Motivation, Stress & Emotion MK Flashcards

1
Q

Hypothalamus

A

couples body states to systemic and neural-behavioural responses

The hypothalamus is a group of nuclei which INTEGRATE VITAL INFO:

  • sensory input
  • physiological input
  • direct smapling of blood and CSF
  • Time (internal clock, internal cues)
  • threat/stress information (amygdala and others)
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2
Q

What is the job of the hypothalamus?

A
  • Core of the CNS -
  • Head ganglion of the ANS
  • Group of nuclei concerned with body maintenance eg. feeding, drinking, sexual activity, sleep/wake cycle, hormones.
  • Homeostatic relfexes
  • Drives, which interact with memory, judgement and experience, to shape behaviour
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3
Q

which responses does it organise?

A

PITUITARY: for hormone output
AUTONOMIC CONTROL
influences behaviour via drives (thirst, hunger etc).

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4
Q

How does the pituitary control hormonal regulation

A

The pituitary, endocrine controller, is half CNS tissue (posterior) and half epithelial (anterior)

Hormone secretion from both are under direct hypothalamic control (also hormonal feedback)

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5
Q

Explain : DRIVES

A

‘drives occur when you force the cortex to help’
Drive = a motivation of behaviour to suit physiological (and more complex) needs.
Can be ignored at onset, biasing behaviour
- Become more dominant as the need increases
- Eventually push aside other behavioural considerations, judgement, taboos
- Satiety relieves pressure on behavoiur

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6
Q

Explain the THIRST drive

A

Low water in the body is detected byt he kidneys, vessel sensors, the hypothalamus (osmoreceptors in the lamina terminalis)

Acts on the lateral hypothalamus, influencing:
- –> the posterior pituitary: systemic ADH response (kidneys, vasculature)
–> Autonomics sustain BP via vasomotor centre
–> Limbic system (cingulate and amygdala) to cortex etc: behaviour (whatever gets the job done)
HORMONES & AUTONOMICS ARE A SHORT TERM FIX -> drive reflex = The hypothalamus creates a behavioural drive, thirst through

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7
Q

Explain the THERMOREGULATION drive

A

HYPOTHALAMUS monitors core temperature;

  • low in medial preoptic area
  • high in anterior hypothalamus

OUTPUTS:

  • anterior pituitary -> thyroid stimulating hormone : metabolic regulation (as appropriate),
  • autonomics (piloerection, blood flow, shivering, sweating)
  • limbic system (cingulate, amygdala) to CORTEX etc -> behavioural change: put on clothing, seek shade etc.
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8
Q

There is no drive for BLOOD PRESSURe, why?

A

Maintaining BP is important. - multiple levels of redundant control: pacemakers, renal arteries, brainstem
Changes in BP stimulate SNS and PSNS, alters pacemaking and cardiac output appropriately, BUT it doesnt create a behavioural drive, WHY?
Behaviour cant effect BP much, beyond the things the brainstem is already doing, so this information is not passed on to consciousness.

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9
Q

How do people get MOTIVATED?

A

Reward and reinforcement system:

  • Berridge made a useful distinction- between wanting and liking behaviour.
  • Wanting isa state or urgency, a way to sustain behaviour over long periods.
  • Liking is the positive reinforcement- the satisfaction when behaviour achieves a goal
  • You also have to figure out what you need
  • In neurobiological terms, this means reward systems influence the cortex and vice versa.
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10
Q

How is PLEASURE involved?

A

Pleasure is an added emotional dimension to an ordinary stimulus

  • a neural code- activity in the septal nuclei : tagging something we want to seek or do
  • Signalled independently, since we may change our minds about what’s pleasant.
  • For example, you can be driven to seek something without particularly enjoyin git
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11
Q

What is the anaotmy of seeking and reward?

A
Ventral Tegmental Area (VTA) - midbrain
Ventral pallidum (VP) - base of striatum
Nucleus accumbens (Acb) - basal forebrain
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12
Q

Explain a classical reward system

A

Forebrain dopamine systems are called the REWARD pathways of the CNS
VTA projects dopaminergic fibres to ventral forebrain as a motivator (drives action)
Nucleus Accumbens uses DOPAMINE to signal satiety ot the cortex- goal has been met, stop seeking now
- the goals of behaviour are negotiated

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13
Q

The brain works on a VALUE system -> explain.

