Emotion and Motivation Flashcards
What type of behaviour does the brainstem control? What evidence supports this?
Stereotypes, reflexive behaviour
- Chewing, swallowing, tastes
Evidence:
- Decerebrated rates cannot eat or approach food but can chew and swallow if food placed in mouth
- Mike the headless chicken
What are the main areas of the hypothalamus and what are their roles?
- Arcuate nucleus: food intake centre (NPY production)
- OVLT: homeostatic inputs (osmolality detection)
- Paraventricular nucleus: autonomic responses (metabolic rate control, decreased insulin secretion)
- Ventromedial centre: “satiety centre” and sex drive in females
- Lateral hypothalamus (LHA): “ hunger centre”
- Mammillary bodies: memory connection (hippocampus)
What are the inputs that the hypothalamus receives?
Homeostatic inputs:
- From OVLT
- Temperature and osmolality
Hormonal inputs:
- Ghrelin (increases sensitivity of NPY neurons)
- Leptin (inhibits NPY neurons and PVN signalling)
- Insulin (high glucose increases NPY)
- T3/4
- Cortisol
Somatic afferents:
- Olfactory, somatosensory, visual
- Controls melatonin production
Visceral afferents:
- Vagal nerve from brainstem
- Gustatory inputs (solitary tract)
Neural inputs:
- Limbic system (amygdala for emotional context)
What are the main mechanisms for satiety?
Short-term:
- Sensory signals: taste; smell (not enough as animals with gastric fistulas eat indefinitely)
- Gut hormones: CCK, reduction of ghrelin
- Gut-brain axis: stomach distension (feedforward)
Long-term:
- Leptin (shown by ob/ob mouse)
What are the outputs from the arcuate nucleus?
NPY/AgRP neurons = GABAergic:
- Increases feeding drive (LHA)
- Reduces metabolic rate, decreases insulin, increases lipolysis, decreases body temperature (PVN)
POMC neurons: CART transcripts and αMSH produced:
- Inhibits NPY
What evidence is there for the roles of NPY and αMSH from the arcuate nucleus?
NPY injection:
- Induces voracious eating (even with bitter food)
- Induces eating even paired with -ve stimulus (electric shock)
- Increases work put in to gain food
αMSH Function:
- αMSH receptor (MC-4) mutations can cause obesity
What are the outputs from the LHA?
Neuropeptides: Melanocyte concentrating hormones (MCH) and Orexin produced:
- Reduces metabolic rate: spinal cord control of autonomic NS
- Control of stereotyped behaviours (PAG)
- Influences complex motivated behaviour (VTA and nucleus accumbens)
What is the evidence that LHA (output) is both necessary and sufficient for feeding behaviour?
Sufficient for feeding: injections of MCH and orexin induce feeding; food deprived animals show higher levels of MCH and orexin mRNA in LH
Necessary for feeding: MCH knockout mice eat less than WT (consistently underweight)
Describe experimentation used to determine the mechanisms/brain areas involved in hunger and satiety signalling:
Lesions:
- Permanent: burn out or toxically inactivate (also damages upper regions E.g. dopaminergic bundles)
- Temporary: Intracerebral microinfusion
- Collateral damage to neuromodulator systems over-represents hypothalamic role
Selective lesioning of modulatory molecules:
- Dopamine neurons using 6-OHDA: causes aphagia (inability to swallow) and adipsia (absence of thirst) (similar to LH syndrome)
- Glutamate antagonist infusions: excitotoxin (AP-5 used inducing high Ca2+ (toxic causing cell death and further Ca2+ release)
- Excitotoxic animals do better (gain more weight) than electrolytic lesioned animals
What are the different stimuli for thirst? Where do they converge?
Osmometric thirst = interstitial fluid become hypertonic:
- Detected by osmoreceptors (stretch inactivated Na+) in OVLT
Volumetric thirst = blood volume decreases
- Detected by baroreceptors in the aortic arch - Vagal afferents to nucleus of solitary tract
- Cause juxtaglomerular apparatus secretion of renin and angiotensin II
Converge on median preoptic nucleus:
- Inputs: Stretch receptors on stomach and atrial baroreceptors
- Outputs: PVN for physiological mechanisms (ADH); LH for behavioural responses (drinking)
What is the mesolimbic system? How
Incentive motivation = potentiates apperceptive behaviour:
- Works in parallel with nigrostriatal dopamine projections
- Maps DA effect on brain regions involved in executive motivation and reward functions
Compare and contrast 6-OHDA and LH syndromes. What does this suggest?
6-OHDA taken up by dopaminergic neurons, causing reduction of DA production.
LH syndrome caused by electrolytic stimulation of LH.
