Psych Exam 3
Chapter 24: Memory — Concepts and Explanations
How do we know there are different types of memories?
Different types of memories exist because brain lesions affect different memory types differently. Some brain injuries impair one type (e.g., declarative memory) but not others (e.g., procedural memory), showing separate systems.
Examples of Memory Types:
Declarative Memory: Facts/events. Example: Knowing Bangkok is the capital of Thailand.
Procedural Memory: Skills/habits. Example: Learning how to ride a bike.
Associations: Classical conditioning. Example: Salivating at the sound of a bell because it was paired with food.
Emotional Responses: Stored in the amygdala. Example: Fear response to a previously neutral sound.
Basic Differences: Declarative vs. Non-Declarative Memories
Declarative (explicit): Conscious recall (facts, events).
Non-Declarative (implicit): Unconscious skills (motor responses, emotional reactions).
Differences: Working, Short-Term, and Long-Term Memory
Short-Term Memory: Lasts hours, vulnerable to disruption.
Working Memory: Lasts seconds, requires active rehearsal, very limited capacity.
Long-Term Memory: Stable over time, formed via consolidation.
How do we know these are different types?
Observations of patients: some lose short-term memory but keep long-term memory or vice versa, indicating distinct systems.
What is Consolidation?
The process of converting short-term memories into stable long-term memories.
Where is sensory information stored for short-term memories?
Likely in various cortical areas, depending on the sensory modality (visual cortex for sight, auditory cortex for sound).
Retrograde vs. Anterograde Amnesia
Retrograde Amnesia: Loss of memories before trauma.
Anterograde Amnesia: Inability to form new memories after trauma.
Evidence that memory storage changes over time
Retrograde amnesia shows a graded loss: more recent memories are more vulnerable, suggesting memories "move" or become more stable over time.
Hebb’s Model of Short-Term Memory
Hebb proposed that memories are stored as the activation of groups of interconnected neurons called cell assemblies.
Neurons and Memory of Stimuli
Perception neurons activate memory neurons through simultaneous activity, strengthening their connections.
What is a Cell Assembly?
A network of neurons that, once activated together, can reactivate each other, maintaining short-term memory.
Hebb’s Description of Consolidation
Consolidation occurs when repeated activation of a cell assembly leads to long-lasting changes (stronger connections).
If Memory Is Based on One Sensory Modality
It would be stored in the corresponding sensory cortex (e.g., visual information in visual cortex).
Experiment with Monkeys (Visual Information)
Delayed non-match to sample task: Monkeys with medial temporal lobe damage could not remember previously seen objects, showing visual memory depends on higher-order visual cortex areas like the inferotemporal cortex.
Inferotemporal Cortex: Location and Function
Location: Temporal lobe.
Function: Visual object recognition and long-term visual memory.
Experiment Figure 24.6
Single neuron recording: Neurons in inferotemporal cortex fire selectively to particular faces, suggesting visual memories are encoded there.
Temporal Lobe Stimulation (Humans)
Stimulating the temporal lobe sometimes evokes vivid memories, but not reliably, suggesting partial involvement but not straightforward memory storage.
H.M.’s Brain and Symptoms
Removed: Medial temporal lobes, including hippocampus.
Symptoms: Severe anterograde amnesia (could not form new declarative memories), intact procedural memory.
Brain Regions and Memory Types
Connections: Medial Temporal Lobe, Hippocampus, Diencephalon
Sensory input → Perirhinal & Entorhinal cortex → Hippocampus → Fornix → Mammillary bodies → Thalamus.
Delayed-Non-Match to Sample Task (DNMS)
Task showed monkeys with medial temporal lobe damage could not perform, supporting its role in memory.
Which Medial Temporal Lobe Area Is Most Important?
Hippocampus appears critical.
N.A.’s Brain Damage and Symptoms
Damaged: Dorsomedial thalamus.
Symptoms: Severe anterograde amnesia, some retrograde amnesia.
Korsakoff’s Syndrome
Damage: Mammillary bodies, thalamus.
Development: Chronic alcoholism → Thiamine deficiency.
Symptoms: Severe anterograde and some retrograde amnesia.
Hippocampus and 3 Memory Functions
Declarative Memory (facts/events).
Spatial Memory.
Relational Memory (relationships between different types of information).
Hippocampal Lesions in Rats
Radial Arm Maze: Rats forget which arms they already visited (spatial memory loss).
Morris Water Maze: Rats struggle to find hidden platform (impaired spatial learning).
Place Cells
Neurons in the hippocampus that fire when an animal is in a specific location.
Human Hippocampus and Memory
Damage leads to deficits in episodic memory, supported by H.M.’s case.
Relational Memory Hypothesis
Hippocampus stores relationships among items (rather than items individually), important for episodic memories.
Striatum and Procedural Memory Studies
Rats: Striatal lesions impaired habit learning.
