Biological Psychology: Emotion, Memory, and Brain Function

Chapter 11: Emotion

What Is Emotion?

• Psychologists discuss emotion in relation to four components:
  • Cognition: Mental process/thought (e.g., “this seems dangerous”).
  • Feeling: E.g., the feeling of fear.
  • Action: E.g., running away.
  • Physiological changes: Can be combined with the “action” (e.g., increased heart rate).
• There is some difficulty in distinguishing emotions from motivations:
  • Similar components exist when examining the motivation of thirst.

Emotion and Autonomic Arousal

• Emotional situations arouse the autonomic nervous system (ANS):
  • Sympathetic nervous system: Prepares the body for immediate action.
    • Fight-or-flight response (e.g., increased heart rate).
  • Parasympathetic nervous system: Helps the body rest/recuperate and prepares the body for future action.
    • Restoring energy (e.g., decreased heart rate).
  • Most emotions evoke a combination of sympathetic and parasympathetic arousal:
    • Feelings of fear activate different systems based on the situational context.

Common Sense View of Emotion

• How does the autonomic nervous system relate to emotions?
  • Three to four components:
    • Situation: Stimulus.
    • Emotion: Feeling.
    • Action/physiological change.
• Common Sense View:
  • The situation causes the emotion/feeling, which then causes the physiological response and action.
    • E.g., frightening situation → fear → running away.
  • This view is contradicted by the James-Lange Theory.

James-Lange Theory of Emotion

• The situation causes the physiological response and action, which then causes the emotional feeling:
  • Autonomic arousal and skeletal action occur first.
  • The emotion felt is the cognitive awareness of the arousal of the organs and muscles.
    • E.g., frightening situation → running away → fear.
• This theory leads to two predictions:
  • People with a weak autonomic or skeletal response should feel less intense emotion.
  • Increasing one’s physiological response should enhance an emotion.
• It is correct in some aspects, but emotion is likely more complex than it indicates.
• Physiological arousal by itself can sometimes, but very rarely, directly produce those emotional feelings:
  • E.g., panic attack → physiological changes cause fear.
• Generally, physiological arousal by itself will instead increase emotional feelings, but won’t cause those emotional feelings themselves:
  • E.g., cold rooms can enhance fear towards a horror movie, but you won’t feel fear just from being in a cold room.

Emotion and Autonomic Arousal

• Patients with paralysis still experience fear/emotion to some degree:
  • This somewhat contradicts the James-Lange Theory.
  • These individuals can still make facial expressions.
• Pure autonomic failure: Output from the ANS to the body fails.
  • Supports the James-Lange Theory.
  • Functions like heart rate continue but are not regulated by the ANS.
  • Patients report feeling the same/correct emotion but at a lesser intensity.
    • Suggests other factors are involved in the perception of emotion.
• Botox blocks transmissions at synapses of neuromuscular junctions:
  • Supports the James-Lange Theory.
  • Results in weaker than usual emotional responses after watching short videos.
  • Implies some bodily changes are an important part of feeling an emotion.

Cognitive Arousal Theory

• Stimulus → action/physiological change → cognition → emotion.
• The cognition interprets the action/physiological change depending on the context.
• Sympathetic nervous system activity increases:
  • Playing with friends: Interpreted as “happiness”.
  • Stranger annoying you: Interpreted as “anger”.
• Contradiction: Some emotions are triggered too quickly for cognitive labeling.
  • E.g., if a snake appears in front of you, you immediately feel fear before cognition occurs.

Brain Activity

• The limbic system becomes active during emotional feelings:
  • The forebrain areas surrounding the thalamus, such as the amygdala, hippocampus, hypothalamus, cingulate gyrus, and mammillary bodies.
• No specific brain area is critical for only emotion:
  • Multiple cortical areas are activated for the same emotion.
  • Brain regions activated are involved in other functions besides emotion.
• Emotional experiences may arouse many areas of the brain (limbic system and cerebral cortex), making it difficult to identify specific emotions physiologically:
  • E.g., does a heart rate increase indicate fear or anger?
• Emotion is useful because it is tied to survival; however, the concept of categorizing different feelings might not be.

Emotions Based on Facial Expressions

• Emotional feelings are commonly divided into six categories:
  • Happiness, sadness, fear, anger, disgust, and surprise.
  • Other emotions are subdivisions of these six.
  • This classification is based on facial expressions, since a specific brain region isn’t tied to a specific emotion.
• Multiple problems exist with splitting emotions into these six categories based on facial expressions:
  • It is more difficult to identify the emotion when looking at just one image of a face without a comparison image.
  • Certain cultures are better or worse at identifying certain emotions.
  • We rarely use facial expressions alone; we also use context and body gestures.

Alternative Identification of Emotional Feelings

• Behavioral Activation System (BAS):
  • Associated with increased activity of the frontal and temporal lobes of the left hemisphere.
    • Indicative of low to moderate arousal of the ANS and a tendency to approach a situation.
    • Stimulates emotions such as happiness or anger.
• Behavioral Inhibition System (BIS):
  • Associated with increased activity of the frontal and temporal lobes of the right hemisphere.
    • Indicative of increased attention and high arousal of the ANS.
    • Inhibits actions, leading to avoidance.
    • Stimulates emotions such as fear and disgust.

Functions of Emotion

• Adaptive value:
  • Fear leads to escape.
  • Anger leads to attack.
  • Disgust leads to avoiding potential illness.
  • Happiness and sadness let us communicate our needs to others.
• Helps in quick decision-making:
  • We do not want to wait around thinking about what to do in a crisis.

Emotions and Moral Decisions

• Moral decisions:
  • Utilitarian aspect: How many people can I save?
  • Emotional aspect: How will that decision outcome make us feel?
• Comparing the utilitarian and emotional aspects involves the ventromedial prefrontal cortex (vmPFC):
  • Damage to the vmPFC leads to basing decisions on just the utilitarian/end-result component.
  • Individuals are no longer able to predict how a decision will make them or others feel, even if they understand what the result of the decision is.
• What we consider the “right” decision is not always the utilitarian one.
• Emotions can interfere with correct decision-making:
  • E.g., a car is skidding on ice, so you incorrectly decide to jerk the steering wheel out of fear.

Decision-Making After Brain Damage

• Damage to different parts of the prefrontal cortex (PFC) causes different emotional impairments:
  • Dorsolateral PFC: Damage leads to difficulty inhibiting emotional responses and regulating intensity.
  • Orbitofrontal cortex: Damage leads to impulsive, risky behaviors.
  • Ventromedial PFC: Damage leads to difficulty inhibiting emotional responses and intensity, as well as a decrease in empathy and understanding the emotions of others.
    • Inability to predict how decisions will affect the emotions of oneself and others.
    • Decreased guilt and trust.
    • Can determine the consequence of an action but not if it is moral or not.

Attack and Escape Behaviors

• Attack and escape behaviors and corresponding emotions: anger and fear.
  • Closely related physiologically (sympathetically) and behaviorally (individuals commonly alternate between attack and escape behaviors).
• Attack behaviors depend on the individual and the situation:
  • We can see this when priming someone for aggression; they are more likely to act aggressively afterward.

