psych 202: final exam

Chapter 2: Cells and Structures of the Nervous System

Cells of the Nervous System

• Neurons: Basic unit of the nervous system

  • Receive, integrate, and transmit information

• Glial cells: Support and protect neurons

  • Astrocytes, microglia, oligodendrocytes (CNS), Schwann cells (PNS)

Anatomy of a Neuron

• Dendrites: Receive information

• Cell body (soma): Integrates information

• Axon: Conducts information

• Axon terminals: Release neurotransmitters

Synapse

• Junction between neurons

• Includes presynaptic membrane, synaptic cleft, postsynaptic membrane

Neural Communication

• Electrical: Within neuron

• Chemical: Between neurons (neurotransmitters)

Nervous System Organization

• Central Nervous System (CNS): Brain and spinal cord

• Peripheral Nervous System (PNS): Cranial and spinal nerves

  • Somatic (voluntary)

  • Autonomic (involuntary): Sympathetic (fight or flight), Parasympathetic (rest and digest)

Chapter 3: Neurophysiology

Resting Membrane Potential

• Difference in electrical charge across the membrane

• Inside is negative relative to outside

• Maintained by sodium-potassium pump (3 Na+ out, 2 K+ in)

Action Potential

• Rapid reversal of membrane potential

• All-or-none response

• Threshold of excitation (~-40mV)

• Phases: Depolarization, Repolarization, Hyperpolarization

Synaptic Transmission

• Arrival of action potential at axon terminal causes release of neurotransmitter

• Neurotransmitter binds to receptors on postsynaptic membrane

• Types: Ionotropic (fast), Metabotropic (slow)

Neurotransmitters

• Examples: Acetylcholine, Dopamine, Serotonin, GABA, Glutamate

Chapter 4: The Chemical Bases of Behavior

Neurotransmitter Systems

• Cholinergic (Acetylcholine): Learning, memory

• Dopaminergic: Motor control, reward

• Noradrenergic: Alertness

• Serotonergic: Mood, sleep

Drugs and Behavior

• Agonists: Enhance neurotransmitter action

• Antagonists: Block neurotransmitter action

Chapter 5: Hormones and the Brain

Hormone Types

• Peptide, Amine, Steroid

Endocrine Glands

• Pituitary (master gland), adrenal, thyroid, gonads

Stress Response

• HPA axis: Hypothalamus → Pituitary → Adrenal cortex → Cortisol

Chapter 7: Life-Span Development of the Brain and Behavior

Neurodevelopmental Stages

• Neurogenesis, Cell migration, Differentiation, Synaptogenesis, Neuronal cell death, Synapse rearrangement

Influences on Development

• Genetics, Environment, Experience

Chapter 8: General Principles of Sensory Processing, Touch, and Pain

Sensory Processing

• Labeled lines, Receptor cells, Sensory transduction

Somatosensory System

• Touch: Merkel’s discs, Meissner’s corpuscles, Pacinian corpuscles, Ruffini’s endings

• Pain: Nociceptors, A-delta fibers (fast), C fibers (slow)

• Pain modulation: Endogenous opioids

Chapter 9: Hearing, Vestibular Perception, Taste, and Smell

Auditory System

• Outer, middle, inner ear

• Cochlea: Hair cells, basilar membrane

• Auditory pathways: Cochlear nuclei, superior olivary nuclei, inferior colliculus, medial geniculate nucleus, auditory cortex

Vestibular System

• Semicircular canals, otolith organs

Taste

• Papillae, taste buds

• Five basic tastes: Sweet, sour, salty, bitter, umami

Smell (Olfaction)

• Olfactory epithelium, olfactory bulb

Chapter 10: Biological Rhythms and Sleep **

Circadian Rhythms

• Suprachiasmatic nucleus (SCN): Circadian clock, receives direct light information (from ganglion cells)

  • Lesions eliminate circadian rhythms

  • Transplant experiment: when adult hampsters received a transplant of SCN tissue from a donor hamster, the recipients adopted the donor's circadian rhythm, demonstrating the SCN's critical role in regulating these biological cycles.