Electrolytic method far more invasive (large 6-OHDA dose needed to compare)
Similarities (due to ascending DA system damage):
- Recovery trajectory: Acute aphagia and adipsia ➡ anorexia and adipsia ➡ adipsia with dehydration aphagia ➡ prandial drinking only ➡ residual deficits (E.g. to osmotic challenge and glucoprivation)
- Hypokinesia, catalepsy and neglect
Differences (LH cell function):
- Akinesia/sensorimotor deficiencies are DA related (LH cell independent)
- Regulatory mechanisms for homeostatic mechanisms (feeding, drinking etc…) have hypothalamic substrate – DA may converge on these mechanisms
What were the Olds and Milner experiments? What did they uncover?
Rats would self-administer (intracranial self-stimulation ICSS) small electric current through electrodes along mesolimbic DA pathway (including LH)
- Animals would powerfully want to press lever (over food; to exhaustion): suggests rewarding
- Measured how many mA of stimulation a particular stimulus was ‘worth’
Dopamine was responsibe:
- Increasing DA transmission decreases threshold
- DA receptor blocker increases reward threshold
- DA levels measured by microdialysis (rises in anticipation of sex/eating)
How is dopamine release influenced?
- State: more DA released if reward is needed (E.g. hunger increases reward value of food)
- Timing: maximum DA release occurs in anticipation of reward (rather than during)
Memory: required for anticipatory response
- Trained Pavlovian cue increases DA
- DA release occurs at earliest predictive cue before reward (DA release shifts to first cue when series of sequential cues trained)
What are the underlying principles of addictive drugs? How has addiction been modelled?
Different targets but all converge on dopaminergic system (VTA and NAc) increasing reward stimuli.
- Drug high is due to INCREASE in DA not absolute levels
- Drugs decrease D2 density level (requiring higher DA concentration for response)
Experimentation:
- Animals self-administer drugs to increase DA levels (level causing intravenous drug infusion)
- Will compensate amount infused per level press with number of times pressed (to cause high)
- Predisposition relevant (lower initial D2 receptor levels)
Describe the mechanism of action of two recreational drugs:
Cocaine:
- Blocks DA/5-HT reuptake transporters
- Increases DA/5-HT concentration in synaptic cleft
- Increases stimulation of DA receptors
Opioids (heroin):
- Binds µ opioid receptor (mimics natural agonist)
- Hyperpolarises GABAergic neurons causing inhibition of dopamine antagonist release
- Therefore DA effect increased
- Also reduces nociceptive stimulation (increasing pain tolerance)
- Increases µ opioid receptor density over time (causing withdrawal symptoms)
What are the classes of emotion? How do they manifest?
Primary = anger, disgust, joy, fear, sadness
Secondary = embarrassment, envy, love, guilt, nostalgia
Requires coordination of integrated physiological (endocrine/ANS), behavioural and subjective responses. Manifest as:
- Subjective feelings (verbal reports of)
- Behavioural (observations of actions)
- Psychophysical (bp, HR, plasma adrenaline, EEG, galvanic skin response)
What is the Schachter theory? What experimentation supports this?
Assimilation of bodily state and situational cues: Body state + appraisal of situation ➡ emotion/feeling.
Experimentation:
- Adrenaline (and placebo) injection in two groups (one placed in stressful; on in joyful environment).
- Informed subjects suppressed their natural tendency
- Uninformed subjects followed actor emotion
Which parts of the brain are useful for emotional processing?
- Insula activation: pairs with autonomic awareness
- Orbitofrontal cortex: assessment of pleasantness
- Amygdala provides stimulus value: pairs emotional significance to stimuli (and memory)
- NAc provides motivation for certain behaviour (Synergism crucial)
Discuss different experimentation types which have lead to understanding of amygdala role:
Klüver-Bucy syndrome (damage to temporal lobe, amygdala and hippocampus):
- Loss of fear (tameness)
- Hypermetamorphosis (exploration)
- Compulsive oral behaviour
- Suggests a disconnect between sensory and affective properties of stimuli (know which items are food due to past experiences)
FMRI studies show amygdala involvement in fear:
- Activation when shown fearful faces
Hypothalamic stimulation:
- Coordinates ‘switching on’ of stereotyped behaviours: stimulation in cats causes sudden aggressive behaviour
Lesion in basal lateral amygdala reduces effect:
- Causes disconnect between reinforcement and emotional connection
- Preparatory behaviour lost but retain consummatory behaviour (mating)
What are the inputs and outputs to different areas of the amygdala?
Medial/central nucleus = mainly physiological information/actions
- Sensory and neuroendocrine inputs (direct and indirect routes): olfactory ➡ medial; gustatory ➡ central
- Neuroendocrine/ANS/behavioural outputs (to hypothalamus/medulla)
Basolateral nucleus = mainly higher order
- Sensory (via thalamus/cortex) inputs
- Output: complex action selection ➡ ventral striatum/thalamus
Describe experimentation showing amygdala role in fear conditioning (pairing stimulus with emotional significance):
Freeze experiments with mice (pair light (CS) with shock (US))
- CS takes on value of US
- Requires PAG activation (a CPG controlling freezing)
- Lateral amygdala lesions impair conditioned freezing
Geller-Seifer test: reward vs. fear (from US) changes depending on context
- E.g. Fear suppressed when responding for food while hungry