Priming Aggressive Behaviors

• Initially preventing a child from playing with a toy:
  • Shows anger (screaming/thrashing) after ~30 seconds.
  • The child is not yet in the “mood” to get angry, so they become angry slowly.
• Wait 30 seconds, then prevent the child from playing with the toy again:
  • Shows an anger response much faster and with more intensity.
  • The child was already in the “mood” to get angry, so they became angry quickly.
• Brain areas related to anger have been more recently activated/primed:
  • The child is now more prepared to act aggressively.
  • Activation of the corticomedial nucleus in the amygdala is involved in priming aggressive behaviors.

Effect of Hormones: Aggressive Behavior

• Male aggressive behavior heavily depends on testosterone:
  • Young adult men have the highest testosterone levels and the highest rates of aggressive behaviors and violent crimes.
  • The effect of testosterone on aggressive behavior may be based more on how often/strong the bursts of testosterone are rather than baseline levels.
• Aggressive behavior depends on the ratio of testosterone to cortisol:
  • Cortisol is secreted during high levels of stress.
  • Cortisol inhibits violent impulses/aggression.
  • Anger decreases cortisol levels.
• Impulsiveness, aggressive behavior, and suicide have been linked to low levels of serotonin:
  • Serotonin turnover: The amount of serotonin that neurons release, absorb, and replace.
    • Low turnover → lower serotonin release/replacement → higher impulsiveness and suicide rates.
  • Serotonin turnover seems to play a role in inhibiting violent actions (though not as much as cortisol).

Violence

• Environmental factors associated with increased violent tendencies:
  • Witnessing or being a victim of violence in childhood.
  • Living in a violent neighborhood.
  • Exposure to lead.
• Twin studies suggest genetic contributions to the likelihood of violent behavior:
  • Monozygotic twins resembled each other much more than dizygotic twins with regard to violent and criminal behavior.
  • Studies failed to find a strong link between aggression and a single specific gene, although there does seem to be a genetic component.
• The interaction between genetics and childhood environment shows a strong link to aggression:
  • Variability in genes controlling the enzyme MAO (which breaks down serotonin).
  • Low MAO causes irregularities in brain development (antisocial behavior).
  • Effects are only seen when in conjunction with environmental factors.

Fear and Anxiety

• Startle reflex: Innate fear response to unexpected loud noises.
  • Auditory information stimulates the part of the pons that commands tensing of the neck and other muscles.
    • Information reaches the pons within 3–8 ms.
    • The startle response occurs within two-tenths of a second (200 ms).
  • The startle reflex is more vigorous if the individual is already tense.
    • PTSD and the startle reflex.
  • The startle reflex can be used as a behavioral measure of anxiety.
    • Can be used with laboratory animals to explore brain mechanisms.

Fear in Rodent Models

• Pairing a stimulus with a shock:
  • Stimulus (tone/light) → becomes a fear signal → startle response is enhanced.
• The stimulus is associated with pleasure or the absence of danger:
  • Stimulus (tone/light) → becomes a relaxing signal → startle response is inhibited.
• Amygdala: Limbic system structure in the medial temporal lobe which is involved in fear/anxiety.
  • Enhances the startle reflex.
    • The central amygdala sends signals to the midbrain, which then sends signals to the pons and medulla to enhance that startle reflex.
    • Although the startle reflex will still occur, damage to the amygdala prevents the enhancement of that reflex.
  • Important for fear learning (prepares animals for fearful situations).

Klüver-Bucy Syndrome

• Impairments in fear learning.
• Bilateral damage to the amygdala (not genetic):
  • If the amygdala of only one hemisphere is damaged, the undamaged one can compensate for it.
  • Damage to other regions of the temporal lobe can still be considered Klüver-Bucy syndrome, but the symptoms will be different.
• Monkeys with this syndrome are tame:
  • Display less than normal fear of snakes and larger, more dominant monkeys.
  • Have impaired social behaviors.
• Non-damaged monkeys with a vigorously active amygdala (no Klüver-Bucy syndrome) show fear of noise/intruders.

Long-Term Fear and Anxiety

• The amygdala is related to fear of a particular stimulus (e.g., snakes).
  • Has multiple pathways involved in fear of different stimuli (pain, predators, aggressive peers).
• Bed nucleus of the stria terminalis:
  • Related to being more fearful in general (not stimulus-dependent).
  • Controls long-term anxiety/fear and generalized emotional arousal.
  • If a person is attacked or has a fearful experience, they may become fearful in a wide variety of circumstances.
  • Thought process of “the world is a dangerous place, so I need to prepare for a sudden threat.”

Response of the Human Amygdala to Visual Stimuli

• fMRI studies show the amygdala responds strongly to photos that arouse fear or faces showing fear.
• The amygdala responds more strongly when facial expressions are harder to interpret.
• The amygdala responds more strongly to a “frightened” face directed toward the viewer, and “angry” faces directed elsewhere.

Amygdala Response and Anxiety

• Anxiety remains fairly consistent over time:
  • An anxious child often grows into an anxious adult.
• Individual differences in anxiety are correlated with amygdala activity:
  • More amygdala activity is correlated with being more anxious.
  • Other cortical regions, such as the prefrontal cortex, can inhibit the amygdala, reducing that fear/anxiety response.
    • Reappraising a situation in a less threatening way.

Damage to the Human Amygdala

• Urbach-Wiethe disease: A rare genetic condition where calcium accumulates in the amygdala until it wastes away.
• Case study of a person called S.M. who experienced fearlessness to snakes:
  • Led to her casually approaching dangerous situations (gunpoint, assault).
  • Still had a fear response from a lack of oxygen.
    • A lack of oxygen directly affected the body, rather than having the amygdala interpret external signals.
    • The amygdala is important for imagining fear and thinking about danger from the outside world.
• Patients can correctly draw faces with various emotions, but have trouble drawing a fearful face:
  • Did not look people in the eyes, focusing instead on the nose/mouth.
  • Although not fully understood, the amygdala may be important for detecting emotional information and directing attention to it, rather than actually feeling fear or other emotions.

Anxiety Disorders

• Anxiety disorders: Conditions in which one’s anxiety seems excessive for the circumstance.
  • Too little anxiety is bad, but too much can also be detrimental.
• Generalized anxiety disorder: An anxiety disorder characterized by excessive worry about everyday situations and issues that persist for at least six months.
  • Most common anxiety disorder.
  • Can cause restlessness, fatigue, difficulty concentrating, muscle tension, and sleep disturbances.
  • Linked to abnormalities in the amygdala and the bed nucleus of the stria terminalis.
  • Risk factors include both environmental and genetic factors.

Panic Disorder

• Panic disorder: A type of anxiety disorder characterized by frequent periods of anxiety and occasional attacks of extreme sympathetic nervous system arousal (rapid breathing, increased heart rate, sweating, and trembling).
  • Fear of the next panic attack will affect behavior.
  • More common in women than men, and in adolescents and young adults.
  • Possible genetic component.
  • Linked to abnormalities in the hypothalamus as well as irregularities in GABA release.
    • Increased release of the neuropeptide orexin.
    • Lower levels of GABA: Cannot inhibit regions related to anxiety as effectively.

