HNS55 Behavioural Neuroscience Flashcards
Brain, Cognition, Behaviour
Behaviourism: Study of observable behaviour (e.g. feeding)
Cognitive science: Study of mental processes (e.g. perception, thinking)
Neuroscience: Study of nervous system
—> different levels of explanations that are complementary
—> integration: Cognitive and Behavioural neuroscience
Motivation
Initiate, Maintain, Direct behaviour
Motivating factors (can be instincts):
—> Internal states (e.g. thirst, hunger, pain)
—> External stimuli (e.g. water, food, predator)
Instinct
Inborn (not learned) patterns of behaviour common to a biological species
e. g.
1. Infants’ attachment to parents (vice versa)
2. Fight, flight, freeze in response to danger
3. Feeding in response to food and hunger
Instinctive behaviour can be elicited by both Internal state + External stimuli —> Hypothalamus
Drive theory
Drive: mechanism of maintaining homeostasis —> internal state required for proper functioning
Need: deviation of internal state from normal range requiring correction (e.g. low blood glucose)
—> Drive: induce state of tension in the nervous system (e.g. hunger)
—> Behaviour: action that reduces drive (eating) and returns body to normal range
***Need —> Drive —> Behaviour —> Need
Hypothalamus
Maintains constant internal environment (Homeostasis)
- Receives multiple ***chemical signals through median eminence which lacks effective BBB
—> Chemical signals provide information about metabolic state of body
—> Hypothalamus respond to energy-deficient state
—> Activate Orexin neurons
—> ↑ Arousal and food seeking
GI tract: Episodic appetite signals
—> Appetite stimulating hormones: ***Ghrelin
—> Appetite inhibiting hormones: CKK, PYY, GLP-1
Body composition: Tonic appetite signals
—> Fat mass (inhibit appetite): ***Leptin
—> Fat-free mass (stimulate appetite): Resting metabolic rate, energy demand and drive to eat
Eating disorder
Hypophagia:
- Hypothalamic lesions
Hyperphagia:
- Ventromedial hypothalamic lesions
- Raised Ghrelin (Prader-Willi Syndrome - chromosome 15 micro-deletion)
- Leptin deficiency
Anorexia nervosa:
- suppressed eating despite ↑ Ghrelin and ↓ Leptin
—> indicate ↓ influence from Hypothalamus + ***↑ top-down control by cortical regions (e.g. Insula, Anterior cingulate, Prefrontal cortex)
—> due to distorted self-image
Incentives
- Drive theory cannot explain all behaviours
- Some people eat even not hungry
- Tend to eat more when greater variety of food available (e.g. Buffet)
—> Certain stimuli (food) have incentive (rewarding) properties that can motivate behaviour even in absence of internal drive
Incentives / Rewards: Powerful stimuli that can **alter behaviour / **induce learning
Associative learning - Beyond instincts
- Hard-wired instincts have evolved because they help animals survive and reproduce —> however it is rigid
- Ability to learn from past experiences —> further improve evolutionary “fitness”
- Behaviourism considers all animal behaviours: result of **Instincts + **Associative learning
- Classical conditioning
- Instrumental / Operant conditioning: Ventral striatum, Lateral hypothalamus
- Aversive stimuli: Amygdala
- Classical conditioning - Associative learning
- Associate 2 different stimuli —> Same response
- Dogs repeated exposed to pairing of sound with food —> develop salivating response to sound alone
Food: Unconditioned stimulus (US)
Food-induced salivation: Unconditioned response (UR) —> Instinctive
Sound: Conditioned stimuli (CS)
Sound-induced salivation: Conditioned response (CR) —> Learned
- Response is automatic (not under conscious control)
- when CS is dissociated with US —> eventually cease to elicit CR —> ***Extinction
- Instrumental conditioning - Associative learning
Positive reinforcement:
- Action consistently followed by a reward tends to ↑ in frequency
- Action: “Goal-directed”
- If reward cease to pair with action —> action ↓ in frequency —> ***Extinction
- Positive reinforcement slowed in Parkinson’s disease —> suggest involvement of ***Dopamine
Incentive salience and Dopamine
Stimuli with Positive incentive value (Reward)
—> elicit internal state of focused attention + eagerness for action (Incentive salience)
Incentive salience is mediated by Dopamine
—> via **Mesolimbic (Ventral Striatum: Nucleus Accumbens + Olfactory tubercle) + **Mesocortical pathway
(Dorsal striatum: Caudate nucleus + Putamen)
Food increases Dopamine
Reduction of Raclopride binding (used in assessment of D2 receptor binding capacity) following feeding in PET scan
—> Dopamine release induced by feeding
—> Food: example of natural reward
Intracranial self-stimulation
- Direct stimulations of some brain regions electrically / chemically can be a potent reward for positive reinforcement
- Regions: **Ventral striatum (Nucleus Accumbens) + **Lateral hypothalamus
—> normally activated by natural rewards (e.g. food) -
**Ventral striatum + **Lateral hypothalamus
—> Important for reinforcement learning
—> form a “reward circuit”
—> Dopamine play crucial role in circuit - Self-stimulation eventually become intensive —> “Compulsive” quality (at the expense of other behaviours e.g. feeding)
Drug abuse
1. Drug use Amphetamine (and others): ↑ dopaminergic neurotransmission —> activate ***Ventral striatum —> activates reward circuit —> reinforce further drug use
- Drug cues
When drug use become more frequent
—> external stimuli (e.g. needles, syringes) associated with drug use
—> elicit **craving for drug
—> drug use becomes less pleasurable, more compulsive
—> behaviour driven more by **Dorsal striatum (dopamine in Caudate nucleus + Putamen) than Ventral striatum
- Aversive stimuli - Associative learning
Aversive stimuli: Pain / other distressing sensations / situations
Behaviours that ↑ aversive stimuli —> become less frequent (Punishment)
Behaviours that ↓ aversive stimuli —> more frequent (Negative reinforcement)
***Amygdala: Important for associative learning of aversive stimuli
—> closely related to Hippocampus + Striatum
—> involved in emotion disorder (anxiety, phobias, depression)
