Emotions, Memory

James-Lange Theory

physiological arousal → emotion

e.g., HR faster → conclude that I’m scared/sad

-consistent with facial feedback hypothesis

Cannon-Bard Theory

(Cannon-ball: fires simultaneously)

physiological arousal + emotion occur simultaneously

thalamus simultaneously sends to CC + SNS

Schachter and Singer’s Two-Factor Theory

-aka cognitive arousal theory

-second factor = cognitive appraisal

Emotion = (1) physiological arousal + (2) cognitive appraisal

-Differences in emotions are d/t cognitive appraisal (can’t be d/t physiological arousal, since it’s so similar)

-cognitive appraisals depend on environmental cues

S-S epinephrine studies found

participants were injected with epinephrine → people looked to external cues (confederate bx) to determine their emotion

misattribution of arousal = tendency to misattribute arousal when it’s unknown/ambiguous

Zillman’s excitation transfer theory

≠ just misattribution of arousal

-emotional excitation from 1st event transfers to and intensifies 2nd unrelated event

-Based on assumptions:

-arousal decays slowly, persisting after 1st event

-residual arousal intensifies arousal during 2nd event

-cognitive misattribution of arousal all to the later unrelated event (ppl often have limited insight into their arousal)

e.g., fear excitation => more intense sexual attraction + joy

Lazarus’s Cognitive Appraisal Theory

-Cognitive appraisal comes FIRST, which determines physical response + emotion

-Primary (stressful?) + secondary appraisal (coping options + effectiveness), and reappraisal (monitor situation, reappraise primary/secondary appraisals as needed)

LeDoux’s Two-System Theory

Cortical (conscious, high-road) and subcortical (amygdala, low-road) response of fear

-contrasted with theories that link fear to subcortical regions only

-may not only be specific to fear

Papez circuit

-hippocampus, mammillary bodies, thalamus, and cingulate gyrus (interconnected)

-Papez – one of the first to link emotions to brain areas

-Papez circuit = memory (not emotion)

Brain areas linked to emotion

Cerebral cortex

Hypothalamus (damage → rage; stimulation → pleasure or fear)

Amygdala

Damage to L hemisphere of CC → (emotional impact)

-“catastrophic reaction” – depression, anxiety, fear, and paranoia

Damage to R hemisphere of CC → (emotional impact)

-“indifference reaction” – inappropriate indifference and/or euphoria

Damage to amygdala → (emotional impact)

-loss of fear, but not other emotions

Selye’s General Adaptation Syndrome

-argues that body response to stress is always the same (alarm, resistance, exhaustion)

-critique = stress response isn’t always the same

McEwen’s allostatic load model

-allostasis and consequences of allostatic load vary across people (d/t genetics, prior xps)

Allostasis

Adaptive processes that maintain stability during stress

e.g., elevation in BP + cortisol as processes that help adapt to stressor

Allostatic state

-Can only be maintained for short-term, w/o adverse consequences

Extended allostasis state → allostatic load/overload

-immune system dysregulation

-PTSD, depression, SUDs

Major memory brain areas

Hippocampus – LT declarative memory, spatial memory (NOT procedural or STM)

Basal ganglia and cerebellum – procedural/implicit memory

Thalamus

Amygdala – emotional content of memory

PFC

Damage to basal ganglia + cerebellum → (memory effect)

difficulty learning new skills, and performing previously learned skills

(both have role in procedural memory + voluntary movement)

Amygdala damage → (effect on memory retrieval)

-People with intact amygdalas remember emotional memories better (than non-emotional)

-People with damaged amygdalas remember emotional/nonemotional memories the same

(emotions haven’t been attached to the emotional memories)

PFC Memory Functions

-WM

-prospective memory – memory for future plans/intent (‘remembering to remember’)

-item memory – what happened, content (got lost)

-source memory – where/when (5 yo in China)

(knowing what happened, where, and when = PFC)

Damage in thalamus → (effect on memory)

Anterograde (can’t learn) + retrograde (old memories) amnesia

anterograde amnesia = cannot form LTMs after the damage (e.g., can't learn people’s names now)

Kandel’s sea slug research on memory (findings)

-with classical conditioning, STM storage involved serotonin

-with classical conditioning, LTM storage involved actual changes in neuron structure (new synapses)

Long-term potentiation

-Essential cellular-level mechanism in learning/memory formation

-LT increased strength of synaptic connections through glutamate

-Seen in glutamate receptors in hippocampus, amygdala, and entorhinal cortex

-Glutamate → increase in glutamate receptors → increased sensitivity to glutamate

-Occurs in neuron from rapid/high-frequency stimulation

-When one neuron repeatedly triggers another, the connection grows (neurons that fire together wire together)

Role of RNA synthesis in LTM formation

-RNA synthesis is required for synaptic changes associated with LTM formation

-drug that inhibits RNA synthesis → prevents LTM formation (but not STM formation)

Electroencephalography (EEG)

-provides info on frequency/amplitude of brain waves

-through electrodes that measure electrical impulses generated by large groups of cortical neurons