Lecture 17: The Limbic Brain Flashcards
What are the 3 primary ways the body uses energy
1) Basal metabolism: 55% of energy usage is to maintain body heat and other resting function (varies with body size).
2) Digestion of food: 33% of energy is used to process food and break it down into molecules to be used by the body.
3) Active behavioural processes: 12-13% of energy usage is for behaviours other than rest (varies greatly depending on activity level).
Remaining energy is typically stored as energy reserves. (In liver or as fatty tissue)
What are the 4 nutrients the body needs?
1)Carbohydrates (Saccharides): ~4 kcal* per gram, carbs get converted to glucose
and provide principle source of energy for brain and muscles. Storable form of carbohydrates are
called glycogens: stored in liver and muscles –
2. Amino Acids (Protein): ~4 kcal per gram. Comes from proteins, basic building
blocks for all cells. 20 amino acids, 9 cannot be produced by body = essential
amino acids. Amino acids can be converted to glucose.
3. Lipids (Fats): ~9 kcal per gram. Long term energy storage. Source of glucose. Fats
can be converted to free fatty acids as alternate energy source (essential).
4. Vitamins and Minerals: needed to assist in bodily functions (digestion, cell
building, homeostasis, etc.). Need to be sourced from diet. Not a source of
glucose. (essential)
Define a calorie
amount of energy (heat) needed to raise the temperature of water by 1 oC.
Why are carbohydrates not essential
short term storage (non-essential
from a building block perspective, and because they are not the only source of
glucose) We can get glucose from protein and lipids.
Describe traditional ideas like the glucostat theory
Traditional ideas (the “glucostat” theory: Mayer, 1954) saw absolute blood glucose as variable that needs to be at equilibrium:
– Glucose is the main source of energy
– Lack of glucose would represent nutrient deficit»_space; drive to eat
What are the two basic types of set-points thought to regulate food intake?
1)Glucostatic Set-Point Theory:
Eating is controlled by deviations
from a hypothetical blood glucose
set-point (Glucostat receptors)
2)Lipostatic Theory: Eating is
controlled by a hypothetical body-fat set-
point (long-term homeostatic
maintenance).
Describe the dual-centre hypothesis and evidence for it
There are two areas of the brain (the lateral hypothalamus and the ventromedial hypothalamus) which are hunger/satiety dedicated areas involved in starting to eat (LH) and stopping to eat (VH).
Research showed that lesions to the ventromedial hypothalamus increase feeding and weight + lesion to the lateral hypothalamus decreased feeding and weight.
Damage to lateral hypothalamus (LH) causes a large decrease in feeding (aphagia) & reduced body size.
Stimulation of LH using optogenetics leads to eating behaviour.
» Hunger center - start eating center
* Damage to the ventromedial hypothalamus (VMH) has opposite effect by increasing feeding (hyperphagia)
» Satiety center – stop eating center
Explain appetite as a mechanism to maintain homeostasis and how does it work
Appetite as a negative feedback homeostatic system based
competitions between hunger and satiety signals:
1. Dedicated drive signals indicating the need for nutrients
(hunger)
a) Lateral Hypothalamus
b) Hormones, e.g., Ghrelin, orexin
2. Dedicated signals relating to food ingestion (satiety)
a) Ventral Medial Hypothalamus
b) Hormones, e.g., CCK, PYY, Leptin
Problems with dual centre hypothesis and what was found instead through rat experiments
Self-stimulation experiments using electrical
stimulation:
* Rats were placed in skinner boxes with an
electrode attached to their lateral hypothalamus.
* Pressing a lever, delivered small electrical
currents to their lateral hypothalamus (i.e., self- activation of the LH)
* This was rewarding. Rats love this, and press more than they would for drugs like heroin.
* So if LH is the “initiate eating” or hunger
center, we should not see this behaviour.
If researcher stimulates the lateral
hypothalamus using an electrode to the LH,
does the animal eat?
* Yes, but, just as often, other behaviours occur (if there is food, the animal eats; if there is water available, the animal drinks; if there is an intruder in the cage of the rat, the animal fights; if there is a receptive female in the cage, the animal will mount the female)
» Effects of LH stimulation depend on the
situation. LH is not a dedicated hunger center, but more generally involved in motivated behaviours (including feeding).
- Where research has moved is that maybe there are dedicated receptors, or dedicated hormones that act on receptors. Maybe there are dedicated hunger or satiety hormones that play the role of the effector mechanism and lead to feeding or stopping feeding?
What are some hormones that could be related to hunger signals?
Ghrelin (growth=eating) and orexins (anorexia=not eating) are peptide hormones
secreted in the gut and from adipose tissue +
hypothalamus
* Orexin and Ghrelin administration increase hunger
What are some peptides that could be related to satiety signals?
