Biopsych exam 4

Learning

  • Definition: Learning is a relatively permanent change in behavior due to experience. It improves with repetition.

Types of Learning:

  1. Classical Conditioning (e.g., Pavlov’s dogs)

    • Involves associating a neutral stimulus with a stimulus that naturally causes a response.

  2. Operant Conditioning (e.g., Thorndike’s cats)

    • Learning through consequences (rewards or punishments).

Hebbian Synapse (Mechanism of Learning):

  • Hebbian Plasticity: Repeated communication between two neurons (presynaptic and postsynaptic) strengthens their connection.

    • Synaptic Plasticity: The strength of synapses changes based on neuronal activity.

    • This is central to Long-Term Potentiation (LTP) and Long-Term Depression (LTD).

    • LTP: Prolonged increase in synaptic response.

    • LTD: Prolonged decrease in synaptic response.

  • Properties of LTP:

    • Specificity: Active synapses strengthen while inactive ones weaken.

    • Cooperativity: The more neurons involved, the stronger the LTP.

    • Associativity: Pairing a weak stimulus with a strong one increases LTP.

Memory

  • Atkinson-Shiffrin Model: Memory is like a computer (information is processed, stored, and retrieved).

    • Three Components:

      1. Sensory Register: Briefly stores sensations from the environment.

      2. Short-Term Memory (STM): Stores 7±2 items for 20-30 seconds.

      3. Long-Term Memory (LTM): Unlimited storage for long durations.

Brain Areas and Memory Types:

  1. Dorsolateral Prefrontal Cortex (DLPFC):

    • Active during STM tasks (e.g., Luria’s tapping test).

    • Damage impairs short-term memory.

  2. Long-Term Memory Areas:

    • Hippocampus: Involved in episodic (events) and spatial (locations) memory.

    • Damage to the hippocampus affects memory tasks with delays.

    • Lateral and Anterior Temporal Gyri: Involved in semantic memory (e.g., facts).

  3. Procedural Memory:

    • Involves skills and motor tasks, stored in the Striatum (part of the basal ganglia).

    • Cerebellum also plays a role in procedural memories (e.g., motor control).

Memory Types:

  • Non-declarative (Implicit) Memory: Includes procedural memory and classical conditioning.

  • Declarative (Explicit) Memory: Includes:

    • Episodic Memory: Memory of events.

    • Semantic Memory: Memory of facts and concepts.

    • Spatial Memory: Memory of locations and routes.

Key Findings from Articles:

  • Bartsch & Butler, 2013 (Transient Amnesic Syndromes):

    • Hippocampus Damage: Predicts poor memory performance on tasks with delays but does not affect procedural memory (e.g., mirror tracing task).

  • Binney et al., 2010:

    • Lateral and Anterior Temporal Gyri: Involved in semantic memory (e.g., facts). This article highlights the role of these brain regions in memory retrieval, particularly for facts and knowledge.

  • Elyoseph et al., 2020 (Machado-Joseph Ataxia):

    • Parkinson’s Disease: Affects procedural memory due to damage in the striatum. This article explores the impact of basal ganglia disorders on procedural learning.

  • Nuefeld & Mintz, 2001:

    • Classical Conditioning in Rats: The cerebellum and amygdala are involved in classical conditioning (e.g., eyeblink response to a light and shock pairing).

Emotions

  • Definition: Emotions are temporary states triggered by specific stimuli and have four aspects:

    1. Valence: Positive or negative value of the emotion (pleasant vs. unpleasant).

    2. Physiology: Involuntary bodily responses, influenced by the autonomic nervous system (e.g., sympathetic = high, parasympathetic = low).

    3. Behavior: Voluntary actions (e.g., approach vs. avoid).

    4. Cognition (Appraisal): How we determine the emotion.

Valence in the Brain:

  • Bipolar Hypothesis: Positive and negative emotions are opposites. Brain areas active during positive emotions should be less active during negative emotions.

  • Bivalent Hypothesis: Positive and negative emotions are separate but coexist. Different brain areas should be active during each.

  • Affective Workspace Hypothesis: Emotions occur in a general brain space, with the whole brain activated during both positive and negative emotions.

  • Key Article: Lundquist et al. (2016) supports the Affective Workspace Hypothesis, showing that whole-brain activation occurs during both positive and negative emotions.