Post-Traumatic Stress Disorder (PTSD)

• Post-Traumatic Stress Disorder (PTSD): An anxiety disorder characterized by frequent distressing recollections and nightmares about a traumatic event, as well as vigorous reactions to noises and other stimuli.
  • Not all people who endure trauma experience PTSD.
  • Having a smaller hippocampus increases the risk of developing PTSD from a distressing event.

Anti-Anxiety Medication

• Benzodiazepines: A class of anti-anxiety drugs which inhibit areas related to anxiety (amygdala, hypothalamus, midbrain, etc.) through increased GABA binding.
  • E.g., diazepam (Valium), alprazolam (Xanax).
  • Bind to the alpha site on the GABA receptor → facilitates the effects of GABA → neuron is less likely to fire.
  • Fast-acting.
  • Carries a risk of addiction.
• Selective Serotonin Reuptake Inhibitors (SSRIs): A class of drugs commonly used to treat depression, but also found to decrease anxiety.
  • Decrease the reuptake of the neurotransmitter serotonin, stabilizing mood.

Reducing Anxiety with Alcohol

• Alcohol is also able to reduce anxiety.
• Alcohol affects GABA receptors, which in turn inhibits brain activity in regions responsible for anxiety:
  • Works similarly to benzodiazepines.

Reducing Anxiety to Phobias through Behavior

• Extinction:
  • Pairing the learned fear-causing conditioned stimulus (e.g., tone) without the unconditioned stimulus (e.g., electric shock).
  • Extinguishing a fear behavior is often referred to as flooding.
    • E.g., putting a person in a room with a large, calm dog that doesn’t bite.
• Systematic desensitization:
  • Pairing relaxation with fear (one cannot be relaxed and anxious at the same time).
  • Hierarchy of fear: Start with a stimulus that causes a small amount of fear, then work your way up.
    • E.g., picture of a dog → small dog far away → petting a large dog.
• Hybrid approach:
  • Exposed to the stimulus (extinction), but gradually approaches it (hierarchy of fear).

Stress and Health

• The definition of stress is broad:
  • Some define it as the nonspecific response of the body to any demand made upon it, whether it be favorable or unfavorable.
  • Better definition of stress: Events that are interpreted as threatening to an individual and which elicit physiological and behavioral responses.
• General adaptation syndrome: The physiological changes the body goes through in response to stress.
  • Stage 1: Alarm - Cortisol release, sympathetic nervous system becomes more active.
  • Stage 2: Resistance - Cortisol continues to release (still alert), but sympathetic nervous system activity declines.
  • Stage 3: Exhaustion - Inactive and tired, not enough energy for a proper immune system response.

Stress and the HPA Axis

• Stress activates two systems in the body:
  • Sympathetic nervous system: Fight-or-flight response.
  • Hypothalamic-pituitary-adrenal (HPA) axis: Recruits activity from the hypothalamus, pituitary gland, and adrenal cortex.
• Activation of the hypothalamus induces the pituitary gland to secrete adrenocorticotropic hormone (ACTH), which then stimulates the adrenal cortex of the adrenal gland, causing it to secrete cortisol.
  • Cortisol will enhance metabolic activity, elevate blood sugar levels, and increase alertness.
• The HPA axis reacts more slowly than the sympathetic nervous system, but becomes the dominant response to prolonged stressors.
• Moderate stress can improve memory and immune response, while prolonged stress can lead to impairments in memory and the immune system.

Immune System

• Protects the body against viruses and bacteria by producing leukocytes:
  • B-cells: Mature in the bone marrow and secrete antibodies.
    • Antibodies: Y-shaped proteins that attach to particular kinds of antigens (key).
    • Antigens: Surface proteins that serve as antibody-generator molecules (lock/identification system).
  • T-cells: Attack intruders directly and help other T-cells or B-cells multiply.
  • Natural killer cells: Attack tumor cells and cells infected with viruses.
• During an infection, leukocytes and other cells produce small proteins called cytokines:
  • Combat infection and communicate with the brain to inform it of illness.
  • Cytokines stimulate the release of prostaglandins.
    • Stimulate the hypothalamus, producing fever, sleepiness, and lack of energy.
    • Sleep and inactivity conserve energy to fight illness.

Effects of Stress on the Immune System

• In response to a short-term stressful experience, the nervous system activates the immune system:
  • Increases production of natural killer cells and cytokines.
  • Cytokines combat infections, but also trigger prostaglandins, which send signals to the hypothalamus causing fever and lack of energy.
  • Brief stressful experiences do not affect the risk of illness.
• Prolonged stress:
  • Produces symptoms similar to depression and weakens the immune system.
  • Cortisol increase removes the energy needed to produce proteins for the immune system, causing a decrease in leukocytes.
  • Cortisol increases metabolic activity in the hippocampus, making it more vulnerable to toxic chemicals and overstimulation.

Coping with Stress

• People’s responses to stress vary.
• Resilience: The ability to recover well after a traumatic experience.
• Methods to control stress responses:
  • Genetics.
  • Previous experiences with stress.
  • Breathing routines, exercise, meditation, distraction, and addressing issues.
  • Social support from a loved one helps to reduce stress.

Chapter 12 - Learning and Memory

Classical Conditioning

• Involuntary/automatic:
  • The stimulus causes the behavior.
• Step 1: The unconditioned stimulus automatically causes the unconditioned response.
  • US (food) → UR (salivation).
• Step 2: The neutral stimulus causes no response.
  • NS (bell) → no response / no salivation.
• Step 3: Pair the neutral stimulus with the unconditioned stimulus.
  • NS (bell) → US (food) → UR (salivation).
• Step 4: The neutral stimulus has become a conditioned stimulus, which elicits a conditioned response.
  • CS (bell) → CR (salivation).

Operant Conditioning

• Voluntary:
  • You perform certain behaviors because you expect that they will yield certain consequences.
• Reinforcement: The consequence increases the chance you will perform that behavior again in the future.
  • E.g., mouse turns left → gets a fruit loop (more likely to turn left in the future).
• Punishment: The consequence decreases the chance you will perform that behavior again in the future.
  • E.g., mouse turns left → gets shocked (less likely to turn left in the future).

Early Views of Types of Memory

• Recent research has changed the distinction between STM and LTM, and is updated from what is listed below.
• Short-term memory (STM): Memory of events that have just occurred.
  • Limited capacity (~5–9 items).
  • Fades quickly without rehearsal (less than a minute).
  • Cannot be stimulated with a cue/hint; once forgotten, the memory is lost.
• Long-term memory (LTM): Memory of events from times further back.
  • No limited capacity.
  • You can reconstruct LTM that you haven’t thought about in a long time, although accuracy may decrease.
  • Can be stimulated with a cue/hint.
• Research once proposed all information enters STM and the brain consolidates it into LTM.
  • Later research disproved this simple distinction.

