Motivation Flashcards

1
Q

What is motivation?

A

Driving force
Various factors control motivation:
- Physical need
- Wanting, liking

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2
Q

What role does the hypothalamus play in motivation?

A

Maintain homeostasis by regulating three interrelated functions
- endocrine secretion
- autonomic nervous system
- emotions and drive/behaviour
· Motivated behaviour, e.g. drinking, eating

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3
Q

What does loading and emptying of the body’s reserves entail?

A

Absorbed nutrients are used for the cells in your body but any excess glucose gets stored as triglycerides in adipose tissue and as glycogen in the liver and muscle
This is called anabolism
After hours the cells will still need nutrients so that’s when the triglycerides and glycogen get broken down to various nutrients for the cells
This is catabolism

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4
Q

What effect does parabiosis have on body weight in mice?

A

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

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5
Q

When is leptin produced?

A

Fatty tissues produce leptin when satisfied

Leptin travels to the arcuate nucleus of the hypothalamus and bind to leptin receptors to tell you to stop eating

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6
Q

What is the frontal section of the hypothalamus composed of?

A

Hypothalamus is found under the thalamus adjacent to the third ventricle of the brain
Contain small sub-hypothalamic nuclei
Paraventricular nucleus adjacent to the third ventricle
Lateral hypothalamic area below
Ventromedial hypothalamic nuclei below that
Arcuate nucleus at the base

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7
Q

What is ventromedial hypothalamic and lateral hypothalamic syndrome?

A

Lateral hypothalamic syndrome: diminished appetite for food; anorexia
Ventromedial hypothalamic syndrome: overeating and obesity
Both related to leptin signaling

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8
Q

What happens during an anorexic response?

A

The response to elevated leptin levels
A rise in leptin levels in the blood is detected by neurons in the arcuate nucleus that release peptides alphaMSH and CART
These neurons project axons to the lower brain stem and spinal cord, the paraventricular nuclei of the hypothalamus and the lateral hypothalamic area.
Each of these connections contributes to the coordinated humoral, visceromotor and somatic motor responses to increased leptin levels
The connection between the arcuate nucleus and the lateral hypothalamic area will induce inhibition of feeding behaviour
At the paraventricular nucleus of the hypothalamus will induce the release of corticotrophin releasing factor and thyrotrophin releasing factor which will be released in the portal system which will induce release of ACTH and TSH from the anterior pituitary and eventually cortisol and thyroxin which increases metabolism
Stimulation of the neurons to the brain stem and preganglionic neurons os the sympathetic ANS will activate sympathetic activity leading to increased metabolism and elevated temperature
As such alphaMSH and CART are anorexic peptides

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9
Q

What happens during an orexigenic response?

A

The response to decreased leptin levels
A reduction in blood levels of leptin detected by neurons in the arcuate nucleus in the hypothalamus which release another two important peptides; NPY and AgRP
These neurons inhibit the neurons in the paraventricular nuclei that control the release of ACTH and TSH
They activate the neurons in the lateral hypothalamic that stimulates feeding behaviour
Some of the activated lateral hypothalamic neurons contain the peptide MCH (melanin-concentrating hormone)

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10
Q

What substances compete for activation of MC4 receptor?

A

The anorectic peptide alphaMSH and the orexigenic peptide AgRP both induce their effects by acting on the MC4 receptor with opposing effects
The AgRP has an antagonistic role
This is one way peptides modulate feeding behaviour

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11
Q

What other peptides does the lateral hypothalamus use to stimulate feeding behaviour?

A

LH neurons stimulating feeding behavior contain:
- Melanin-concentrating hormone (MCH)
· Widespread connections in the brain
· Prolongs food consumption
- Orexin
· Also with widespread cortical connections
· Promotes meal initiation

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12
Q

What is satiety?

A

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

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13
Q

What are the three stages of digestion?

