Emotion, Reward, Addiction

Emotions

autonomic and unconscious

reactions to events or a state due to the release of chemicals in the brain
instant
help us understand what we like and do not like
can be seen through expressions

Feelings

cortex > conscious

includes your interpretation, influenced by culture, religion, society

feelings can be hidden

long term

Duchenne Findings

voluntary smile v. true smile are different due to triggering of different smiles

Volitional Movement

descending pyramidal and extrapyramidal projections from motor cortex and brainstem

Duchenne Smile

descending extrapyramidal projections from medial forebrain and hypothalamus

Limbic Lobe

forms a rim, around corpus callosum and diencephalon

Cingulate gyrus

Papez Circuit

proposed circuit for emotional processing

main pathways to the hypothalamus

missing amygdala, frontal cortex (emotional centers)

Classic Hypothalamus

controls the pituitary gland

sleep/wake circadian rhythms

feeding and breeding

hunger, thirst

Emotional hypothalamus

autonomic expression of emotions through activation of sympathetic system

expression of innate and conditioned defensive behaviors

specific changes in heart rate, temperature, sweating depending on the situation

Sham rage exp. overarching

Hypothalamus coordinates the visceral and somatic motor components of emotional behaviors

Shame rage exp. What happened? Results?

Philip Bard exp in 1920s

removed both cerebral hemispheres, underlying white matter, and basal ganglia

left the Hypothalamus

resulted in spontaneous rage response despite no apparent target

MAJOR point of sham rage exp

Hypothalamus is necessary and sufficient for the coordinated rage response

necessary

if hypothalamus is ______, then without it, there would be no rage response

sufficient

if the only thing there is the hypothalamus and no cortex, and there is still a coordinated rage response

Amygdala

responsible for relating sensory stimuli with emotional expereince

found in the temporal lobe, adjacent to hippocampus (MEMORIES)

site of associative learning – fear with snakes

connections with cortex, hippocampus, hypothalamus, thalamus, basal ganglia

Amygdala and the rest of the systems

Connectivity between Amygdala and higher order cortical areas are required for higher order processing of emotion and ultimately behavior

Patient SM

had no amygdala due to Urbach-Wietha dieases

as a result — NO FEAR

Bilateral lesions of the Aymgdala

physically unable to feel fear

cannot recognize fear in facial expressions of others

does not have a concept of personal space

DOES HAVE startle response – that is REFLEXIVE not FEAR

CAN follow group fear responses due to voices and body responses in others

Innate responses

born with it

Learned responses

depend on experience
can be conscious but often subconscious

emotion learning

construction of implicit memories linking a situation or event to an emotion body state

Fear conditioning

innate reflex (conditioned) is modified by associating the normal trigger stimulus with an unrelated stimulus

How Fear Conditioning works

a neutral auditory tone is paired with a shock
the experience of the shock is relayed by somatosensory system as pain – negative reinforcement

this association is learned by strengthening of the auditory inputs through long term potentiation

leads to better activation of amygdala circuits by the tone

enhances survival response– freezing, changes in BP

Fear conditioning v. memory

different brain regions

no deficit in a memory task despite the fear response to conditioned stimuli

amygdala required for fear but not memory

hippocampus required for memory but not fear

3 Dopamine Pathways

Nigrostriatal (dorsal striatum) DA projections – motor

Mesolimbic (ventral striatum) DA projections – reward

Mesocortical DA projections – alertness, executive functions

Nigrostriatal System Origin

Substantia Nigra

Nigrostriatal System Location of Terminal Buttons

Neostriatum (caudate and putamen)

Nigrostriatal System Behavior Effects

control of movement

Mesolimbic System Origin (reward)

Ventral tegmental area (mid brain)

Mesolimbic System Location of Terminal Buttons

Nucleus accumbens

Mesolimbic System Behavioral Effects

Reinforcement, effects of addictive drug

Mesocortical System Origin

Ventral tegmental area (mid brain)

Mesocortical System Location of Terminal Buttons

Prefrontal Cortex

Mesocortical System Behavioral Effects

Short-term memories, planning, strategies for problem solving

Reward system….

helps to promote our survival

VTA to NA Pathway

THE primary reward synapse in the brain

reinforcement of behavioral movements

more DA signaling increases motivation to perform these behaviors again in the future

DO IT AGAIN SYNAPSE

VTA releases Dopamine on nucleus accumbens

The Motivation Control System

Reward system interacts with other systems too

Ventral Tegmental area (VTA) w/ reward

source of dopamine cell bodies sending axon projections to the nucleus accumbens

Nucleus accumbens w/ reward

receives dopamine inputs (axon terminals) from the VTA

all addictive drugs produce an increase of dopamine

Basal Ganglia w/ reward

increases motor output to produce an overall increase in behavior

Hippocampus

tells the nucleus accumbens where we are and what is happening around us (our context)

Prefrontal cortex w/ reward

provides the nucleus accumbens with several options for behavior

Rats will work to…

electrically stimulate the VTA to NA pathway – push a lever that self-administers drgus to activate pathway

Blockade of DA recepts in the NA will block this behavior

DA neurons in the VTA change their activity pattern during reward learning

A. no conditioning: increased firing after reward

B. after condition: increased firing after stimulus but BEFORE reward

C. no reward: increased firing after stimulus then NO firing when NO reward given

Brain Reward Circuits

all abuse-prone drugs, morphine, cocaine, alcohol, and marijuana,a have found to enhance brain stimulation reward or lower brain reward thresholds in these circuits.

Drugs —> increased dopamine 

All drugs of abuse…

increase dopamine release in the nucleus accumbens

Nicotine

binds to ACh receptors on VTA —> Depol

Increased glutamate released onto VTA neurons

booth effects increase DA release from VTA neurons onto NAc

Cocaine and Amphetamine

block DA reuptake into VTA axon terminals

large, extended concentration of dopamine in NAc

Opiates (morphine, heroin)

bind to the opioid receptors on the axon terminals of GABAergic interneurons

____ are inhibitory – therefore decrease GABA release

Disinhibits VTA neurons —> INCREASES dopamine release

Addiction

Corruption of the dopaminergic system extending from the ventral tegmental area

addictive drugs artificially increase dopamine levels in situations that would normally have lower levels of dopamine

affects the perception/processing of reward

reinforce addictive behavior by increasing dopamine at the wrong time/circumstance

D2 receptors + Anhedonia

addicted subjects were found to have lower D2 recept expression and lower baseline dopamine releases

These changes cause a blunted response to natural rewards such as food and sex

drug-induced dopamine overcomes baseline deficiencies

As a result, addicted subjects don’t feel normal unless they have dopamine levels increased by their drug of choice