1)Cholecystokinin (CCK) is a hormone released in the intestines in response to fat
– CCK injections inhibit subsequent feeding
2) Peptide YY (PYY) is also released in the gut in response to food
– Injections of PYY inhibit eating. PYY may be
abnormally low in obese individuals.
3)Leptin: Leptin discovered in obese mice.
* We now know that leptin is produced
by adipose tissue and interacts with six types of receptors (Leptin receptor)
* Leptin receptor is present in a number of hypothalamic nuclei, where it exerts its effects.
* Leptin binds to receptors in the ventromedial nucleus of the hypothalamus (i.e. what was thought to be the satiety center)
* Genetic leptin deficiency associated with obesity
What’s a behaviourist theory related to appetite?
Stimulation or reduction of appetite through
learned associations
* Stimulation of appetite through taste and
smell even when satiated/full
e.g. learned association with cinema and popcorn.
Motivation to eat or not in these cases does not depend on homeostatic mechanisms.
How does anticipatory eating behaviour show in babies
Prior to 3 months, babies are homeostatic machines.
They take large breast feeds first thing in the morning to relieve hunger when they wake up.
* At around 3-6 months they switch to a large feed last thing at night
– This large meal anticipates the relative difficulty of obtaining night-feeds. So this is not to relieve hunger, but in anticipation of possible hunger.
Evidence for anticipatory eating behaviours in rats
Rats are nocturnal animals – they eat and
drink when it’s dark, and sleep in the day.
They increase their intake of food and drink before the lights go off and going to sleep in anticipation to not having it as they sleep.
But this is not related to whether the lights are on or off. It is related to their own internal body clock. Rats eating & drinking is the same way even when they are always in the dark.
Describe cue-potentiated feeding in satiated rats by Peter Holland
Step 1: Pavlovian conditioning – cue (CS+) is paired with food delivery when hungry (CS- is unpaired control cue)
* Step 2: Satiate with free feeding (i.e., take away the homeostatic ‘drive’).
* Step 3: Play back Conditioned Stimulus (CS+) and it produces (over)eating.
This effect is due to influence of the amygdala on the lateral hypothalamus.
Peter Holland
Describe cue potentiated feeding in humans
Food specific visual and auditory cues enhance feeding in children.
The experiment involved children in a cafeteria eating their favourite food and as much of it as they wanted. Meanwhile the cafeteria would play different sounds and different coloured lights.
The day after they presented the same food and cues and the children showed increased consumption and speed of consumption than before.
How does deprivation relate to behaviour and motivation as a theory
There needs to be deprivation in order to have a drive/motivation for the behaviour.
What is one of the main motivators for why we eat apart from feeling hungry and needing it to survive?
Pleasure (as a reward e.g. eating an ice cream on a hot day vs. on a freezing day): Kent Berridge measured taste hedonics in humans and rats and found that they show tongue protrusions if they like something sweet and gaping if they dislike a bitter taste. Obliviously pleasure and reward relates to dopamine in the brain so it is expected that if the link is removed in the mesolimbic dopamine system of a rat, that it would decrease eating behaviour.
What was observed after causing damage to the mesolimbic dopamine system of a rat in terms of eating behaviour? What about when increasing dopamine activity in the
mice?
> Damage:
1. Animal became aphagic and adipsic
(didn’t eat/drink)
2. If forced to eat/drink, rats showed pleasure
responses and drank sweet but not bitter
solutions.
3. Depleting dopamine in the nucleus
accumbens makes rats aphagic but does
not change taste pleasure.
Increased dopamine:
Genetic mutation that increases dopamine activity makes mice want more sucrose, without changing their liking of sucrose.
Genetically altered mice with high dopamine levels ‘want’ food more (run faster for food) but ‘like’ it just as much (or even less).
Describe the dissociation between liking and wanting in nucleus accumbens
Wanting involved dopamine, liking involves opioid, GABA and cannabinoid systems in the nucleus accumbens.
Summarise how the areas of the brain are involved in eating and drinking behaviour
Regulatory processes interact with learned associations in the amygdala and the nucleus accumbens involved in liking/pleasure to initiate non-regulatory motivation.
Lateral hypothalamus and ventromedial hypothalamus involved in taste hedonics/aversions, learned associations in the amygdala and peripheral/hormone hunger and satiety signals in hypothalamus.
Overall interaction between the hypothalamus and the limbic system.
Briefly describe the structure of the limbic system and how it relates to the hypothalamus in eating and homeostasis
It involves the frontal lobe, thalamus, hippocampus, hypothelamus, amygdala and olfactory bulb.
Limbic brain areas such as cingulate cortex, hippocampus, amygdala and nucleus accumbens alter hypothalamic processes to
influence motivation and emotion.
Connections between the limbic system and hypothalamus integrate homeostatic and non-homeostatic mechanisms in feeding,
drinking (and temperature regulation).