• Retinohypothalamic pathway: Specialized retinal ganglion cells → send light information → SCN

• Melatonin: Secreted by pineal gland at night

Sleep Stages (EEG)

1. Alert, awake: Desynchronized EEG

2. Non-REM sleep

   • Stage 1: Vertex spikes

     • note: reticular formation

   • Stage 2: Sleep spindles

   • Stage 3 (SWS): Delta waves

     • note: basal forebrain

3. REM sleep: Paradoxical sleep

   • note: pons

Sleep Disorders

• Orexin: A lack of orexin, which helps keep us awake, causes narcolepsy with extreme sleepiness and sudden sleep attacks

• Sleep apnea: when breathing stops and starts during sleep, causing poor rest. It can be caused by a blocked airway or brain issues

• REM behavior disorder (RBD): people act out their dreams during sleep, sometimes with violent movements

Sleep Physiology

• Basal forebrain: Promotes slow-wave sleep (SWS) and helps initiate deep sleep by releasing acetylcholine

• Hypothalamus (VLPO): Sends GABA to arousal centers; regulates the sleep-wake cycle and circadian rhythms

• Reticular formation: Regulates wakefulness and helps control the transition between sleep and wake states, maintaining alertness

• Pons: key role in REM sleep and controls muscle paralysis during REM to prevent acting out dreams

• Molecular clock steps

  1. Clock/Bmal1 dimers promote the transcription of Per and Cry genes.

  2. Per and Cry proteins interact with tau proteins to form Per/Cry/tau complexes.

  3. These complexes inhibit the Clock/Bmal1 dimers, halting the transcription of new Per and Cry proteins.

  4. Per, Cry, and tau proteins degrade over 24 hours, resetting the cycle.

  5. The process is influenced by melanopsin in the retina, which sends light information to the SCN, helping synchronize the cycle with the environment.

  6. Glutamate activation in the SCN helps maintain and regulate the cycle

Chapter 11: Emotions and Stress

Neural Mechanisms

• Brain-self stimulation: Electrical stimulation (septum)

• Fear conditioning: Neutral stimulus + unpleasant stimulus → fear response

• Polygraph test: Measures heart rate, blood pressure

• Relaxation training: Mindfulness-based stress reduction (MBSR)

Conditions & Disorders

• Capgras delusion: Believe loved ones are impostors (low-road connection damage)

• Maternal aggression: Mother defending offspring

• Decorticate (sham) rage: Sudden rage without clear direction

• Klüver-Bucy syndrome: Reduced fear/anxiety (bilateral amygdala damage)

Stress Response

• Adrenal medulla: Releases epinephrine (E) & norepinephrine (NE)

• HPA axis: Hypothalamus → anterior pituitary → adrenal cortex

  • ACTH → adrenal corticosteroids (e.g., cortisol)

  • Glucocorticoid receptors: Respond to cortisol, form stress/fear memories

Stress Pathways

1. FAST: Hypothalamus → adrenal medulla → E & NE

2. SLOW: Hypothalamus → CRH → anterior pituitary → ACTH → adrenal cortex → cortisol

Effects of Stress

• Amygdala activity increases

• PFC activity decreases

Theories of Emotion

• Folk psychology: Emotion → autonomic arousal

• James-Lange: Autonomic arousal → emotion

  • Facial feedback hypothesis: Sensory feedback from facial expressions affects mood (James-Lange theory)

• Cannon-Bard: Simultaneous emotion & arousal

• Schachter-Singer Theory (Two-Factor Theory of Emotion): Perception + arousal → emotion

  • Experiment (1962):

    • Epinephrine (uninformed): Increased emotional response

    • Epinephrine (informed): No increase in emotional response

    • Participants' emotions matched the context (happy or angry), showing that interpretation of arousal influenced emotion.

