BIOL 2052 - Pleasure and Behaviour

pleasure

• powerful influence over behaviour and choices we make

• consimung pleasurable foods drives us to seek out more of those foods

eating and reward

• eating serves an essential role in homeostasis

• food intake can also be affected by the pleasurable effects of food

• the pleasure of eating food, driven by the “liking” reaction in the brain (also called hedonic circuits)

• hedonic feeding driven by the pleasure of consuming food —> component of reward

• 3 main components make up reward:

  • liking

  • wanting (also referred to as incentive salience)

  • learning - make associations and prediction reward value

• motivational circuit can be activated by specific sensory cues like seeing or smelling good tasting food

eating disorders

• can induce obesity, bulimia, anorexia

• obesity associated with reduced life expectancy and a range of diseases (liver, respiratory conditions, T2D)

homeostatic circuitry

• circuit which drives us to seek out food to maintain constant levels

• key component is the hypothalamus

• recieve signals from the pancreas and brain stem which can change activity

• 2 types of neurons:

  • orexigenic: increase appetite

  • anorexigenic: decrease apetite

reward circuit

• olds and milner: identified reward centre in brain by delivering electrical activity to a certain region of the brain via an electrode

• mice self administered stimulation of the brain —> chose to stimulate the reward region of the brain over and over

• position of teh electrode was changed and the experiment repeated as a control

circuitry

• the reward system is the neural network that recieves and evaluates the rewarding properties of stimuli

• network consists of multiple interacting neural circuits

• robust self stimulation behaviour obtained with electrodes along the medial forebrain bundle

• self stimulation observed from electrodes located in several brain areas including:

  • nucleus accmubens

  • lateral hypothalamus

  • ventral tegmental area

  • cortical structures (insula cortex, orbitofrontal cortex)

key structures of reward circuit

• medial forebrain bundle

• reward circuit that includes axons that project from the VTA —>Nac (mesolimbic dopamine pathway)

• hypothalamus recieves inputs from structures within reward circuits)

hedonic vs neural motivational

• conserved facial expressions associated with either liking or adverse reactions

  • positive facial liking: tongue protrusion

  • negative facial liking: gaping

• tastants are administered to rats, monkeys, babies and the behaviour is quantified by facial liking

signalling pathways

OPIODS

• endogenous opiods: enkephalins, dynorphins, endorphins

• the opiod receptors: mu, kappa, delta

• receptors: all GPCRs

• agonists: morphine

• antagonists: naloxone

ENDOCANNABANOIDS

• lipid molecules such as: anadamide and 2 arachidonoylglycerol

• there are 2 subtypes of receptors: CB1 and CB2

• receptors are GPCRs

• CB1 receptors in CNS

opioid pathways - ate they involved with reward?

• morphine increases hedonic pathways

• naloxone decreases food intake in rats, especially when sucrose is used

• opioid receptors against DAMGO (mu opioid agonist) administered and the measure of facial liking allows us to identify:

  • role for mu receptors

  • prescise map for nucleus accumbens

  • hedonic hotspots (10% of Nacc)

  • larger region for food intake wanting

hedonic hotspots of the brain

• additional liking structures in addition to the Nacc

• mu opiod receptors activation increases in these areas enhanced by hedonic responses to sucrose, by way of increased liking reactions

• the different hotspots identified are connected anatonically via neural pathways to create an interconnected circuit for liking

• to map the functional connectivity between these hotspots an approach called Fos plume was used

• recruitment of hotspots important mechanism for causing increased liking responses

• disruption of one hotspot can disrupt liking reactions and the function of the circuit

• another experiment done where DANGO injected into one region and naloxone —> activity is recorded

• blocking opioid receptors whilst simutantaneously stimulating another hotspot causes the expression of ehanced liking responses

• the ventral palladium is an integral hub for liking —> if inhibited/removed it supresses all enhanced liking

Fos plume

• one region of the animals brain is injected with the DAMGO and teh brain is removed

• immunhistochemical staining is used to quantify the expression of a protein called cFos in regions of the brain outside the injection site

• cFos is a protein that is expressed when neurons are activated and so increased expression of this protein provides a readout for when neurons are being activated by the drug injected

endocannabanoid pathway

• anecdotal evidence: active ingredient for cannabis is 9 tetrahydrocannabanoidal increases food intake, particularly sugary food

• targeted injection of anandamide into Nacc increases facial liking expression to sucrose

• therefore, theres an endocannabanoid hotspot in the Nacc that overlaps with the opiod hotspot

• CB1 receptors and mu receptors have been identified as co localised and can function together to coordinate release of GABA/glycine

motivational pathway

• dopamine is the key neurotransmitter for reward

• hypothesis testing used the facial expression paradigm compared with the neurochemical lesions in the brain to reduce dopamine signalling

  • depletion of dopamine did not affect orofacial expression of liking response to sweetness

  • but reducing dopamine caused rats to no longer seek out or consume food

  • so: dopamine more involved with motivation component rather than pleasure

further evidence

• G OHDA is able to remove the effect of dopaminergic neurons —> doesnt affect pleasure but does surpass wanting

• mice with increased dopamine have increased wanting for sweet food but no increase in liking

• individuals with low dopamine (parkinsons) show no difference in pleasure

cross talk of reward homeostasis

• orexin is a signalling molecule for cross talk between reward and homeostatic signalling

• cross talk occurs at the hypothalamus

• evidence for this:

  • orexic neurons project from the lateral hypothalamic neurons to structures of the reward system

  • orexin microinjections in hedonic hotspots enhances liking reactions to sucrose

eating disorders

• some individuals have the wanting circuitry which exceeds the liking circuitry causing them to be vulnerable to food wanting triggered by associated sensory cues

• this leads to overeating

• incentive sensation caused by hyperactivity of the dopaminergic pathways in the reward circuitry

• more intense triggering of wanting pathways in reponse to palatable food cues and associated with visual image

• future direction: tracking changes in brain function and activity using neuroimaging to understand changes that take place before/after obesity develops