Approach and Avoidance in the Brain:

  • Biopsychological Theory of Personality (Gray, 1970):

    • Behavioral Activation System (BAS): Reward system, associated with left frontal activation. Related to approach emotions like hope and happiness.

    • Behavioral Inhibition System (BIS): Punishment system, associated with right frontal activation. Related to avoidance emotions like fear and anxiety.

  • BIS Activation Example:

    • People high in BIS sensitivity avoid situations that may lead to negative experiences (e.g., avoiding clowns or hiding behind a parent when meeting strangers).

  • Key Article: Harmon-Jones (2006) explores how hand contraction (squeezing a stress ball) can influence approach-related emotions, showing the connection between physical actions and emotional response.

Threat and Fear:

  • Amygdala:

    • Part of the limbic system, the amygdala activates in response to threat-related stimuli like fear-inducing pictures or faces.

    • This activation is moderated by individual differences in anxiety proneness and emotion regulation ability.

  • Key Article: Balderston (Paper) discusses how the amygdala responds to emotional stimuli like fear and anger.

Emotion Regulation:

  • Definition: Emotion regulation is the ability to change one's emotional state.

    • Examples:

      • Suppression: Tamping down an unwanted emotion.

      • Reappraisal: Reframing a negative event in a positive way.

      • Mindfulness: Identifying and accepting an emotion without judgment.

  • Brain Regions Involved:

    • Dorsolateral Prefrontal Cortex (DLPFC): Important for regulating emotions, involved in complex mental processes required for goal-directed behavior.

  • Key Article: Lutz et al. (2014) studied mindfulness and its effects on the amygdala and DLPFC activation. They found that mindfulness reduces amygdala activation and increases DLPFC activation during emotional processing.

Stress

  • Definition: Stress is a negative situational experience, typically accompanied by emotional, behavioral, cognitive, and physiological responses.

Stress Response:

  1. Emotion: Negative emotional states motivate action to mitigate stress.

  2. Behavior: Fight (approach) or flee (avoid).

  3. Cognition: Focus on the stressor, making it hard to concentrate on anything else.

  4. Physiology: Bodily changes occur to help deal with stress (e.g., increased heart rate, blood pressure).

Acute Stress Response:

  1. Sympathetic-Adrenal-Medullary (SAM) Axis:

    • Activates quickly, releasing catecholamines (epinephrine and norepinephrine) from the adrenal medulla.

    • Increases heart rate, blood pressure, etc.

  2. Hypothalamic-Pituitary-Adrenal (HPA) Axis:

    • Slower response, releasing cortisol (a glucocorticoid) from the adrenal cortex.

    • Mobilizes energy and regulates inflammation.

Chronic Stress:

  • Dysregulation of SAM and HPA Axes:

    • Excessive cortisol release (Hypercortisolism): Linked to conditions like Cushing’s syndrome and depression.

    • Blunted cortisol response (Hypocortisolism): The body fails to respond effectively to stress, potentially leading to chronic stress-related health problems.

Physiological Effects of Chronic Stress:

  1. Not Adaptive:

    • Elevated Blood Pressure: Can lead to cardiovascular diseases like coronary heart disease.

    • Immune System Dysregulation: Immunosuppression, making the body more vulnerable to infections and diseases.

  2. Key Concept - Allostatic Load (McEwen & Stellar, 1993):

    • Allostasis: The body’s process of adapting to environmental stressors.

    • Allostatic Load: The wear and tear from constantly adapting to stress. More stress leads to more wear and tear on the body’s systems.

  • Chronic Stress Impacts:

    • Dysregulation of SAM and HPA can lead to cardiovascular disease, immune dysfunction, and mental health issues.

  • Key Article References:

    • Lundquist et al. (2016): Discusses valence in the brain.

    • Harmon-Jones (2006): Investigates physical actions influencing emotions.

    • Lutz et al. (2014): Studies mindfulness and brain activation in emotion regulation.

    • McEwen & Stellar (1993): Introduces the concept of allostatic load.

Psychological Disorders

Major Depressive Disorder (MDD)

  • Primary Clinical Features:

    • Dysphoria: Depressed mood (e.g., sad, tearful).

    • Anhedonia: Loss of interest or pleasure in activities.

    • Other Symptoms: Changes in appetite, sleep, psychomotor activity, fatigue, feelings of worthlessness, trouble concentrating, etc.