Constructing Emotions

• Low Road (Fast): Thalamus → Amygdala (Lateral Nucleus). Quick, unconscious emotional reactions.

  • High Road (Slow): Thalamus → Sensory Cortex → Amygdala. Slower, conscious evaluation.

• Lateral Nucleus: Main input region of the amygdala, receives sensory info.

  • Central Nucleus: Main output region, triggers emotional responses (via hypothalamus and brainstem).

• Key cortical areas modulating emotion:

  • Insula: Bodily awareness and emotional feelings.

  • Cingulate Cortex: Emotional regulation and attention.

  • Prefrontal Cortex (PFC): Interprets and regulates emotional responses

Chapter 12: Psychopathology

Defining Psychopathology

• Psychopathology: The study of mental disorders, including their symptoms, etiology (origins), and treatment.

• Criteria for diagnosis often include distress, dysfunction, and deviance.

Major Categories of Psychiatric Disorders

• Schizophrenia Spectrum Disorders

  • Characterized by psychosis, hallucinations, delusions, disorganized thinking.

• Mood Disorders

  • Includes depression and bipolar disorder.

• Anxiety Disorders

  • Includes generalized anxiety, panic disorder, phobias.

• Obsessive-Compulsive and Related Disorders

  • Includes OCD, body dysmorphic disorder.

• Trauma- and Stressor-Related Disorders

  • Includes PTSD and acute stress disorder.

Biological Basis of Schizophrenia

• Dopamine Hypothesis: Overactivity of dopamine pathways (particularly D2 receptors) contributes to positive symptoms.

• Glutamate Hypothesis: NMDA receptor hypofunction may contribute to cognitive symptoms.

• Structural Abnormalities:

  • Enlarged ventricles

  • Reduced hippocampus, amygdala, and thalamus volumes

• Hypofrontality: Reduced activity in the frontal lobes.

Depression and Bipolar Disorder

• Monoamine Hypothesis: Depression results from deficits in serotonin, norepinephrine, and/or dopamine.

• HPA Axis Dysregulation: Elevated cortisol levels linked to depression.

• Brain Changes:

  • Reduced hippocampal volume

  • Increased amygdala activity

• Bipolar Disorder: Alternating periods of mania and depression; may involve dysregulated dopamine signaling.

Anxiety Disorders

• Amygdala Hyperactivity: Increased fear responses.

• GABAergic Dysfunction: Reduced inhibitory neurotransmission may underlie anxiety.

• Treatment:

  • Benzodiazepines enhance GABA activity.

  • SSRIs increase serotonin availability.

PTSD (Post-Traumatic Stress Disorder)

• Amygdala: Hyperresponsive to trauma cues.

• PFC: Hypoactivity may fail to inhibit fear responses.

• Hippocampus: Reduced volume may impair context processing.

• Treatment: CBT, exposure therapy, SSRIs.

Obsessive-Compulsive Disorder (OCD)

• Cortico-striato-thalamo-cortical (CSTC) circuit dysfunction

• Serotonin Hypothesis: SSRIs are effective treatments.

Treatments for Psychopathology

• Pharmacotherapy:

  • Antipsychotics (e.g., D2 antagonists)

  • Antidepressants (SSRIs, MAOIs, tricyclics)

  • Mood stabilizers (e.g., lithium)

  • Anxiolytics (e.g., benzodiazepines)

• Psychotherapy:

  • Cognitive Behavioral Therapy (CBT)

  • Exposure therapy

• Neuromodulation:

  • Electroconvulsive Therapy (ECT)

  • Transcranial Magnetic Stimulation (TMS)

Chapter 13: Learning and Memory

Types of Memory

• Declarative (Explicit) Memory: Facts and events; consciously recalled

  • Episodic memory: Personal experiences (e.g., first day of school)

  • Semantic memory: Factual knowledge (e.g., capital cities)