A

Three phases: cephalic, gastric, substrate (intestinal)
Cephalic- before consumption
- Saliva increase
- PNS and enteric activation
- Digestive juice secretion
Gastric- during consumption from mouth to distention of stomach
- Much more intense secretion when chewing and swallowing
Substrate/intestinal- food gets absorbed through intestine

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14
Q

What happens during the cephalic phase (hunger)?

A

Cephalic: hunger

- Ghrelin released when stomach is empty
- It activates NPY/AgRP-containing neurons in arcuate nucleus
- Removal of ghrelin-secreting cells of stomach thought to cause loss of appetite
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15
Q

What happens in the intestinal phase?

A

Intestinal Phase- satiety signals which ends meal
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

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16
Q

What are the natural rewards?

A
Natural rewards
Food
Water
Sex
Nurturing
Natural rewards such as food, water, sex, and nurturing allow the organism to feel pleasure when eating, drinking, procreating, and being nurtured.  Such pleasurable feelings reinforce the behavior so that it will be repeated.  Each of these behaviors is required for the survival of the species.
17
Q

What is the rewards pathway?

A

This is a view of the brain cut down the middle.
An important part of the reward pathway is shown and the major structures are highlighted: the ventral tegmental area (VTA), the nucleus accumbens and the prefrontal cortex.
The VTA is connected to both the nucleus accumbens and the prefrontal cortex via this pathway and it sends information to these structures via its neurons.
The neurons of the VTA contain the neurotransmitter dopamine which is released in the nucleus accumbens and in the prefrontal cortex
Note: the pathway is not the only pathway activated by rewards, other structures are involved too, but only this part of the pathway is shown for simplicity.

18
Q

Describe the stages of the addiction cycle?

A

Drug addiction is defined as a chronic relapsing disorder characterised by compulsive seeking of the drug, loss of control over drug taking and emergence of negative emotional states (anxiety, dysphoria, irritability) and physical states when the drug is not provided (withdrawal symptoms).
Drug intake begins with social drug-taking during which the drug induces a hedonic, pleasurable effect which will trigger further drug administration.
This is called positive reinforcement when drug taking is triggered by the positive, pleasurable effects of the drug which is process also triggered by natural rewards.
The mesolimbic dopaminergic system which consist of dopaminergic neurons projecting from the VTA to the Nacb are long been considered the major neurobiological substrate mediating all drugs positive reinforcement (including alcohol, opioids, cannabis, nicotine.
They all induce dopamine release in the nucleus accumbens.
After further administration of the drug, people tend to move to a pattern of escalating compulsive use due to tolerance and finally to dependence which is characterised by a state of emotional and physical withdrawal symptoms (anxiety, depression ect) in short and sometimes long periods of abstinence.
Now this negative emotional state triggers the craving, the wanting of the drug which will drive the drug administration which is called negative reinforcement.
In other words the aversive, dysphoria experience of drug withdrawal drives now the drug intake NOT the positive hedonic property of the drug.
Regions of the extended amygdala such as the amygdala, hypothalamus, hippocampus as well as nucleus accumbens and release of NA, CRF, GABA are known to be involved in the aversive negative reinforcement in dependent people.
There is a basically a transition from positive reinforcement in non dependent people to negative reinforcement in dependent people which drives the drug intake.
Relapse is very likely in the withdrawal period (induced by the drug itself, stressors, cues), and therefore the cycle is repeated.
Acute/long term withdrawal.
Million dollar question of how to prevent relapse

19
Q

What role does dopamine play in motivation?

A

Dopamine release in the nucleus accumbens is correlated with motivation but not liking (hedonic)
Its also release in anticipation of reward
Note that dopamine also involved in movement because it is a big part of motivation, the movement of going to get what you want

20
Q

What role does serotonin play in motivation?

A

Mood and food are connected
5HT in hypothalamus
- Rises in anticipation of food
- Spike during a meal (carbohydrates in particular)
- Association anorexia nervosa, bulimia with depression (low serotonin)