Consolidation

• Consolidation: Strengthening a memory to make it longer lasting.
• Later research weakened the distinction between STM vs. LTM:
  • Not all rehearsed STM becomes LTM.
  • The time needed for consolidation varies.
• Emotionally significant memories form quickly:
  • Flashbulb memories: Emotional events that are remembered in vivid detail.
  • The locus coeruleus (in the pons) is excited, releasing norepinephrine in the cerebral cortex and dopamine in the hippocampus.
  • Emotional events trigger epinephrine and cortisol.

Working Memory

• Working memory (WM): Temporary storage of information to actively attend to it and work on it for a period of time.
  • Expands on the concepts of STM and LTM.
• A common test of WM is the delayed response task:
  • Keeping a representation of the stimulus in the brain during a delay when you can no longer sense the object.
  • Screen comes down → brain activity represents where the food stimulus is.
• The prefrontal cortex is involved in storing this representation:
  • Damage impairs performance.
  • Declining activity of the prefrontal cortex in the elderly is associated with memory decline.

Anterograde and Retrograde Amnesia

• Amnesia: Loss of declarative/explicit memories (episodic/semantic).
  • Two major types of amnesia:
    • Anterograde amnesia: Loss of the ability to form new declarative memories after the brain damage.
    • Retrograde amnesia: Loss of old declarative memories of events prior to the occurrence of brain damage.
  • Patient H.M. showed both types of amnesia after his surgery; however, the anterograde amnesia was more extreme.

Memory in Patient H.M.

• H.M.’s WM remained intact:
  • Was able to remember a number after 15 minutes without distraction.
  • When distracted, the memory was gone in seconds.
• H.M. showed impairments in explicit/declarative long-term memory:
  • Not being able to state the date or his age.
  • Read the same magazine repeatedly without losing interest.
  • Was able to form some very limited new semantic memories.
    • Semantic memory: Memories of facts and concepts.
      • Memories of facts such as the last name of a famous person.
      • New semantic memories were still very impaired; old semantic memories were not as impaired.
• Severe impairments in episodic memory:
  • Episodic memory: Memories of personal experiences and events.
    • Could not form new memories of personal events from his life.
    • Would not remember what he did that day.
• Better implicit than explicit memory:
  • Explicit/declarative memory: Deliberate and conscious recall of information.
    • Consciously remembering that a person was kind to you.
  • Implicit memory: An unconscious influence of experience on behavior.
    • Unconsciously remembering someone was kind to you (you think they are friendly but don’t know why).
• Intact procedural memory.

Function of the Hippocampus

• Research on hippocampus function suggests it is critical for declarative memory functioning, especially episodic memory.
• It is hypothesized that the hippocampus connects to the regions needed to recall and consolidate information:
  • Various parts of a memory are stored in different brain areas.
  • The hippocampus reconstructs this context so we can recall episodic memory, and allows us to consolidate that context into LTM.
  • Damage leads to severe anterograde amnesia.
    • Personal experiences are exhibited in working memory but never get consolidated into conscious memory.
• Damage to the hippocampus also impairs abilities on spatial memory tasks such as:
  • Radial maze: A subject must navigate a maze that has 8+ arms, with a reinforcer at the end.
  • Morris water maze: A rat must swim through opaque water to find a resting platform just underneath the surface.

Entorhinal Cortex

• Entorhinal cortex: Limbic system structure located in the medial temporal lobe.
  • Important for forming new semantic memories.
  • H.M. had both the hippocampus and the entorhinal cortex removed.
• The hippocampus and anterior temporal cortex are also important for semantic memories:
  • The entorhinal cortex connects the hippocampus to the cerebral cortex.

Striatum

• Striatum: Part of the basal ganglia (caudate nucleus and putamen).
  • Important for implicit and procedural memory.
    • People with damage to the striatum will have impairments in learning new motor skills.
    • H.M. had an intact striatum, so he was able to improve on reading words backward.

Amygdala

• Amygdala: Associated with fear learning.
  • Fear conditioning.
  • Urbach-Wiethe disease (genetic) and Klüver-Bucy syndrome (injury) involve a damaged amygdala.
    • People exhibited fearlessness.

Memory Disorders

• Two common types:
  • Korsakoff’s syndrome:
    • Brain damage caused by prolonged thiamine (vitamin B1) deficiency.
      • Impedes the brain’s ability to metabolize glucose.
      • Leads to a loss of or shrinkage of neurons in the brain.
    • Often due to chronic alcoholism.
      • Alcohol limits the body’s ability to absorb vitamins.
      • The majority of damage is in the thalamus and hypothalamus (mammillary bodies).
    • Symptoms:
      • Confabulation: The production of fabricated, distorted, or misinterpreted memories.
  • Alzheimer’s disease:
    • A neurodegenerative disease characterized by the loss of memory beyond that of normal aging, particularly explicit/declarative (episodic and semantic) memories.
    • Affects ~3% of people aged 65–74 and potentially ~32% of people over age 85.
    • Two types of Alzheimer’s disease:
      • Late-onset: Occurs at ages 65+.
        • Has genetic (APOE gene) and environmental components.
      • Early-onset: Occurs before the age of 65 (usually in the 40s–50s).
        • Mainly has a genetic component (PSEN1, PSEN2, APP genes).
    • Accumulation and clumping of toxic proteins in the brain, mostly starting in the cerebral cortex and hippocampus but spreading to other areas as the disease progresses.
      • Amyloid-beta protein: Accumulates into “plaques”.

How Are Memories/Learning Stored in the Brain?

• Not every physiological change in the brain is going to be a memory.
• Hebbian synapse: A synapse that increases in effectiveness because of simultaneous activity in the presynaptic and postsynaptic neurons.
  • Neurons that are near each other and fire together, wire together.
  • Pavlov’s dog:
    • Axon A is strongly activated by the sight of food (US) → causes salivation (UR).
    • Axon B is simultaneously activated by the bell (CS) → weaker salivation (CR).
    • A and B are paired together; the effects of B increase.

Examining Aplysia to Understand the Physiology of Learning

• Studies of how physiology relates to learning often focus on invertebrates and try to generalize to vertebrates:
  • The nervous system is organized differently, but many aspects are generalizable.
    • Action potentials, neurons, neurotransmitters, receptor binding.
• Aplysia (sea slug) is a commonly studied invertebrate:
  • Fewer number of neurons.
  • Neurons are nearly identical between individuals.
  • Neurons are very large.

Aplysia Withdrawal Response

• Withdrawal response: Touching the siphon, mantle, or gill causes that structure to withdraw.
• Used to study basic processes, such as habituation and sensitization.

Habituation

• Habituation: A decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli.
  • Clock ticking: Seems loud at first, then you ignore it.
  • Smelly food: Strong smell at first, but you notice it less later.
  • The stimulus does not change, but your response to it does.
• Withdrawal response of Aplysia:
  • The gill stops retracting after repeated presentations of the stimulus.
    • Not due to muscle fatigue or changes in the sensory neurons.
  • Sensory neurons fail to excite motor neurons as they did previously.

