NSCI 201 eating, drinking, motivation

what is motivation about?

• Behaviour

• Choice

• Goals

• Habits (motivation turns in habits over time)

• Emotions

• Values

• Hedonism

• Learning

Regulatory vs purposive motivation

Regulatory motivation

• External control

• Focused on rules, consequences, pressure

• Driven by rewards & punishments

• “I have to do this”

Purposive motivation

• Internal meaning

• Focused on goals, values, identity

• Driven by purpose & intention

• “I want to do this

Regulatory = Rules
Purposive = Purpose

ex. external (grades) vs internal (enjoyment)

Habit vs Goal-directed

Habit

• Automatic

• Triggered by cues

• Little conscious thought

• Hard to change

Goal-Directed

• Deliberate

• Based on outcomes

• Flexible and thoughtful

• Sensitive to consequences

Habit = Auto
Goal-directed = Aware

Model-free vs model based

Model-Free

• habit system

• don’t have to think about it

Model-Based

• need a pathway/ need to think about it before you do it

• ex. thinking about how you will change your pathway to the bus
  Model-Free = React
  Model-Based = Reason

seeking appetitive outcomes vs avoiding aversive outcomes

• we approach things we like and avoid things we don’t like

• the hedonic axiom

Preference vs persistence vs vigour

• persistence: if we like something we will spend more time one it

• vigour: you will put in more effort into something that your like

Averages vs individual differences

• ex. finding the differences between all ubc students vs ubc neuro students

Homeostasis

• the bodys regualtory system

• main goal is maintainign a set point like a thermostat

• the hypothalamus seems to regulate many aspects of homestasis

What are the three components to homestasis response?

1. Humoral response

   1. hormone: a change in endocrine system

   2. a change in your glands that release hormones

2. visceromotor response

   1. sympathic and parasympathetic systems

   2. efferent system

3. somatic motor response

   1. involuntary: outside of conicous control

   2. voluntary: you have thought and act on it conscious

**these components are all driven by different parts of the brain

homorones vs neurotransmitters

• homorones: are released in blood stream

• neurotransmitters: are electrically sent (not via blood stream)

Example of homeostatic response when you are cold?

1. Humoral response:

   1. Thryoid releasing hormone (TRH) in hypothalamus (Hth) is released

   2. antioeri pituary gland released throid stimulate homrone (TSH)

   3. T4 and T3 thryoid horomes are released

   4. hormones increase metabolism which generates warmth

2. Visceromotor response:

   1. increased sympathetic NS activty

   2. contrict blood to your core

   3. increased heard rate

   4. breakdown of fat and glycogen for energy (into ATP)

   5. helps generate heat

3. Somatic motor response

   1. involuntary (shivering)

   2. Voluntary (going inside/seeking warm)

**all these responses involve the hypothalamus

what is a hypothesis for why do we eat and why may this be inaccurate?

Hypothesis: we start/stp[ eating to maintain “balance” fro energy in our bodies

-but energy deficits are super rare!

What is body mass index

• BMI

• tool used to understand ratio between hieght and weight

• in kg/m²

what is considered overweight and obese with the BMI

• overweight: BMI = 25-29

• obese: BMI = 30+

what stigmas are around obesity?

• soical

• self

• cultural

does oiesty cause health issues?

• not cause, but correlated

what health risks are obesity correlated with?

• cariovascular diease (CVD)

• diebates (type 2)

• sleep apnea

• some cancers

how many people who are consider overweight/oibese dont have health issues?

• more than 50% of people that are considered overwieght are healthy

• more than 30% of people are considered obese are healthy

what is obese survival?

• paradoxical

• is someone has cancer they may have some what of a higher chance to survive it they obese compared ot someone who is not

what are the 2 basic proposed mechanisms on eating?

1. lipostatic (longer term)

2. glucostatic (shorter term)

lipostatic theory on eating

• fat is providing some sort of signalling about your body weight

Glucostatic theory on eating

• “blood sugar”

• glucose

• proposes that short-term appetite is regulated by blood glucose levels, with decreasing glucose utilization in the brain triggering hunger and high levels causing satiety

Prandial state

anabolism

anabolism

body is in storing energy mode.

→ glycogen: stored in muscles but they have limits

→ fat stored all around the body

postabsorptive state

catabolism

catabolism

breakdown of energy storage

→ breaking down glycogen and fats

Leptin

• protein hormone secreted by fat cells

• fat cells aren’t galnds even though they release the hormone

• more fat = more leptin in the blood stream

ob/ob mutations in mice

• ob/ob: double recessive gene in mice

• stands for obesity

• mice would eat excessivly and gain a lot of wieght

• if they were injected with aritifcal dose fo leptin then they didn’t become obese/would go back to their normal body weight

*note: these mutation in humans are very rare and did not explain human obesity

Ghrelin

• hunger hormone

• released by the gut

Lateral hypothamalus’s (LH) role in eating stimulated vs lesion

• when stimulated in animals, these animals will be eating

• when lesion, will cause:

  • aphagia: not eating when you should

  • adipsia: not drinking when you should

ventromedial hypothalamus (VMH) role in eating

• oppsite effect of LH when stimulated the animals stop eating

• when lesion:

  • Hyperphagia: higher amounts of eating than usual

Arcute nucleus

• has multiple neuron types that detect leptin levels in blood

• lots of porous spots that detect leptin

What hypothalamic neurons detect leptin (in response to eating alot) and what do they release?

