar to the practical, they looked at VMH lesioned rat brain and brain of sister of lesioned rat.
They found that VMH-legioned rat showed a dramatic increase in food intake and body weight. In conclusion, the VMH plays a role in controlling the cessation of eating. Damage to the VMH results in prolonged and dramatic weight gain.
The ventromedial hypothalamus of the rat was damaged and her body weight was monitored for a year. Her sister was normal.
What is VMG and LH effects on food intake?
Lateral hypothalamic syndrome: diminished
appetite for food; anorexia
Venteromedial hypothalamic syndrome: overeating and obesity
Both related to leptin signaling
What is the Arcuate Nucleus?
Arcuate Nucleus: important for control of feeding (effect of leptin on arcuate nucleus)
What is the anorexic response?
Elevated leptin levels will get sensed by specialised neurones, whose cell bodies are found in the Arcuate nucleus. These neurohormones, release 2 peptide hormones (CART/a-MSH). These neurones project to axons to the lower part of the brain stem and spinal cord, the paraventricular nuclei of the hypothalamus, and the lateral hypothalamic area. Each of these are connections contribute to the coordinated humoral, visceromotor and somatic motor responses to increased leptin levels.
The neurones would induce the release of corticotrophic releasing factor and thyrotrophin releasing factor. CRH released in the portal system gets transported to the anterior pituitary, where they will induce the release of ACTH and TSH into the circulation, which will eventually release cortisol and thyroxine. This increases the basal metabolic rate, increasing metabolism.
Injection of CART/aMSH mimics high concentration of leptin
What is a response to elevated leptin levels?
*Activation of arcuate neurons that
release αMSH and CART peptides
–Anorectic peptides—diminish appetite
–Project to regions that orchestrate
coordinated response of humoral,
visceromotor, and somatic responses
*Paraventricular nucleus (humoral response)
*Intermediolateral gray matter of spinal cord
(visceromotor response)
*Lateral hypothalamus (somatic response)
What is orexigenic?
This contributes to the response to decreased leptin levels. A reduction in blood levels of leptin is detected by neurons in the arcuate nucleus that contain the peptides NPY and AgRP. These arcuate nucleus neurones inhibit the neurons in the paraventricular nuclei that control the release of TSH and ACTH from the pituitary, In addition, they activate the neurones in the lateral hypothalamus that stimulate feeding behaviour. Some of the activated lateral hypothalamic neurons contain the peptide MCH (melanin-concentrating hormones).
Injection of NPY/AgRP mimics low concentration of leptin, increasing appetite.
How does the competition for activation of the MC4 receptor work?
One way that a-MSH, an anorectic peptide and AgRP, an orexigenic peptide exert opposite effects on metabolism and feeding behaviour is via an interaction with the MC4 receptor on some hypothalamic neurons. While a-MSH stimulates the MC4 receptor, AgRP inhibits it.
MC4 receptor:
+ aMSH acts as an agonist, so activates it and inhibits feeding behaviour.
- AgRP acts as an antagonist, blocking the aMSH from binding to the receptor.
How is feeding controlled by Lateral Hypothalamic Peptides (2 other players)
*LH neurons stimulating feeding behavior
contain:
–Melanin-concentrating hormone (MCH)
*Widespread connections in the brain
*Prolongs consumption
–Orexin
*Also with widespread cortical connections
*Promotes meal initiation
This peptide is also connected to sleep -eg. Narcolepsy having very low levels of Orexin. It also plays a role in addiction.
How is bodyweight and food intake controlled?
Hypothalamus and the control of
bodyweight 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)
* Disruption of this regulation leads to
–Hyperphagia
–Anorexia
–Bulimia nervosa
How is feeding regulated in the short term?
*Motivation to eat also depends on:
-How long it has been since last meal
-How much one has already eaten
-What type of food has already been eaten
What is satiety?
*Satiety is the feeling of fullness and the
suppression of hunger for a period of time
after a meal
*Feelings of satiety can influence how soon
and how much you next eat
*The feeling of satiety occurs due to a
number of bodily signals that begin when a
food or drink is consumed and continue as
it enters the gut and is digested and
absorbed
What is the model for short term regulation of feeding?
Before meal:
- Satiety signals decrease continuously until 0
- This will induce feeding
- Orexigenic signals are high
During meal:
- Satiety signals continually increase.
- Orexigenic signals decrease along with feeding.
After meal:
-Will start to decrease again.
- Orexigenic signals will start to increase again.
What is the satiety cascade?
*Three phases: cephalic, gastric, substrate (intestinal)
1) Cephalic stage:
Sight of pancakes (before eating)
PNS and enteric activation
Saliva secretion
Digestive juices secretion
2) Gastric stage:
Much more intense secretions
when chewing/swallowing
3) Substrate (intestinal) stage:
CCK released by intestine in response to fatty food. Acts on vagus nerve to inhibit feeding
Insulin is a satiety signal
What happens in the Caphalic phase?
Short-Term Regulation of Feeding
(Cephalic phase)
*Cephalic: hunger
–Ghrelin released when stomach is empty
–Activates NPY/AgRP-containing neurons in
arcuate nucleus
–Removal of ghrelin-secreting cells of stomach
thought to cause loss of appetite. Eg. In bariatric surgery, when a large portion of the stomach is taken out, the Ghrelin-secreting cells are lost with it. This plays a role in the treatment for morbid obesity.
What are the short term regulation of feeding satiety signals?
–Gastric distension signals brain via vagus nerve.
–Works synergistically with CCK released in intestines in response to certain foods
–Insulin also released by β cells of the pancreas— induces satiety by acting on arcuate nucleus of the hypothalamus
What do we eat?
*We like food
–Hedonic aspect
*We want food
–Drive reduction
*Liking and wanting mediated in part by separate brain circuits
*Dopaminergic system involved in wanting/
craving (or liking?)