A

VTA pushes motivation to the nucleus accumbens which is put into an unresolved state of ‘goal not met’ stage, ‘wanting’
The prefrontal cortex negotiates with nucleus accumbens with Acb about what needs to be done and when its been achieved.

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14
Q

Feedback on what we like/dislike

A

“Hedonistic” transmitters – opioids, GABA, endocannabinoids – are used to signal “good things”

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15
Q

Sugar and sweet

A

When we taste something sweet, neuronal firing INCREASES In nucleus accumbens etc. versus when we taste something salty, firing decreases.
BUT when we are salt depleted, sugar still tastes nice, but salt is more tasty, and neuronal firing is increased–> THE IDEA OF PLEASANT HAS CHANGED, because the needs of the mouse have changed

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16
Q

Evaluation

A

Cortex also feeds into evaluation process: we enjoy doing what we identify as worthwile and fun. -> through emotion
Emotion = evaluation: global, high level assessment of the current cognitive state:
ALL COGNITION HAS EMOTIONAL DIMENSIONS:
- a behavioural bias/preference (we behave differently in different emotional states)
- socially, emotion is communicated (eg. facial expressions, emotion behaviours, interpretation) - a signal to heed.

17
Q

what are the emotion related brain regions?

A
  • anterior cingulate cortex – forms emotional states which shape behaviour
  • orbitofrontal / ventromedial cortex – couples drive-related activity to behaviour motivation
  • anterior insula – visceral sensation, perhaps registering “gut reactions” to mental states
18
Q

What is the AMYGDALA for

A

Alarm and emotion centre
of the brain
- Activates when things are threatening or exciting
- Allows memory of emotional states by sending input to hippocampus
- Activated when we identify new threats based on experience, and reacts to them as well
- Often pre-conscious – triggered before you know why it was triggered (CNS hits panic button)

19
Q

ADRENAL GLAND

A
  • STRESS!!!

Stressors activate the SNS and the endocrine system

20
Q

What happens in ACUTE STRESS

A

Combined actions of the SAM axis and HPA axis act to fire up the somatic muscles and provide them with needed resources
(Nor)adrenaline released systemically, but also within the CNS from locus coeruleus
–positive cardiac chronotropic / inotropic effects
- bronchodilation; vessel effects (muscle, viscera)
- gluconeogenesis

21
Q

How does anxiety work?

A

when the senses pick up a threat the information goes:

  1. straight to the amygdala- gives out fear response: increased adrenaline , sweaty, racing heart, shut down GIT
  2. Roundaway: thalamus -> cortex -> if it is legitimate, back to amygdala to create fear response
22
Q

Explain the HPA axis

A

Paraventricular nucleus in hypothalamus secretes CRH (corticotropic releasing hormone) via posterior pituitary –> ACTH released by anterior pituitary —> cortisol and other glucocorticoids released by adrenals —> under normal conditions, cortisol feeds back to suppress CRH and ACTH

23
Q

What does cortisol do?

A
  • Essential for normal physiology
  • Normally secreted at low levels
  • Elevates on waking – fires you up
24
Q

What does chronic cortisol elevation cause?

A

Chronic stress causes overproduction of

cortisol for long periods, with many e

25
Q

What does chronic cortisol elevation cause in the cns?

A
- Blood-brain barrier does not apply to
steroid hormones (including glucocorticoids)-> chronic cortisol elevation has a range of significant e
26
Q

How does cortisol effect memory?

A

Cortical processing is affected: working memory is disrupted.
- Hippocampal stem cells have glucocorticoid
receptors which regulate neurogenesis
- Depression therapies all interact with this regulatory mechanism
- High cortisol impairs hippocampal output during REM sleep: long term memory formation is disrupted

27
Q

What are the knock on effects of high stress => high cortisol

A

Sleep is disrupted - less REM, more nREM, more waking (may -> insomnia)
- Insomnia and chronic cortisol elevation affect metabolism, including glucose intolerance and abnormal brain glucose uptake
Dietary shift – high fat/sugar – in some
- SNS secretes neuropeptide Y onto fat cells’ Y2R receptors, causing abdominal fat deposition
- “Metabolic syndrome” – type 2 diabetes (insulin insensitivity); coronary disease
- May depend on genetics, and epigenetics – including maternal stress