Sensitization

• Sensitization: An increase in response to a mild stimulus as a result of previous exposure to more intense stimuli.
• Aplysia: A strong shock to the tail (intense stimulus) will cause a touch to the siphon (mild stimulus) to produce a more intense withdrawal response in the future.
  • An intense stimulus causes a facilitating interneuron to release serotonin to multiple sensory neurons.
  • Serotonin blocks the potassium channels in the sensory neurons.
  • The action potential of the mild stimulus lasts longer than normal, causing more neurotransmitters to be released.
  • The motor response is enhanced from that mild stimulus.

Long-Term Potentiation and Long-Term Depression

• Long-term potentiation (LTP): Occurs when one or more axons bombard a dendrite with stimulation; this leaves the synapse “potentiated” for a period of time and the neuron is more responsive.
  • Specificity: Only highly active synapses are strengthened.
  • Cooperativity: Simultaneous stimulation by two axons produces LTP more strongly than repeated stimulation by one axon.
  • Associativity: Pairing a weak input with a strong input enhances later responses to the weak input.
• Long-term depression (LTD): A prolonged decrease in response at a synapse that occurs when axons have been less active than others.

Biochemical Mechanisms of LTP

• LTP depends on changes at glutamate synapses (and to a lesser extent GABA synapses).
• Two major types of glutamate receptors:
  • AMPA receptors and NMDA receptors:
    • Both are ionotropic receptors.
    • When glutamate binds to AMPA receptors, Na+ flows into the post-synaptic neuron.
    • NMDA receptors have a magnesium ion blocker; when glutamate binds to NMDA receptors, Na+ initially still cannot enter.
      • The magnesium blocker will move depending on the membrane potential.

Calcium’s Role in LTP

• Calcium is needed for LTP.
• Calcium activates the protein CaMKII:
  • Causes more AMPA receptors to be inserted into the postsynaptic neuron’s membrane.
  • Leads to increased dendritic branching.
• The postsynaptic cell becomes more sensitive to glutamate (is potentiated).
• CaMKII also activates the protein CREB, which can cause epigenetic changes.
• LTD involves the opposite process, where a lack of calcium leads to a recession of AMPA receptors.

How We Get LTP: Step-By-Step

1. Repeated glutamate excitation of AMPA receptors depolarizes the membrane.
2. Depolarization displaces magnesium molecules that had been blocking NMDA receptors.
3. Glutamate is then able to excite NMDA receptors, opening a channel for Ca2+ to enter the neuron.
4. The entry of calcium through the NMDA channel activates CaMKII, with the activation of the CaMKII protein setting a series of events in motion.
5. More AMPA receptors are built and dendrite branching is increased.
6. These changes potentiate the dendrite’s future responsiveness to incoming glutamate (the synapse is strengthened).

Presynaptic Changes

• Changes in the presynaptic neuron can also cause LTP.
• Retrograde transmitter: Extensive stimulation of a postsynaptic cell causes the release of a neurotransmitter that travels back to the presynaptic cell.
• This retrograde transmitter is often nitric oxide (NO), which causes the following effects on the presynaptic neuron, making it more likely to fire an action potential and achieve LTP:
  • Decreases its action potential threshold.
  • Increases neurotransmitter release.
  • Expands the axon.
  • Releases neurotransmitters from additional sites.

Improving Memory

• Mechanisms of change impacting LTP may lead to drugs that improve memory.
• Caffeine and Ritalin enhance learning by increasing arousal.
• Herbs have doubtful effects.
• Altering gene expression in mice (e.g., more NMDA receptors):
  • Can cause chronic pain.
  • Slight benefits to certain types of memory.
  • Improvements come with a cost.
    • Generally impairs a different type of memory.
• Behavioral methods are the best way to improve memory:
  • Studying and rehearsing.
  • Living a healthy lifestyle (exercise, eating healthy, sleeping, and managing stress).

Intelligence

• Intelligence involves multiple cognitive skills:
  • Learning, memory, problem-solving, etc.
  • Many of these skills are correlated with one another.
• Some scientists assume that there might be a single underlying factor “g”.
• The brain is related to intelligence.

Comparing Brains of Different Species

• Why are some animal species, such as humans, more intelligent than others?
• Does brain size matter?
  • Comparing families of animals: Larger brains show more intelligence.
  • Not true when comparing species of different families (e.g., humans vs. whales).
• Does the brain-to-body ratio matter?
  • Humans score well here, but it is still not entirely consistent.
• Does the total number of neurons in the brain matter?
  • Seems to be the best answer when comparing species.
  • Non-human intelligent animals also score well here (monkeys, crows, parrots, etc.).

Human Data: Men vs. Women

• If two individuals of the same species have the same size neurons, you might falsely assume the larger brain would have more neurons.
• In humans, the male brain is 10% larger than the female brain:
  • Men and women have roughly equal IQ.
• Women have deeper sulci (which makes the number of neurons about equal).
• Women’s brains are organized differently:
  • More efficient to make up for size.

Genetics and Environmental Influences

• Twin studies:
  • Monozygotic twins resemble one another more than dizygotic twins on intelligence, specific cognitive abilities, and brain volume.
  • The effect of genetics/heritability increases with age.
• People who inherit higher cognitive skills seek out more cognitively challenging environments:
  • Heritability has a smaller influence in poor living environments.
  • One needs a good environment to express those genetics.
• Slight mutations on common genes can cause intellectual impairments.
• Multiple genes correlate to academic success, but there is no single overarching gene.

Brain Evolution

• The organization and components of the nervous system are similar between species:
  • Differences are quantitative (size/number) instead of the type of structure/neuron.
• Cost efficiency plays a large role in how brains have evolved:
  • The brain is metabolically expensive (in humans, it is 2% of mass and 20% of fuel consumption).
  • Energy can be spent elsewhere (e.g., reproduction in fish).
• Humans devote a lot of time to development:
  • Cooperativity in humans can reduce parental burdens.

Chapter 13 - Cognitive Functions

Corpus Callosum and the Split-Brain Operation

• Epilepsy: A condition characterized by repeated episodes of excessive, synchronized neural activity (affects 1–2% of people).
  • Results in frequent and severe seizures.
• Anti-epileptic drugs block Na+ flow across the membrane or enhance GABA’s effects.
  • Most people with epilepsy respond to drugs.
• Surgical options:
  • Removing the focus point where seizures begin.
  • Corpus callosotomy: Cutting the corpus callosum such that the hemispheres can no longer communicate with one another, preventing epileptic signals from rebounding between hemispheres.
    • Individuals who have undergone the surgery are referred to as split-brain patients.

Specialization of the Right Hemisphere

• Left hemisphere:
  • Important for processes involving speech/language.
• Right hemisphere:
  • Important for comprehending spatial relationships.
  • Important for perceiving emotional stimuli.
• Although rare, people can be right-brain dominant for speech and left-brain dominant for spatial relationships/emotion.