• detected in arcutate nucleus that release neuropeptide alphaMSH and CART

• these are part of the anorectic pathway meanign that they suppress eating

• the neuropeptides will be projected into the PVN, brainstem, and LH via the arcute nuclues axons

neuropeptide

• large molecules part of proteins

How does the PVN contribute to leptin’s effects?(in response to eating alot)

• after it recieves the alphaMSH and CART

• it will release hormones (CRH, TRH) which stimulat ehte release of ACTH and TSH from anterior pituitarty

How does the Brain stem/spinal cord contribute to leptin’s effects?(in response to eating alot)

• stimulates the sympatheic NS

• breaks down glycogen and promtoes loss of fat

How does the LH contribute to leptin’s effects?(in response to eating alot)

• inhibts feeding

What happens when lepin levels decrease (due to a decrease in eating)?

• arcute nuclues detects the drop of leptin levels

  • released neurpeptides called NPY and AgRP

• are orexigenic pathway

  • stimulating eating

• projects into the PVN, and LH

• there is also a decrease in sympathic output and shifting balance to the parasympathetic NS

What happens to the PVN when leptin levels drop?

• recieves NPY and AgRP

• inhibits release of ACTH and TRH to ant. pit.

• decreases metabolism to save energy

What happens to the LH when leptin levels drop?

• stimulate feeding behaviour

• voluntary motor response

what type of neurotransmitter is in the LH

• MC4 receptor

  • is a G-protein-coupled-receptor

• antagonistic

• is like “the switch” in LH

How do α-MSH and AgRP interact at the MC4 receptor?

• α-MSH binds to MC4 → activates the receptor → tells the neuron to inhibit feeding.

• AgRP binds to MC4 → blocks or inhibits the receptor → tells the neuron to promote feeding.

• Competition:

  • Only one ligand can “control” the receptor at a time.

  • So if α-MSH is bound, the receptor is active → feeding suppressed.

  • If AgRP binds first or is in higher concentration, it blocks α-MSH → feeding promoted.

• like tug-a-war

How does the LH drive feeding behaviour?

1. LH receives a signal from arcuate neurons (e.g., when you’re hungry) to start driving feeding.

2. LH neurons release MCH and orexin (hypocretin).

3. MCH neurons release:

   • GABA: suppresses inhibitory signals from other neurons (like PVN neurons) that would stop feeding. Think of it as “removing the brakes.”

   • Glutamate: excites feeding circuits, helping to drive eating behavior.

4. Orexin neurons: project to VTA and nucleus accumbens (NAc), increasing dopamine → enhancing motivation and reward for eating.

5. Both MCH and orexin are orexigenic neurotransmitters (promote feeding).

co-occurrence

• neurons that release 1 molecule and a large molecule

Short-term regulation of feeding behavior

refers to the mechanisms that tell you when to start and stop eating during a single meal, rather than long-term body weight regulation.

Old theory of short-term regulation of feeding

glucostatic hypothesis

• Idea: changes in blood glucose levels signal the brain to start or stop eating.

• Low blood glucose → feel hungry → eat.

• High blood glucose → feel full → stop eating.

• Insulin regulates blood glucose.

• Because of this, scientists thought insulin levels could also signal short-term feeding behavior

• no longer the believed theory

lipolysis

• breakdown of fat

What are the three stages of short term feeding behaviour?

1. Cephalic (brain)

2. gastric (stomach)

3. intestinal (intestines)

Describe the cephalic phase of short-term feeding behaviour

• signal: ghrelin (empty stomach)

• grhelin will activate NPY/AgRP neurons of arcute nuclues

• this promotes feeding behaviour

Describe the Bastric and intestinal phase of short term feeding behaviour

• signals: Gastric distension (sensory signal from when intestines get stretched mechonreceptors will sense it) (vagus nerve - 10th cranial nerve), CCK, PYY, GLP-1 (intestine), insulin (pancreas)

• projects to the nucleus of the solitary tract

• inhibits feeding behaviour

What are predication of these homesotatic mechaims for eating?

• Hunger/eating triggered by changes in blood sugar

• Hunger/eating suppressed by increases in body fat

• There must be accompanying body/brain mechanisms for initiation/cessation of these motivated behaviours

• We should probably “know” what to eat and when

• Body weights should be stable

• Unrelated stimuli should not influence eating

• Taste/flavour is relatively unimportant