• Nondeclarative (Implicit) Memory: Skills and habits; does not require conscious thought

  • Procedural memory: Motor skills (e.g., riding a bike)

  • Priming: Exposure to one stimulus influences response to another

  • Conditioning: Classical and operant learning associations

Brain Regions Involved in Memory

• Hippocampus: Critical for consolidation of declarative memories; spatial memory (place cells)

• Amygdala: Emotional memory; fear conditioning

• Cerebellum: Procedural learning, motor memory, classical conditioning

• Prefrontal Cortex (PFC): Working memory, decision making

• Mammillary bodies and Thalamus: Memory relay; implicated in Korsakoff’s syndrome

Memory Processes

• Encoding: Converting sensory input into a form that can be stored

• Consolidation: Stabilization of memory traces (sleep plays a key role)

• Storage: Retention of information over time

• Retrieval: Accessing stored information when needed

• Reconsolidation: Memories become unstable when retrieved and need to be restabilized

Long-Term Potentiation (LTP)

• Persistent strengthening of synapses based on recent activity

• Found primarily in the hippocampus

• Involves NMDA and AMPA receptors

• Basis for synaptic plasticity and memory formation

Memory Disorders

• Amnesia

  • Retrograde amnesia: Loss of pre-existing memories

  • Anterograde amnesia: Inability to form new memories (e.g., H.M.)

• Korsakoff’s Syndrome: Thiamine deficiency; damages mammillary bodies; severe anterograde amnesia and confabulation

• Alzheimer’s Disease: Progressive loss of memory; neurofibrillary tangles and amyloid plaques

Chapter 15: Schizophrenia, Affective Disorders, and Anxiety Disorders

Schizophrenia

• Symptoms:

  • Positive: Hallucinations, delusions

  • Negative: Flat affect, social withdrawal

• Dopamine Hypothesis: Overactivity of dopamine, especially at D2 receptors.

• Treatments: Antipsychotics (D2 antagonists)

Depression (Affective Disorders)

• Monoamine Hypothesis: Low levels of serotonin, norepinephrine, or dopamine.

• HPA Axis Dysfunction: Elevated cortisol linked to depressive symptoms.

• Treatments:

  • Antidepressants: SSRIs, MAOIs, tricyclics

  • Electroconvulsive Therapy (ECT)

  • Cognitive Behavioral Therapy (CBT)

Anxiety Disorders

• Types: Generalized anxiety, panic disorder, phobias

• Mechanisms:

  • Amygdala hyperactivity

  • GABAergic dysfunction

• Treatments:

  • Benzodiazepines (enhance GABA)

  • SSRIs

  • CBT

Chapter 16: Autism Spectrum Disorder, ADHD, and Stress-Related Disorders

Autism Spectrum Disorder (ASD)

• Core features: Social communication deficits, restricted/repetitive behaviors.

• Associated with: Theory of mind deficits, sensory sensitivities.

Attention-Deficit/Hyperactivity Disorder (ADHD)

• Symptoms: Inattention, hyperactivity, impulsivity.

• Neurobiology: Dopamine dysregulation in frontal-striatal circuits.

• Treatments: Stimulants (e.g., methylphenidate), behavioral interventions.

Post-Traumatic Stress Disorder (PTSD)

• Symptoms: Re-experiencing trauma, avoidance, hyperarousal.

• Neural basis: Amygdala hyperactivity, reduced PFC regulation, hippocampal atrophy.

• Treatments: CBT (exposure therapy), SSRIs

Chapter 16: Autism Spectrum Disorder, ADHD, and Stress-Related Disorders

Autism Spectrum Disorder (ASD)

• Social communication deficits, restricted interests

• Theory of mind deficits

ADHD

• Inattention, hyperactivity, impulsivity

• Treatments: Stimulants (methylphenidate)

PTSD

• Re-experiencing trauma

• Hyperarousal

• Treatments: Cognitive-behavioral therapy (CBT), SSRIs