Inactivated Left and Right Hemispheres

• We can explore these differences when we inactivate either the left or right hemisphere.
• Brain surgery patients with an inactivated left hemisphere:
  • Cannot produce speech.
• Brain surgery patients with an inactivated right hemisphere:
  • Can use speech to describe a traumatic/emotional event but cannot remember the emotions they felt during that event.

Hemispheric Specializations in Intact Brains

• Structurally, the two hemispheres are very similar to one another, but there are some minor anatomical differences.
• Planum temporale: Area of the temporal cortex that is larger in the left hemisphere in 65% of people.
  • Part of Wernicke’s area on the language-dominant side (usually the left).
  • Related to language processing.
  • The size of this area differs in infancy, indicating this is a difference individuals are born with.
• Other asymmetries in structure size/activity between the lobes exist, but they are much more minor:
  • May contribute to right-hand / left-hand preference.

Evolution and Physiology of Language

• Nonhuman animals can communicate with one another in the natural world, but they communicate through more limited and inflexible means:
  • Visual communication - body language.
  • Auditory communication - growling.
  • Tactile communication - hugging.
  • Chemical communication - pheromones.
• Human language is much more flexible and has very high productivity.
  • Productivity: The ability to improvise new combinations of signals to represent new ideas.

Nonhuman Precursors of Language

• Human language is likely a modification of a behavior also found in other species.
• We examine animals ancestrally close to us to explore how language has evolved.
• We can teach chimpanzees to communicate using sign language, but this communication is less developed than what we see in humans:
  • They rarely use symbols in new, original combinations (low productivity).
  • The use of symbols is primarily used to request and not to describe.

Bonobos

• Bonobos’ social order resembles humans’:
  • Male and female interactions and relationships.
  • May contribute to showing a better capacity for language.
• The most famous example involves the bonobos Kanzi and Panbanisha:
  • Understand more than they can produce.
  • Use symbols/names to describe objects.
  • Request items that are not seen.
  • Use symbols to describe past events.
  • Make original, creative requests.
  • Had a large lexicon of words (3000+), but syntax/grammar was not fully developed.
• Possible explanations for Kanzi’s and Panbanisha’s results:
  • Perhaps bonobos have greater language potential than other chimpanzees.
  • Language training began early.

Features of Language

• Language is a special category of communication that is able to be manipulated into a near-infinite amount of meaningful ways to represent different ideas:
  • Symbols: Cues used to represent an experience or object that you can share with someone else.
    • Words, gestures, and images.
  • Semantics: The meaning associated when combining symbols.
    • E.g., “the water is leaking from the bucket” vs. “the water is wordy from the bucket”.
  • Syntax: The system of grammatical rules by which the symbols are arranged.
    • E.g., “I drove my car to work” vs. “My car I work to drove”.
• Many animals can demonstrate symbols in the wild.
• Although not naturally developed, some animals can undergo language training to demonstrate semantics; however, very few, if any, can demonstrate consistent syntax.

What Do We Gain from Studying Nonhuman Language Abilities?

• Insights on how to best teach language to those who do not learn it easily:
  • Brain damage.
  • Autism.
• Indicates that language evolved from a precursor found in other species.
• The concept of language is ambiguous:
  • Need a more precise definition of language.
  • Controversial whether animals can use language due to limits in syntax/grammar.

How Did Humans Evolve Language?

• Language likely evolved from communication by gestures (symbols):
  • Primates communicate through gestures.
  • A child’s ability to communicate by gestures predicts the onset of spoken language.
  • Adults accompany language with gestures even when the listener cannot see them.
• Two main theories for how humans evolved language:
  • Byproduct of brain development/intelligence.
  • Specialized brain mechanisms.

Language as a Byproduct of Intelligence

• If this is true, a person with a full-sized brain and normal intelligence should then always have normal language ability:
  • Certain genes can cause difficulty in aspects of language, even when non-language intelligence remains the same.
• Williams syndrome: Intellectual disability characterized by decreased gray matter, especially in visual processing areas.
  • Retains skillful use of language.

Language as a Specialization

• Chomsky & Pinker proposed humans have a language acquisition device:
  • A built-in mechanism for acquiring language that humans are born with.
  • Evidence comes from the ease with which most children develop language.
  • Deaf children will make up their own sign language to teach one another.
• Why did humans develop language and not other animal species?
  • Human children are highly dependent on their parents for a long period of time.
  • Evolved as a byproduct of social interaction.

Sensitive Period and Bilingualism

• Research suggests a sensitive period exists for the learning of language:
  • The period is between birth to around age 6.
  • No early language exposure can lead to permanent impairment.
• Bilingualism:
  • There is no sharp cut-off period for learning a second language, but the ease of learning differs with age.
    • Learning after age 12 → rarely gain fluency equal to a native speaker.
    • Children excel at learning pronunciation and unfamiliar aspects of grammar.
    • Adults are better at memorizing vocabulary and gaining a lexicon.
  • Brain activity:
    • Learning a second language before age 6: Bilateral activity of brain hemispheres during speech.
    • Learning a second language after age 6: Only left brain hemisphere activity during speech (lateralization).

Sensitive Period and Deafness

• Deaf children who began sign language while young learn much better than those who started later.
• A child who learns a spoken language early can learn to use sign language later:
  • A deaf child who learns sign language early can learn a spoken language later.
• Rare cases of children not exposed to language indicate a limited ability to learn language later.
• While a lexicon of words can be learned at any age, syntax/grammar has a sensitive period in which it can develop:
  • Animals likewise can learn words but have issues with syntax/grammar.

Broca’s Aphasia (Non-Fluent Aphasia)

• Serious impairment in language production:
  • Damage is often limited to Broca’s area.
    • Speaking activates much of the brain, not just Broca’s area.
  • Have strong semantics but poor syntax.
• Typical characteristics:
  • Slow and awkward with all forms of language communication, not just spoken.
  • Improper grammatical use (rarely using pronouns, prepositions, helping verbs, and similar words).
  • Can understand most speech/semantics, except when the meaning depends on complex aspects of grammar.
  • Mnemonic: Broca’s banter is broken.

Wernicke’s Aphasia (Fluent Aphasia)

• Impaired language comprehension and ability to remember object names:
  • The person can still speak smoothly and with correct syntax/grammar.
  • Recognition of items is often not impaired; the ability to find the correct word is impaired.
  • Have strong syntax but poor semantics.
• Typical characteristics:
  • Articulate/fluent speech, except with pauses to find the right word.
  • Difficulty finding the word (anomia: Difficulty recalling the names of objects).
  • Poor language comprehension.
    • Difficulty understanding speech, writing, and sign language.

Consciousness of a Stimulus

• Consciousness: A person is in the presence of a stimulus and reports that they were aware of it.
  • Cannot observe directly; difficult to define.
  • This definition requires the individual to be a cooperative and healthy human (usually adults).
  • This definition does not apply to individuals who cannot talk (animals and infants).
• Studying consciousness:
  • Various ways to create experiments to study consciousness.
  • Compare brain responses between conscious and non-conscious groups.