Humans: Patients with Parkinson’s (striatal damage) showed impaired habit formation.
Prefrontal Cortex and Working Memory Studies
Monkeys: Prefrontal lesions impaired delayed-response tasks.
Humans: Damage caused problems in planning and task-switching (Wisconsin card-sorting test).
Class Notes
Overview
• Memory is a complex neurological process involving multiple brain systems
• Memories range from factual knowledge to ingrained motor patterns
• Learning and memory are lifelong adaptations of brain circuitry
Types of Memory
1. Declarative Memory (Explicit)
• Conscious recollection
• Easily formed and forgotten
• Includes:
• Facts
• Events
• Short-term memories
• Long-term memories
2. Non-Declarative Memory (Implicit)
• Non-conscious knowledge
• Long-term experience
• Less prone to forgetting
• Includes:
• Procedural memory
• Skills
• Habits
• Behaviors
• Associations
• Emotional responses
Memory Processes
Memory Consolidation
• Process of converting short-term to long-term memories
• Involves multiple brain regions
• Stages:
1. Sensory information intake
2. Short-term memory storage
3. Consolidation
4. Long-term memory storage
Memory Storage Regions
• Hippocampus:
• Declarative memory processing
• Spatial memory
• Recognition memory
• Relational memory
• Striatum:
• Procedural memory
• Habit learning
• Includes caudate nucleus and putamen
• Prefrontal Cortex:
• Working memory
• Problem-solving
• Planning behaviors
Amnesia Types
1. Retrograde Amnesia
• Forgetting previously known information
2. Anterograde Amnesia
• Inability to form new memories
3. Transient Global Amnesia
• Short-term memory loss
• Disorientation
• Repeated questioning
Key Concepts
Neural Basis of Memory
• Engram: Physical representation of memory
• Stored in:
• Neurons
• Neural circuits
• Firing patterns
• Synaptic connections
Hebb's Memory Model
• "Neurons that fire together, wire together"
• Memory distributed across linked cells
• Can involve neurons from sensation and perception
Research Insights
Experimental Evidence
• Studies on:
• Macaque monkeys
• Rat maze learning
• Temporal lobe patients (e.g., H.M.)
Brain Regions and Memory
• Different cortical areas contribute differently to learning
• Memories are distributed across multiple regions
Practical Implications
• Memory is adaptive
• Involves complex interactions between brain systems
• Can be affected by:
• Disease
• Trauma
• Neurological conditions
Conclusion
Memory is a dynamic, multi-system process crucial for learning, adaptation, and survival.
Chapter 22: Mental Illness — Concepts and Explanations
Freud and Skinner: Causes and Treatments of Mental Illness
Freud believed mental illness came from unconscious conflicts shaped by childhood experiences. His psychoanalysis method aimed to uncover hidden memories and resolve conflict.
Skinner rejected unconscious conflict ideas. He believed mental illness is learned maladaptive behavior. Treatment was behavior modification: replacing bad behaviors with positive ones.
Biological Breakthrough: General Paresis and Arsphenamine
General paresis (severe mental illness) was found to be caused by brain infection with syphilis bacteria (Treponema pallidum).
Arsphenamine (developed by Ehrlich) treated syphilis, showing that biological causes can underlie mental illness.
Anxiety Disorders
Normal Fear Response vs. Anxiety Disorder
Normal fear: Protective, appropriate reaction to real danger.
Anxiety disorder: Inappropriate or exaggerated fear response when there is no immediate threat.
Panic Disorder
Symptoms: Sudden intense terror, palpitations, shortness of breath, dizziness, fear of death or insanity.
Obsessive-Compulsive Disorder (OCD)
Obsessions: Intrusive, inappropriate thoughts (e.g., germs, harm, violence).
Compulsions: Ritualistic behaviors to reduce anxiety (e.g., hand washing, checking things).
Hypothalamic-Pituitary-Adrenal (HPA) Axis
Function: Orchestrates stress response: prepares the body for "fight or flight".
Amygdala and Hippocampus: Roles
Amygdala: Activates the HPA axis (initiates stress response).
Hippocampus: Inhibits the HPA axis, providing feedback to shut off stress once the threat is gone.
How Chronic Stress Affects the Hippocampus
Chronic cortisol exposure leads to hippocampal atrophy, which weakens its ability to regulate the HPA axis, worsening stress and anxiety.
Treatments for Anxiety Disorders
CRH Receptor Antagonists (new class): Block CRH receptors, potentially lowering stress response.
Affective Disorders (Depression and Bipolar)
Types:
Major Depression: Long periods of profound sadness, anhedonia.
Dysthymia: Chronic, low-grade depression.
Bipolar Disorder: Alternating periods of depression and mania.
Monoamine Hypothesis
Depression results from deficiency of monoamine neurotransmitters (serotonin and norepinephrine).
