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.