Masking

• Masking: A brief visual stimulus is preceded and followed by longer interfering stimuli.
  • No masking (blank screen → WORD → blank screen):
    • Most participants were conscious of the word.
  • Masking (interfering stimuli → WORD → interfering stimuli):
    • Most participants were not conscious of the word.
• Compared brain activity when seeing the hidden word:
  • Both conditions activated the primary visual cortex.
  • More brain activity occurred in the conscious condition, and activity spread to other regions (prefrontal cortex and parietal cortex).

Fate of an Unattended Stimulus

• Information from unconscious stimuli is not discarded:
  • More likely to become conscious of meaningful stimuli.
    • Fading in words from your own language vs. another language.
    • Fading in a meaningful image vs. an unmeaningful image.
  • We determine if something is meaningful before we are consciously aware of it.
• Much of our brain activity is unconscious, and even unconscious activity can influence behavior.
• Theory: Consciousness is a threshold phenomenon.
  • If a stimulus activates enough neurons to a sufficient extent, the activity reverberates, magnifies, and extends over much of the brain.
  • If a stimulus fails to reach that level, the pattern fades away.

Timing of Consciousness

• Delays exist between an event and our consciousness of it.
• The phi phenomenon occurs when we see a dot in one position alternating with a similar dot nearby:
  • Appears as if the dot is moving back and forth.
  • The second position changed the perception of what occurred before.
• An obscure word changes based on the phrase:
  • “There was a *ent in the car” - dent.
  • “There was a *ent in the forest” - tent.
• A new stimulus can change the consciousness of what came before it.

Conscious and Unconscious People

• Loss of consciousness under anesthesia:
  • Decreased overall brain activity.
  • Decreased connectivity between the cerebral cortex and the thalamus, hypothalamus, and basal ganglia.
  • Initial recovery of consciousness involves reconnecting these areas.
    • Increased activity in the cortex.
• fMRI in a persistent vegetative state:
  • Asked to imagine playing tennis: The individual showed increased activity in motor areas of the cortex, similar to healthy subjects.
  • Asked to imagine walking in a house: The individual showed activity in other regions of the cortex, similar to healthy subjects.
  • Similar results were found in 4 of 53 patients.

Attention

• Attention is closely aligned with consciousness:
  • We are only conscious of the information we direct our attention toward.
• Inattentional blindness: Failing to be conscious of an object when our attention is directed elsewhere.
• Change blindness: Failing to notice if something in a complex scene changes slowly, or changes while your view is briefly blocked.

Brain Areas Controlling Attention

• Bottom-up attention: Reaction to a stimulus.
  • Attention is captured because some aspect of the stimulus stands out.
  • E.g., a deer runs past you in the park, grabbing your attention.
  • Mainly involves activity in the ventral parietal cortex.
• Top-down attention: Intentional.
  • Intentional guidance of attention based on your knowledge.
  • E.g., looking for someone you know in a crowd.
  • Mainly involves activity in the prefrontal cortex.

Stroop Effect

• Stroop effect: Ignoring the words “green, blue, etc.” and instead indicating their color of ink.
  • Increased activity in vision areas of the cortex associated with identifying color.
  • Decreased activity in vision areas of the cortex associated with identifying words.
• The ability to resist distraction varies among individuals:
  • Requires top-down attention to focus on specific stimuli.

Spatial Neglect

• Spatial/hemispatial neglect: The tendency to ignore items on one side of space, very commonly the left side of space.
  • E.g., ignoring the left side of objects or what one feels on the left side of the body.
• Associated with a loss of attention rather than impaired sensation:
  • Someone with spatial neglect can see an entire letter and what composes it (e.g., a circle made of smaller circles).
  • The same person ignores the left half when asked to cross out all the letters that compose a word.

Chapter 14 - Psychopathology

Substance Abuse: Drug Mechanisms

• Substance abuse: An addiction/dependence on a substance.
  • Often a drug such as alcohol, but can also be a habit such as gambling.
• Antagonist: A drug that blocks a neurotransmitter.
• Agonist: A drug that mimics or increases the effect of a neurotransmitter.
• Affinity: A drug’s tendency to bind to a receptor.
  • Low affinity: Rarely binds (weak).
  • High affinity: Commonly binds (strong).
• Efficacy: A drug’s tendency to activate the receptor.
  • Low efficacy: Rarely activates (antagonist).
  • High efficacy: Commonly activates (agonist).
  • High affinity + low efficacy = strong antagonist.
  • High affinity + high efficacy = strong agonist.

Predispositions

• Not all individuals develop addiction, but certain risk factors can make you more likely to:
  • Genetic influences:
    • Individual genes by themselves usually only have a small effect.
    • Multiple genes working together can put you much more at risk.
  • Environmental influences:
    • Prenatal environment and maternal alcoholism.
    • An unstable environment in childhood.
    • Environmental stressors in adulthood.
  • Interaction:
    • When genetic and environmental risk factors are combined, the person is much more at risk.

The Role of Dopamine in Addiction

• The effects of drugs are different (e.g., cocaine vs. alcohol), yet they are both addictive, and this addiction follows similar pathways.
• Dopamine plays a role in forming the addiction characterized in abuse:
  • Nucleus accumbens: A region in the basal forebrain that is very rich in dopamine and is central to the brain’s reinforcement system.
    • The ventral tegmental area (VTA) pathway sends dopamine to the nucleus accumbens.
  • Actions which cause the release of dopamine in the nucleus accumbens can become highly addictive (nicotine, sugar, cocaine, gambling).
• The role of dopamine may be somewhat overemphasized:
  • Many addictive drugs increase dopamine, but some not by much.
  • Reducing addiction by blocking dopamine doesn’t work.

Cravings, Tolerance, and Withdrawal

• Characteristics of addiction:
  • Craving: An insistent search for the substance.
    • Environmental cues can trigger cravings.
    • Cravings can occur after very prolonged periods without the substance (months/years).
  • Tolerance: Decreased effect of the drug after repeated use.
    • Strong initial effects fade (the same amount is no longer enough, so the drug is taken more frequently or in a larger dose).
    • Repeatedly taking the drug in a certain environment may make you more tolerant in that environment.
      • Can lead to an overdose when taking a drug in a place you’ve never taken it before.
  • Withdrawal: The body’s reaction to the absence of the drug.
    • Withdrawal symptoms will depend on the drug but can include sweating, anxiety, fatigue, shaking, and irritability.

Hypothesis for Addiction

• Addiction as a means to cope with stress and relieve withdrawal.
• Hutcheson (2001):
  • Rats learned to press a lever for a heroin injection.
  • Rats went through withdrawal for the first time; halfway through, half of the rats were given the lever (pressing it removed withdrawal symptoms) and the other half were not.
  • Rats went through withdrawal a second time; all rats were given a lever, but it no longer delivered heroin.
  • Rats that previously learned that lever presses would relieve withdrawal symptoms pressed it more frequently, even though it didn’t give them heroin this time.
• Addiction forms as a means to reduce the distress caused by withdrawal:
  • Can be generalized to stressful situations (craving the drug/habit).

