Exam 4, Lec 3; Flashcards: Emotions + Rewards + Addictions

Duchenne smile

True emotional smile; cannot be "faked" or voluntarily produced

Volitional movement

Descending "pyramidal" and "extrapyramidal" projections from motor cortex and brainstem

Pathway of volitional movement

Volitional movement --> Pyramidal smile --> motor neuron pools in facial nucleus --> activation of facial muscles

Break in pathway of volitional movement

Voluntary facial paresis

Neural Systems of Emotional Expression

Descending "extrapyramidal" projections from medial forebrain and hypothalamus

Pathway of Neural Systems of Emotional Expression

Neural Systems of Emotional Expression --> Duchenne smile --> motor neuron pools in facial nucleus --> activation of facial muscles

Break in pathway of Neural Systems of Emotional Expression

Emotional facial paresis

Limbic lobe structure

Forms a rim, "limbus" around corpus callosum and diencephalon

Papez circuit

Proposed circuit for emotional processing, main pathways to hypothalamus

What structures does the papez circuit consist of?

- Cingulate cortex, fornix, thalamus, mammillary bodies, hippocampus
- Missing amygdala, frontal cortex (emotional centers)

Classic hypothalamus

Neuroendocrine function through connections with the pituitary gland

emotional hypothalamus

- Autonomic expression of emotions through activation of the sympathetic system
- Expression of innate and conditioned defensive behaviors
- Specific changes in heart rate, temperature, and sweating depending on the situation

What parts of emotional behavior does hypothalamus coordinate?

Visceral and somatic motor components

"Sham rage" experiments

Philip Bard in 1920:

- Removed both cerebral hemispheres, underlying white matter and basal ganglia

Effects of sham rage experiments

After anesthesia wore off, animals acted "enraged" spontaneously without any obvious target:
- Autonomic correlation: increased blood pressure & heart rate, dilation of pupils, piloerection
- Somatic correlation: arching back, extending claws, snarling/hissing

What is necessary and sufficient for coordinated rage response?

Hypothalamus

Necessary aspect of coordinate rage response

Without hypothalamus, no rage response

Sufficient aspect of coordinated rage response

With hypothalamus but no cortex, there is a coordinated rage response

Amygdala location

found in temporal lobes - adjacent to hippocampus

Amygdala function

- Responsible for relating sensory stimuli with emotional experience
- Site of associative learning
- Connections with cortex, hippocampus, hypothalamus, thalamus, basal ganglia

What is the connectivity of the amygdala and higher order cortical areas required for?

Higher order processing of emotion and ultimately behavior

Effects of patient S.M. with bilateral lesions of the amygdala

- Physically unable to feel fear - will approach spiders and snakes
- Cannot recognize fear in facial expressions
- Does not have concept of personal space
- Does have startle response that does not depend on amygdala
- Can follow group fear responses due to voices and body responses in others

How do stimuli/events attain emotional significance?

Some events are automatic, INNATE or LEARNED

Examples of automatic/INNATE emotional responses

Lab rats display fear when exposed to fox odor

Learned emotional responses depend on?

Experience; can be conscious, but is often subconscious

Emotional learning

Construction of implicit memories linking a situation or event to an emotional body state

fear conditioning

Pairing a shock with a neural auditory tone

Effect of fear conditioning

- Experience of shock is relayed by somatosensory system as "pain" - negative reinforcement
- Association is "learned" by strengthening auditory inputs through long-term potentiation
- Leads to better activation of amygdala circuits by tone

Response of fear conditioning

Enhances survival responses - freezing, changes in blood pressure

Do fear conditioning and memory require different brain regions?

Yes

What is required for fear but not memory?

Amygdala

What is required for memory but not fear?

Hippocampus

Dopaminergic pathways

- Nigrostriatial (dorsal striatum) DA projections
- Mesolimbic (ventral striatum) DA projections
- Mesocortical DA projections

Nigrostriatial (dorsal striatum) DA projection function

Motor; control of movement

Mesolimbic (ventral striatum) DA projection function

Reward; reinforcement, effects of addictive drugs

Mesocortical DA projection function

Alertness, exectuve function (cognitive state); short-term memories, planning, strategies for problem solving

"Do-it-again" syanpse

Invertebrates have a rudimentary dopamine system

Meso meaning

Mid-brain

What structures does the midbrain include?

Substantia nigra and ventral tegmental area

What is the mesolimbic DA pathway synapse important for?

Reinforcement of behavioral movements, where more DA signaling increases motivation to perform those behaviors again in the future

Presynaptic and postsynaptic parts in reward synapse

VTA (presynaptic) to NAc (postsynaptic)

Five major brain regions involved in reinforcement and reward

- VTA (ventral tegmental area)
- Nucleus accumbens
- Basal ganglia
- Hippocampus
- Prefrontal cortex

VTA (ventral tegmental area)

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

Nucleus accumbens

Receives dopamine inputs (axon terminals) from the VTA
All addictive drugs produce an increase of dopamine

Basal ganglia

Increases motor output to produce an overall increase in behavior

Hippocampus

Tells nucleus accumbens where we are and what is happening around us (our "context"

Prefrontal cortex

Provides nucleus accumbens with several options for behavior

What do rats work to electrically stimulare?

Drugs that activate the VTA-NA pathway

How to block the behavior of rats working to electrically stimulate VTA-NA pathway?

Blockade of DA receptor signaling in the NA

What neurons change their activity pattern during reward learning?

DA neuron in the VTA

Steps of change in activity pattern during reward learning of DA neuron in VTA

- VTA neural response to an unexpected juice reward
- After learning, VTA neural response to the cue that predicts impending juice reward
- When juice reward is predicted but not delivered, VTA neural activity is suppressed

Effects of all abuse-prone drugs

- Enhance brain stimulation reward or lower brain reward thresholds in circuits
- Increase dopamine release

Where do drugs of abuse increase dopamine?

Nucleus accumbens (NaC)

Pathway of dopamine increase of nicotine

- Binds to ACh receptors on VTA neurons causing depolarization
- Increases glutamate release onto VTA neurons
- Both effects increase DA release from VTA neurons projecting to the NAc

Pathway of dopamine increase of Cocaine and Amphetamine

- Block DA reuptake into VTA axon terminals -- increasing effect of DA in the NAc

Pathway of dopamine increase of Opiates (e.g. morphine, heroin)

- Binds to opioid receptors on axon terminals of GABAergic interneurons
- Opiates are inhibitory - therefore decrease GABA release
- Disinhibits VTA neurons and increases dopamine release in NAc

Addiction

Corruption of the dopaminergic system extending from ventral tagmental area (VTA)

How do addictive drugs cause addiction?

"Artificially" increase dopamine levels in situations that would normally have lower levels of dopamine

Effect of addiction

- Perception/processing of reward
- Reinforce addictive behavior by increasing dopamine at the wrong time/circumstance

Anhedonia

a diminished ability to experience pleasure

D2 receptor

G-coupled protein that's a common target for antipsychotic drugs and is involved in many physiological and pathological processes

Effects of D2 receptors and Anhedonia in addicted individuals

Lower D2 receptor expression and lower baseline dopamine release --> cause blunted response to natural rewards such as food and sex

Implications of addicted individuals in terms of feeling "normal"

Addicted subjects don't feel "normal" unless they have dopamine levels increased by drug of choice