Monoamine Neurotransmitters:
Serotonin
Norepinephrine
Antidepressant Drugs
All increase monoamine levels in synapse, but relief of depression symptoms takes weeks, suggesting secondary brain changes are needed.
Long-Term Effects of Antidepressants
Promote hippocampal neurogenesis (new neuron formation) and increase glucocorticoid receptor expression, which helps regulate stress.
Diathesis-Stress Hypothesis
Depression arises from the interaction between genetic vulnerability (diathesis) and early life stressors that dysregulate the HPA axis.
Study on Early Sensory Experience and Stress Response
Rats with more maternal care had more hippocampal glucocorticoid receptors, better HPA feedback, and lower anxiety.
Lithium and Bipolar Disorder
Lithium stabilizes mood, likely by affecting second messenger systems like inositol signaling pathways.
Schizophrenia
Genetic and Environmental Evidence
Runs in families (genetic link), but early prenatal environmental factors also contribute.
Brain Changes
Enlarged ventricles, reduced cortex thickness, fewer interneurons.
Neurotransmitter Systems
Dopamine Hypothesis: Excess dopamine activity leads to schizophrenia.
Glutamate Hypothesis: NMDA receptor hypofunction causes symptoms.
Schizophrenia Symptoms Categories
Treatments for Schizophrenia
Conventional antipsychotics: Block D2 dopamine receptors (reduce positive symptoms).
Atypical antipsychotics: Act on multiple receptors (dopamine and serotonin) with fewer motor side effects.
Future therapies: Focus on enhancing NMDA receptor function.
Class Notes
Main Takeaway
This chapter explores the scientific understanding of mental illness, highlighting how neuroscience has transformed our perception of mental health from supernatural explanations to a complex interplay of biological, genetic, and environmental factors.
Introduction to Mental Health Disciplines
Neurology
• Branch of medicine concerned with diagnosing and treating nervous system disorders
• Helps illustrate physiological processes in brain function
Psychiatry
• Branch of medicine focused on diagnosing and treating disorders affecting the mind
• Examples of disorders: Anxiety disorders, affective disorders
Defining Mental Illness
• Definition: A diagnosable disorder of thought, mood, or behavior causing distress or impaired functioning
• Historically viewed as separate from bodily disorders
• Modern understanding recognizes complex interactions between biology and environment
Approaches to Understanding Mental Illness
Traditional Approaches
• Supernatural explanations
• Treatments involving spirit possession and rituals
Modern Psychosocial Approaches
• Secularized understanding
• Based on individual experiences
• Treatment relies on psychotherapy
Key Theoretical Perspectives
Sigmund Freud
• Emphasized the unconscious
• Key points:
1. Much of mental life is unconscious
2. Experience shapes unconscious and conscious life
3. Mental illness results from conflicts between unconscious and conscious elements
4. Psychoanalysis aims to uncover unconscious elements
B.F. Skinner
• Behavioral approach
• Behaviors (including maladaptive ones) are learned responses to environment
• Treatment focuses on behavior modification
Major Psychiatric Disorders
1. Anxiety Disorders
• Characteristics:
• Inappropriate expression of fear
• Approximately 15% of Americans experience annually
• Types:
• Panic disorder
• Agoraphobia
• Generalized anxiety disorder
• Specific phobias
• Social phobia
• Post-traumatic stress disorder (PTSD)
• Obsessive-compulsive disorder (OCD)
2. Affective Disorders
• Major Depression
• Diagnosis requires symptoms for > 2 weeks
• Symptoms include decreased interest, lowered mood, changes in appetite/sleep
• Bipolar Disorder
• Repeated episodes of mania and/or depression
• Types include Type I, Type II, and Cyclothymia
3. Schizophrenia
• Symptoms:
• Positive symptoms: Delusions, hallucinations
• Negative symptoms: Reduced emotional expression, speech difficulties
• Types:
• Paranoid schizophrenia
• Disorganized schizophrenia
• Catatonic schizophrenia
Biological Foundations
Genetic and Environmental Interactions
• Mental illnesses result from complex interactions between:
1. Genetic predispositions
2. Environmental factors
• Stress response regulated by hypothalamic-pituitary-adrenal (HPA) axis
Treatment Approaches
Anxiety Disorders
• Psychotherapy
• Medications:
• Benzodiazepines
• Serotonin-selective reuptake inhibitors (SSRIs)
• CRH receptor targeting drugs
Affective Disorders
• Electroconvulsive Therapy (ECT)
• Psychotherapy
• Antidepressants
• Deep Brain Stimulation
• Transcranial Magnetic Stimulation
• Psychedelics (in clinical settings)
Schizophrenia
• Drug therapy
• Psychosocial support
• Neuroleptic medications
• NMDA receptor drugs
Conclusion
Modern understanding of mental illness emphasizes:
1. Neuroscience's impact on psychiatry
2. Recognition of physical bases for mental illness
3. Complex interactions between genes and environment