Treatments

• Some addicts are able to decrease use or quit on their own.
• Social groups:
  • Alcoholics Anonymous or similar groups.
• Cognitive-behavioral therapy:
  • Contingency management: Rewards for remaining drug-free.
• Medications:
  • Alcohol:
    • Antabuse (disulfiram): Results in sickness after consuming alcohol.
    • Acamprosate: Normalizes chemical imbalances from alcohol abuse.
  • Heroin, morphine, and fentanyl (opioids):
    • Methadone, buprenorphine, levomethadyl acetate (LAAM): Still addicted, but cravings are satisfied in a safer way.
    • Naltrexone: Blocks opiate receptors, reducing the pleasurable effect.
      • Sometimes used to treat alcohol addiction.

Mood Disorders: Major Depressive Disorder

• Major depressive disorder: A condition in which people feel helplessness and an absence of happiness every day for weeks at a time.
  • An absence of happiness is a more reliable indicator than sadness.
  • The nucleus accumbens becomes less responsive to rewards.
  • 5–6% of adults in the U.S. and Canada have major depression.
    • 10% experience it at some point in their life.
    • More common in women than men after puberty.
  • Some people suffer from long-term depression.
    • It is more common to have periodic episodes of depression.

Depression: Genetics

• Moderate degree of heritability:
  • Multiple genes are associated with depression, some of which are more prevalent in certain populations.
• Two main types of depression (which seem to be linked to different genes):
  • Early-onset depression: Depression occurring in individuals before the age of 30.
    • More severe, longer-lasting episodes and suicidal tendencies.
    • Have close relatives with psychiatric issues (depression, anxiety, neuroticism, etc.).
  • Late-onset depression: Depression occurring in individuals aged 30 or older (usually 45–50).
    • Have close relatives with circulatory problems.
• Interaction between genes and environment:
  • Genes make one more at risk for developing depression.
  • Pain and stress (environment) trigger depression.

Depression: Brain Activity

• Abnormalities of hemispheric dominance:
  • Decreased activity in the left prefrontal cortex.
    • The behavioral activation system tied to happiness and approach is less active.
  • Increased activity in the right prefrontal cortex.
    • The behavioral inhibition system tied to avoidance is more active.
  • These abnormalities remain stable over the lifetime.
    • It is likely that depression isn’t causing abnormal hemispheric dominance, but rather individuals with this dominance have a predisposition toward depression.

Antidepressant Drugs

• Many drugs used to treat psychiatric disorders are discovered before we understand the processes behind the disorder:
  • The first antidepressant (iproniazid) was originally made to treat tuberculosis.
• Types of antidepressant drugs:
  • Tricyclics.
  • Selective serotonin reuptake inhibitors (SSRIs).
  • Serotonin norepinephrine reuptake inhibitors (SNRIs).
  • Monoamine oxidase inhibitors (MAOIs).
  • Atypical antidepressants.

How Antidepressants May Work

• Antidepressants increase the availability of serotonin and other neurotransmitters:
  • Initially, it was thought that depression is tied to a lack of serotonin and other neurotransmitters, but this no longer seems to be the case.
    • Some depressed individuals have normal or even increased serotonin levels.
    • Antidepressants affect neurotransmitters very quickly, but it takes at least two weeks to see behavioral effects.
• People with depression have lower than average levels of the neurotrophin brain-derived neurotrophic factor (BDNF):
  • BDNF is important for synaptic plasticity, learning, and the proliferation of new neurons in the hippocampus.
  • Antidepressants seem to increase BDNF levels over the course of weeks in the hippocampus.
  • Antidepressants may work through the proliferation of new neurons in the hippocampus.

Antidepressants: SSRIs

• Selective serotonin reuptake inhibitors (SSRIs): Drugs that block the reuptake of serotonin in the presynaptic terminal.
  • Block serotonin transporter proteins.
  • Blocking reuptake increases the concentration of serotonin in the synapse.
• Examples: fluoxetine (Prozac), sertraline (Zoloft), fluvoxamine (Luvox), citalopram (Celexa), paroxetine (Paxil).

Antidepressants: SNRIs

• Serotonin norepinephrine reuptake inhibitors (SNRIs): Drugs that block the reuptake of serotonin and norepinephrine.
  • Block serotonin and norepinephrine transporter proteins.
  • Blocking reuptake increases the concentration of serotonin and norepinephrine in the synapse.
• Examples: duloxetine (Cymbalta), venlafaxine (Effexor).

Altered Sleep Patterns

• Many individuals with depression suffer from sleep issues, with these issues commonly preceding changes in mood:
  • Falling asleep on time, but awakening early and being unable to fall back asleep.
  • Trouble sleeping is a risk factor for depression.
• Irregularities in sleep patterns:
  • Show a phase-advance in circadian activity (entering REM sooner than normal).
  • Activity matches a healthy individual going to sleep later than normal.
• Sleep deprivation can temporarily improve mood.
• Going to sleep earlier than normal (phase-advance) can temporarily return the sleep schedule to normal and improve mood.

Seasonal Affective Disorder (SAD)

• Seasonal affective disorder: Depression that reoccurs during a particular season, such as winter.
  • Thought to be caused by circadian rhythm irregularities due to a lack of sunlight.
  • Most prominent in winter and closer to the poles.
• Patients show a phase-delay in circadian activity (entering REM later than normal, the opposite of most individuals with non-seasonal depression).
• Many people with SAD have a mutation on a gene responsible for regulating circadian rhythms.
• Treatment often uses very bright lights in the morning:
  • Hypothesized to help regulate circadian rhythms (not conclusive).
  • Has shown potential improvements in individuals with non-seasonal depression.

Autism Spectrum Disorders (ASD)

• Autism spectrum disorder: A family of psychological disorders marked by impaired social and emotional exchange and other symptoms.
  • Includes varying degrees of impairment.
  • Prevalent throughout the world.
  • Four times more common in males than females.
• Characteristics/symptoms of ASD:
  • Deficits in social and emotional exchange.
  • Deficits in nonverbal communication (gestures, facial expressions, etc.).
  • Stereotyped behavior (repetitive movements).
  • Resistance to change in routine.
  • Unusually weak or strong responses to stimuli.

Causes of ASD

• Genetic causes:
  • Strong genetic effect: Multiple genes can cause autism, but there isn’t one main predictor gene.
    • Chromosomes often come from the father.
    • Older fathers are more at risk for having an autistic child.
• Prenatal causes:
  • Higher concordance rate in dizygotic twins than in siblings.
  • Mother exposed to large amounts of chemicals and air pollutants.
  • Some mothers of children with autism have antibodies that attack certain brain proteins.
  • Adequate amounts of folic acid during pregnancy halves the risk of having an autistic child.

ASD: Treatments

• Medical treatment:
  • No medical treatment exists for the central problems of decreased social behavior and communication.
  • Risperidone sometimes reduces stereotyped behaviors.
    • Can have serious side effects.
• Behavioral treatment:
  • Behavioral treatments focus on attention and reinforcing favorable behaviors.
  • Works in most but not all autistic children.