  • Functional Features:

    • Amygdala Activation: Increased negative emotion and stress.

    • Reduced Anterior Cingulate Cortex Activation: Impaired emotion regulation and error monitoring.

  • Neurotransmitters:

    • Monoamines (Serotonin, Norepinephrine, Dopamine): MDD is associated with low levels of these neurotransmitters.

    • Treatments:

      • SSRIs (Selective Serotonin Reuptake Inhibitors) prevent serotonin from being reabsorbed, increasing serotonin levels.

      • NDRIs (Norepinephrine-Dopamine Reuptake Inhibitors) prevent the reuptake of norepinephrine and dopamine.

      • MAO Inhibitors: Inhibit the enzyme that degrades monoamines, leaving more in the synapse.

      • Electroconvulsive Therapy (ECT): Stimulates the release of monoamines to improve mood.

      • Transcranial Magnetic Stimulation (TMS): Increases monoamine production and reduces amygdala activation.

  • HPA Axis Dysregulation:

    • High Cortisol: Predicts depression and is linked to conditions like Cushing’s syndrome.

Obsessive-Compulsive Disorder (OCD)

  • Primary Clinical Features:

    • Obsessions: Recurrent, distressing thoughts or impulses.

    • Compulsions: Repetitive behaviors or mental acts performed to reduce anxiety caused by obsessions.

    • Prevalence: 1-3% globally, 1.2% in the US, more common in women. Average onset is 19 years old.

  • Functional Features:

    • Limbic System Circuit: Abnormalities in the circuit (e.g., orbitofrontal cortex, basal ganglia) impair decision-making and impulse control.

    • Neurotransmitter Dysregulation:

      • Increased Glutamate (excitatory) and Decreased GABA (inhibitory).

      • Increased Dopamine contributes to OCD symptoms.

  • Treatments:

    • Benzodiazepines: Anxiolytic drugs that facilitate GABA binding to reduce anxiety.

    • TMS (Transcranial Magnetic Stimulation): Can reduce overactivity in the cortico-striato-thalamo-cortical (CSTC) circuit, improving OCD symptoms.

  • Key Article: Ruffini et al. (2009) found that TMS of the orbitofrontal cortex reduces OCD symptoms by modulating brain activity.

Schizophrenia

  • Primary Clinical Features:

    • Hallucinations: Sensory experiences that aren't real (usually auditory).

    • Delusions: Beliefs detached from reality (e.g., persecution).

    • Psychosis: Includes disorganized speech and behavior, loss of normal emotional responses.

  • Functional Features:

    • Associative Circuit Dysregulation: Disruptions in the prefrontal cortex and basal ganglia impair cognition and learning.

    • Impaired Cognition and Memory: Linked to abnormal brain circuitry.

  • Neurotransmitters:

    • Dopamine Hypothesis: Schizophrenia results from excessive dopamine (DA) activity in certain brain regions.

    • Origins: Amphetamines can block dopamine reuptake, leading to psychosis similar to schizophrenia.

    • Treatment: DA Antagonists (Antipsychotics/Neuroleptics): These drugs block dopamine receptors, reducing psychotic symptoms.

  • Key Article: Schizophrenia Simulator: This is a tool to simulate the effects of schizophrenia, which may help in understanding the disorder better.

Summary

  • Understand the Key Features of Each Disorder:

    • MDD: Look for low monoamines, especially serotonin, and HPA axis dysregulation (high cortisol).

    • OCD: Focus on limbic circuit dysregulation, especially overactivity in the orbitofrontal cortex and basal ganglia.

    • Schizophrenia: Understand the dopamine hypothesis and the role of overactive dopamine in the disorder.

  • Neurotransmitter Connections:

    • MDD involves low serotonin, norepinephrine, and dopamine.

    • OCD has increased glutamate and dopamine, and decreased GABA.

    • Schizophrenia is marked by too much dopamine.

  • Treatments:

    • MDD: SSRIs, NDRIs, MAO inhibitors, ECT, TMS.

    • OCD: Benzodiazepines, TMS.

    • Schizophrenia: DA antagonists (antipsychotics).

  • Key Articles:

    • Ruffini et al. (2009): TMS reduces OCD symptoms.

    • Schizophrenia Simulator: Provides insight into the experience of schizophrenia.