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Emotions
a fleeting subconscious, physiological response (expression) in reaction to an event; 6 universal emotions include fear, anger, joy, sadness, disgust, and surprise
Feelings
how one is feeling inside of their body, is not always related to emotion, involves cognition, and can be hidden
James-Lange Theory
theory that a stimulus is perceived, causes an emotional expression, and is then perceived cognitively to create an emotional experience (feeling linked to an emotion)
Cannon-Bard Theory
theory that a stimulus is perceived, causes an emotional experience (feeling linked with emotion), and then allows us to act out an emotional expression
Volitional smile
a voluntary smile that does not reflect genuine emotion and is generated by the pyramidal motor pathway (ex. forcing a smile for a photograph)
Duchenne smile (emotional smile)
an involuntary, emotional smile that reflects true emotional experience and is generated by the extrapyramidal motor pathway (ex. smiling in response to a funny joke)
Pyramidal motor pathways
motor pathways that innervate voluntary, skeletal muscles via upper motor neurons
Extrapyramidal motor pathways
where neurons do not originate in the motor cortex, but instead from areas like the brainstem and hypothalamus, creating a closer association with emotions
Hypothalamus
controls hormones secretion via connections to the pituitary gland, and regulates autonomic expression of emotions and innate and conditioned defensive behaviors
Amygdala
responsible for relating sensory stimuli with emotional experience and is required for high order processing of emotion
Patient S.M
physically unable to feel fear or recognize fear in facial expressions due to bilateral lesions of the amygdala - can still be startled and follow group fear response
Emotional learning
the construction of implicit memories linking a situation or event to an emotional body state (most emotional responses are learned)
Fear conditioning
requires the amygdala to show appropriate fear response and the hippocampus to help us predict dangerous stimuli (factual learning)
Emotional symptoms of anxiety
include irrational and excessive fear or worry, panic, feelings of dread, irritability, restlessness, etc
Physical symptoms of anxiety
include shortness of breath, muscle tension, headaches, sweating, etc. (all are manifestations of our fight or flight response)
Role of sympathetic nervous system on anxiety
many signs of anxiety are explained by sympathetic nervous system activation such as increased heart rate and blood pressure, dilation of pupils, sweating, etc
Panic attack
sudden episodes of discrete periods of intense fear or discomfort accompanied by four or more symptoms such as trembling, numbness, dizziness, chest pain, etc.
Locus ceruleus
area of the brain in the brain stem that is involved in fear which is responsible for producing norepinephrine
Norepinephrine
a neurotransmitter and hormone that plays a critical role in the body’s fight or flight response and regulating physical reactions to stress
Hypothalamus
area of the brain involved in fear and is responsible for triggering the sympathetic nervous system to prepare the body for perceived threats
Necessary parts of the brain
proven to be necessary because without that region, a certain behavior is not presented
Sufficient parts of the brain
proven to be sufficient because when everything but this area is removed, the behavior is still presented
Anxiolytics
drugs used to relieve both the psychological and physical symptoms of anxiety by enhancing GABA receptors so that more hyperpolarization can take place and prevent overactive hypothalamus from firing AP (ex. xanax, valium)
Mesolimbic dopamine pathway
pathway between the ventral tegmental and nucleus accumbens that acts as the primary reward synapse in the brain and increases motivated behaviors
Ventral tegmental area (VTA)
source of dopamine cell bodies that send axon projections to the nucleus accumbens
Nucleus accumbens
receives dopamine inputs from the VTA and uses the signal to reinforce behavior that increases dopamine release
Basal ganglia
increases motor output to produce an overall increase in behavior and assist with habit formation
Hippocampus
provides our nucleus accumbens with contextual memory to help us remember where rewards are found
Prefrontal cortex
provides the nucleus accumbens with options to create plans on how to achieve rewards
5 major brain regions involved in reinforcement
ventral tegmental area, nucleus accumbens, basal ganglia, hippocampus, and prefrontal cortex
Dopamine neurons in the VTA can change because…
when a conditioned stimulus is presented with a reward, the VTA will fire for the conditioned stimulus instead of the reward - without the reward, the neural activity in the VTA will be suppressed
Effects of drugs on reward synapse
all drugs exponentially increase dopamine release in the nucleus accumbens, causing down regulation of our dopamine receptors so dopamine release for natural rewards no longer feels rewarding
Positive symptoms for schizophrenia
Delusions, hallucinations, disorganized speech, paranoia, etc.
Negative symptoms of schizophrenia
Decreased motivation, diminished emotional recognition and expression, social withdrawal, etc.
Causes of schizophrenia
mostly include genetic heredity (80-85%) of susceptible genes, but can be caused by environmental factors such as stressful childhood events, prenatal and birth complications, cannabis use during adolescence
The dopamine hypothesis
1) Elevating dopamine in normal individuals produces schizophrenia-like symptoms
2) Increasing dopamine in schizophrenia individuals worsens symptoms
3) Blocking dopamine activity in schizophrenics reduces symptoms
4) Excess dopamine in the mesolimbic DA pathway causes positive symptoms
5) Deficit of dopamine in prefrontal cortex causes negative symptoms and cognitive impairment
Schizophrenia treatments
drugs used to reduce positive symptoms of schizophrenia by reducing dopamine activity in the mesolimbic pathway, however, side effects include Parkinsonian-like symptoms or development of tardive dyskinesia (irreversible)
Patch Clamp recordings
method of measuring neuronal activity that allows us to directly measure action potentials, synaptic currents, and membrane properties; drawbacks include being highly invasive, and only being able to measure one neuron at a time instead of showing network-level dynamics